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PubMed1999

Effects of omega-agatoxin IVA, a P-type calcium channel antagonist, on the development of spinal neuronal hyperexcitability caused by knee inflammation in rats.

Both N- and P-type high-threshold calcium channels are located presynaptically in the CNS and are involved in the release of transmitters. To investigate the importance of P-type calcium channels in the generation of inflammation-evoked hyperexcitability of spinal cord neurons, electrophysiological recordings were made from wide-dynamic-range neurons with input from the knee joint in the anesthetized rat. The responses of each neuron to innocuous and noxious pressure onto the knee and the ankle were continuously assessed before and during the development of an inflammation in the knee joint induced by the injections of K/C into the joint cavity. The specific antagonist at P-type calcium channels omega-agatoxin was administered into a 30-microl trough on the spinal cord surface above the recorded neuron. In most neurons the application of omega-agatoxin before induction of inflammation slightly enhanced the responses to pressure onto the knee and ankle or left them unchanged. Two different protocols were then followed. In the control group (13 rats) only Tyrode was administered to the spinal cord during and after induction of inflammation. In these neurons the responses to mechanical stimuli applied to both the inflamed knee and to the noninflamed ankle showed a significant increase over 4 h. In the experimental group (12 rats) omega-agatoxin was applied during knee injection and in five 15-min periods up to 180 min after kaolin. This prevented the increase of the neuronal responses to innocuous pressure onto the knee and to innocuous and noxious pressure onto the ankle; only the responses to noxious pressure onto the knee were significantly enhanced during development of inflammation. Thus the development of inflammation-evoked hyperexcitability was attenuated by omega-agatoxin, and this suggests that P-type calcium channels in the spinal cord are involved in the generation of inflammation-evoked hyperexcitability of spinal cord neurons. Finally, when omega-agatoxin was administered to the spinal cord 4 h after the kaolin injection, i.e., when inflammation-evoked hyperexcitability was fully established, the responses to innocuous and noxious pressure onto the knee were reduced by 20-30% on average. The shift in the effect of omega-agatoxin, from slight facilitation or no change of the responses before inflammation to inhibition in the state of hyperexcitability, indicates that P-type calcium channels are important for excitatory synaptic transmission involved in the maintenance of inflammation-evoked hyperexcitability.

Animals↗
PubMed2000

FK506 attenuates developing and established joint inflammation and suppresses interleukin 6 and nitric oxide expression in bacterial cell wall induced polyarthritis.

OBJECTIVE: To determine the efficacy of therapeutic administration of FK506 (Tacrolimus) in suppressing developing and established joint inflammation, proinflammatory cytokine expression, and nitric oxide (NO) production in peptidoglycan-polysaccharide (PG/PS) induced experimental polyarthritis in rats. METHODS: Chronic joint inflammation was induced by intraperitoneal injection of PG/PS, and joint inflammation was quantified using arthritis index and paw volume. Serum and joint levels of interleukin 6 (IL-6) were measured by bioassay and Western blot analysis respectively, and serum levels of NO production were determined by the Griess procedure and the expression of the inducible isoform of nitric oxide synthase (i-NOS) in the joints was determined by Western blot analysis. RESULTS: Arthritis induced by PG/PS is biphasic, progressing through an initial acute phase and a remission phase, which is followed by a persistent chronic phase. Daily administration of FK506 initiated during the remission phase significantly attenuated the onset and development of chronic joint inflammation. We observed a significant reduction in joint inflammation and swelling, an apparent suppression of pannus development, and minimal erosive damage to the articular cartilage and subchondral bone. Fully established chronic joint inflammation was also ameliorated by daily administration of FK506. Joint swelling and inflammation was significantly reduced by 5 days post-treatment with FK506 and the erosive activity associated with the pannus appeared diminished. The elevated expression of IL-6 and NO characteristic of chronic joint inflammation in the serum and in joint tissue was significantly reduced by FK506 treatment. CONCLUSION: Therapeutic administration of FK506 has a profound antiinflammatory effect on the development of the chronic, erosive arthritis induced by PG/PS. This attenuation in joint inflammation was associated with suppression of IL-6 and NO production systemically and locally in the joints. Our data suggest that FK506 may be effective in the treatment of chronic joint inflammation associated with rheumatoid arthritis.

Animals↗
PubMed2001

Comparison of microscopic methods for detecting inflammation in expressed prostatic secretions.

PURPOSE: We evaluated microscopic methods of detecting inflammation in expressed prostatic secretions. MATERIALS AND METHODS: Methods of counting expressed prostatic secretion leukocytes were compared in 251 samples from 159 patients with chronic prostatitis/chronic pelvic pain syndrome, including traditional wet mounts, hemocytometer derived concentrations and expressed prostatic secretion smears stained with Gram's method or DiffQuick stain (Dade International, Inc., Miami, Florida). RESULTS: Of 159 initial patient evaluations 84 (53%) showed inflammation by hemocytometer concentration at 500 leukocytes per mm.3 or greater but only 37 (23%) were considered inflammation by the traditional wet mount method (p <0.001). Inflammation was identified in 149 of 251 specimens (59%) by hemocytometer but in only 82 (33%) by wet mount (p <0.001). When inflammation was defined as 1,000 leukocytes per mm.3 or greater the hemocytometer still identified significantly more patients (41%) and specimens (48%) with inflammation than the wet mount. The hemocytometer method had a substantially lower interassay and intra-assay coefficient of variation than the wet mount method. Polymorphonuclear neutrophils and macrophages were the most common cells observed on stained smears, which detected inflammation in 147 specimens (59%) by DiffQuick but in only 98 (39%) by Gram's method. CONCLUSIONS: Detecting inflammation in expressed prostatic secretions is method dependent. Significantly more cases of inflammation were detected by hemocytometer than by the traditional wet mount technique. Because the wet mount method also proved more variable than the hemocytometer and highly sensitive to volume, its use is not recommended. These findings support the adoption of hemocytometer and staining methods for accurate evaluation of expressed prostatic secretion inflammation in men with chronic prostatitis/chronic pelvic pain syndrome.

Adolescent↗
PubMed1996

[Significance of intestinal inflammation in the pathogenesis of spondylarthropathies].

The concept of spondylarthropathy (SpA) gathers together a group of chronic diseases with common clinical, biological, genetic and therapeutic characteristics. The concept forms a distinct entity, different from other rheumatic diseases. The target organs are not only the joint, but also the axial skeleton, the enthesis, the eye, the gut, the urogenital tract, the skin and sometimes the heart. The prevalence of this entity in the general population is estimated 1%, equal to the prevalence of rheumatoid arthritis. Genetical predisposition (HLA-B27) is one of the clues to the pathogenesis of the disease. Since reactive arthritis is induced by specific urogenital or enterogenic bacteria, and since the gut is implied in different forms of spondylarthropathies, especially in IBD, it was clear that the gut could play an important role by permitting exogenous factors to enter the body. This hypothesis was the rationale for investigating the gut in the spondylarthropathies by performing ileo-colonoscopies. In the first ileo-colonoscopic studies of SpA patients, histological signs of gut inflammation were found in a relatively great number of patients, mostly not presenting any clinical intestinal manifestations. These lesions were not seen in other inflammatory joint diseases. Further ileo-colonoscopic studies confirmed the strong relationship between gut and joint inflammation. In patients in whom a second ileo-colonoscopy was performed, remission of the joint inflammation was always connected with a disappearance of the gut inflammation, whereas persistence of locomotor inflammation was mostly associated to the persistence of gut inflammation. The hypothesis was proposed that some patients with a spondylarthropathy had a form of subclinical Crohn's disease in which the locomotor inflammation was the only clinical expression. This hypothesis was confirmed in prospective long-term studies in which the ileo-colonoscopied patients were reviewed 2 to 9 years later:about 6% of SpA patients not presenting any sign of Crohn's disease at first investigation but demonstrating gut inflammation on biopsy, developed full-blown Crohn's disease. By performing electronmicroscopy it was described that in patients with SpA the number of membranous (M) cells, which are scarce in normal ileum, is increased in number in inflamed mucosa. They showed a thin rim of cytoplasm covering groups of lymphocytes. In chronic inflammatory lesions necrotic M-cells, rupture of M-cells and lymphocytes entering the gut lumen was observed. The bursting of M-cells at the top of the lymphoid follicles leads to interruption of the gut epithelial lining and gives the luminal content access to the lymphoid tissue. This can be responsible for an exponential increase of local antigen stimulation. Accelerated luminal antigen presentation through a break in the epithelial layer, together with cytokines released from activated monocytes, might induce a second line of defense aiming at elimination of the massive antigen penetration into the mucosa. The postulated switch from secretory local immunity to a systemic type of local immune reaction could have different consequences:the local down-regulation of J chain in the IgA immunocytes could shift the production of polymeric IgA to monomers, jeopardizing secretory immunity; the disproportionate increase of IgG-producing cells could favor further inflammation and tissue damage through complement activation and arming of the killer cells, and cause autoimmune responses locally and in target organs at a distance (e.g. joint organs). The discovery of subclinical gut inflammation in the SpA had therapeutic consequences. Sulphasalazine (SASP) has been proven to be an active drug in the treatment of IBD. Since the gut could play a crucial role in SpA, it was logic to use this drug in the treatment of this disease. Multiple open and double-blind studies have proven the effectiveness of this drug in SpA.

Animals↗
PubMed2004

The metabolic syndrome, inflammation, and risk of cognitive decline.

CONTEXT: Several studies have reported an association between the metabolic syndrome and cardiovascular disease. Despite an increasing awareness that cardiovascular risk factors increase risk of cognitive decline and dementia, there are few data on the metabolic syndrome and cognition. OBJECTIVE: To determine if the metabolic syndrome is a risk factor for cognitive decline and if this association is modified by inflammation. DESIGN AND SETTING: A 5-year prospective observational study conducted from 1997 to 2002 at community clinics at 2 sites. PARTICIPANTS: A total of 2632 black and white elders (mean age, 74 years). MAIN OUTCOME MEASURES: Association of the metabolic syndrome (measured using National Cholesterol Education Program guidelines) and high inflammation (defined as above median serum level of interleukin 6 and C-reactive protein) with change in cognition (Modified Mini-Mental State Examination [3MS]) at 3 and 5 years. Cognitive impairment was defined as at least a 5-point decline. RESULTS: Compared with those without the metabolic syndrome (n = 1616), elders with the metabolic syndrome (n = 1016) were more likely to have cognitive impairment (26% vs 21%, multivariate adjusted relative risk [RR], 1.20; 95% confidence interval [CI], 1.02-1.41). There was a statistically significant interaction with inflammation and the metabolic syndrome (P = .03) on cognitive impairment. After stratifying for inflammation, those with the metabolic syndrome and high inflammation (n = 348) had an increased likelihood of cognitive impairment compared with those without the metabolic syndrome (multivariate adjusted RR, 1.66; 95% CI, 1.19-2.32). Those with the metabolic syndrome and low inflammation (n = 668) did not exhibit an increased likelihood of impairment (multivariate adjusted RR, 1.08; 95% CI, 0.89-1.30). Stratified multivariate random-effects models demonstrated that participants with the metabolic syndrome and high inflammation had greater 4-year decline on 3MS (P = .04) compared with those without the metabolic syndrome, whereas those with the metabolic syndrome and low inflammation did not (P = .44). CONCLUSION: These findings support the hypothesis that the metabolic syndrome contributes to cognitive impairment in elders, but primarily in those with high level of inflammation.

Aged↗
PubMed1999

Persistent Fos protein expression after orofacial deep or cutaneous tissue inflammation in rats: implications for persistent orofacial pain.

This study was designed to systematically examine the effects of persistent orofacial tissue injury on prolonged neuronal activation in the trigeminal nociceptive pathways by directly comparing the effects of orofacial deep vs. cutaneous tissue inflammation on brainstem Fos protein expression, a marker of neuronal activation. Complete Freund's adjuvant (CFA) was injected unilaterally into the rat temporomandibular joint (TMJ) or perioral (PO) skin to produce inflammation in deep or cutaneous tissues, respectively. Rats were perfused 2 hours, 24 hours, 3 days, or 10 days following CFA injection. The TMJ and PO inflammation-induced Fos expression paralleled the intensity and course of inflammation over the 10-day observation period, suggesting that the increase in intensities and persistence of Fos protein expression may be associated with a maintained increase in peripheral input. Compared to PO CFA injection, the injection of CFA into the TMJ produced a significantly stronger inflammation associated with a greater Fos expression. In TMJ- but not in PO-inflamed rats, Fos-like immunoreactivity (LI) spread from superficial to deep upper cervical dorsal horn as the inflammation persisted and there was a dominant ipsilateral Fos-labeling in the paratrigeminal nucleus. Common to TMJ and PO inflammation, Fos-LI was induced in the trigeminal subnuclei interpolaris and caudalis, C1-2 dorsal horn, and other medullary nuclei. Substantial bilateral Fos-LI was found in the interpolaris-caudalis trigeminal transition zone. Further analysis revealed that Fos-LI in the ventral transition zone was equivalent bilaterally, whereas Fos-LI in the dorsal transition zone was predominantly ipsilateral to the inflammation. The differential induction of Fos expression suggests that an increase in TMJ C-fiber input after inflammation and robust central neuronal hyperexcitability contribute to persistent pain associated with temporomandibular disorders.

Animals↗
PubMed1993

Changes in the proteins coating monosodium urate crystals during active and subsiding inflammation. Immunogold studies of synovial fluid from patients with gout and of fluid obtained using the rat subcutaneous air pouch model.

OBJECTIVE: In this in vivo study, we investigated changes in the proteins that coat monosodium urate (MSU) crystals in human synovial fluid samples and rat air pouch fluid samples obtained sequentially during periods of active and resolving inflammation, in order to evaluate whether in vivo findings are consistent with hypotheses on roles of protein coating based on in vitro findings. METHODS: Crystals from patients with gout were isolated from joint fluids with acute inflammation, and subsequently from the same joints at the time inflammation was resolving. Crystals were also obtained using the rat subcutaneous air pouch model. Immunogold was used to label proteins coating MSU crystals, for light microscopy (LM) and transmission electron microscopy (TEM) studies. RESULTS: Dense immunogold-silver labeling for IgG was observed under LM on crystals from fluid with acute inflammation, whereas other proteins (apolipoproteins [Apo], fibronectin, fibrinogen, albumin) were not labeled significantly. Apo B became strongly positive on crystals as the inflammation subsided, whereas other proteins were only weakly positive and IgG became absent or weakly positive. Quantitative TEM evaluation confirmed the LM observations. CONCLUSION: This study provides the first in vivo evidence supporting the notion derived from previous in vitro studies that proteins coating MSU crystals change as inflammation evolves. Protein coatings may play an important role in the self-limited nature of gouty inflammation. IgG coating MSU crystals may enhance the inflammation. As the inflammation subsides, Apo B could displace the IgG by competitively coating sites on crystals and could contribute in part to the resolution of the acute gouty arthritis.

Aged↗
PubMedDate not supplied

Distortion of iron status indices by acute inflammation in older hospitalized patients.

The relation between acute inflammation and biochemical indices of iron and nutritional status in older in-patients have been investigated. Thirty-nine consecutive patients (25 men and 14 women; median age 79 years) with acute inflammation episode were evaluated. C-reactive protein (CRP) > or = 3 mg/dl was considered to indicate acute inflammation. Iron and nutritional status were explored measuring hemoglobin (Hb), hematocrit (Ht), red blood cell (RBC), white blood cell (WBC), mean erythrocyte volume (MCV), mean corpuscular hemoglobin (MCH), and serum levels of iron (Fe), transferrin (T), percentage transferrin saturation (%TS), ferritin (SF), albumin (Alb) and pre-albumin (pre-Alb), the day after admission (T-basal), the day of onset of inflammation (T0), and successively (T5, T8-15, and T-final). CRP and WBC were significantly higher at T0 than T-basal (CRP: +1014%, P < 0.01; WBC: +30%, P < 0.01) but had reduced on days T8-15 compared to T0 (CRP: -90%, P < 0.01; WBC: -26%, P < 0.01). Fe serum levels fell at the beginning of the acute phase (T0: -24% versus T-basal; P < 0.01), but had recovered at T-final (+36% versus T5; P < 0.01). T levels also varied significantly (P < 0.01) (T0: -16% versus T-basal; T-final: +18% versus T5). SF was slightly higher than normal at T-basal and increased further during inflammation (+41% at T5 versus T-basal) to reduce at T-final (-36% versus T5; P < 0.01). At T-final, pre-Alb and Alb were significantly higher than at T5 (pre-Alb +63%, P < 0.01; Alb +20%, P < 0.05). The indices of iron status are disrupted in elderly patients during acute inflammation, just as they are in chronic inflammation, and cannot therefore be used to diagnose sideropenic anemia. The only variables not influenced by inflammation are MCV and %TS. Low values of these, associated with other symptoms of anemia, suggest sideropenic anemia, irrespective of the values of the other indices of iron status. With the appearance of inflammation, nutritional indices tend to decline as liver activity shifts to the production of acute phase proteins.

Acute Disease↗
PubMed2005

Proteinase-activated receptor 2 activation in the airways enhances antigen-mediated airway inflammation and airway hyperresponsiveness through different pathways.

BACKGROUND: Serine proteinases such as mast cell tryptase, trypsin-like enzymes, and certain allergens are important in the pathogenesis of asthma. These proteinases can activate the proteinase-activated receptor (PAR)-2, which has been shown to be upregulated in the airways of patients with asthma. OBJECTIVE: The purpose of this study was to investigate PAR-2 activation in the airways during allergen challenge and its effects on the 2 principle features of asthma, airway inflammation and airway hyperresponsiveness (AHR). METHODS: Proteinase-activated receptor 2 activating peptide SLIGRL-NH2 (PAR-2 activating peptide [ap]) or control peptide LSIGRL-NH2 (PAR-2 control peptide [cp]) was administered alone or in conjunction with ovalbumin intranasally to mice, and AHR and airway inflammation were evaluated. RESULTS: PAR2ap did not induce AHR or airway inflammation in ovalbumin-sensitized mice that had not been challenged with ovalbumin. When administered with ovalbumin, PAR-2ap enhanced AHR and airway inflammation compared with ovalbumin administered alone or with PAR-2cp. The enhanced AHR persisted for 5 days, whereas the enhancement to airway inflammation dissipated. Mice administered PAR-2ap alone during the 5 days after the final antigen challenge demonstrated an additional enhancement to airway inflammation compared with the control animals. PAR-2ap administered with allergen increased TNF and IL-5 mRNA in lung tissue and IL-13 and TNF in bronchoalveolar lavage fluid. CONCLUSION: Exogenous PAR-2 activation in parallel with allergen challenge enhances allergen-mediated AHR and airway inflammation through distinct mechanisms. PAR-2 activation can also enhance established airway inflammation even when dissociated from exposure to allergen. Therefore, PAR-2 activation may play a pathogenic role in the development of AHR and airway inflammation.

Animals↗
PubMed2003

Inflammation-induced upregulation of AMPA receptor subunit expression in brain stem pain modulatory circuitry.

Our previous study demonstrated an increase in alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor sensitivity in the rostral ventromedial medulla (RVM) associated with enhanced net descending inhibition after inflammatory hyperalgesia. The present study further studied the time-dependent changes in AMPA-produced inhibition after inflammation and the underlying molecular mechanisms. Inflammation was induced by intraplantar injection of complete Freund's adjuvant (CFA, 0.2ml). There was a significant increase in AMPA-produced inhibition at 5h that was further enhanced at 24h (P<0.05), as compared to that at 3h post-inflammation. The AMPA-produced inhibition returned to the control level at 14 days post-inflammation. We analyzed mRNA and protein levels of the GluR1 and GluR2 AMPA receptor subunits in the RVM at 2h to 14 days post-inflammation. AMPA receptor subunits exist in the two 'flip' and 'flop' isoforms that differentially affect the desensitization properties of the receptor. Reverse transcription-polymerase chain reaction analysis indicated that there was a significant upregulation of mRNAs encoding the GluR1-flip (5-24h), GluR2-flip (24h) and GluR2-flop (24h) isoforms in the RVM after inflammation, whereas the levels of GluR1-flop mRNAs showed no significant change. Western blots demonstrated that the GluR1 protein levels were significantly upregulated at 24h-3 days (P<0.05) post-inflammation, compared to that of naive animals. GluR2 protein levels remained unchanged. Immunohistochemistry further demonstrated an increase in GluR1-like immunoreactivity localized to the RVM at 24h post-inflammation. These findings suggest that AMPA receptors in the RVM undergo selective transcriptional and translational modulation following inflammation and may contribute to activity-dependent plasticity in descending pain modulatory systems after prolonged noxious input.

Animals↗
PubMedDate not supplied

Inflammation and neovascularization associated with clinically used vascular prosthetic materials.

This study was designed to evaluate and compare healing characteristics, specifically neovascularization and inflammation, of polymeric vascular graft materials commonly used in clinical applications. Our hypotheses were (i) polymeric materials used in vascular graft manufacture stimulate chronic inflammation and (ii) inflammation and neovascularization of polymeric materials are related. Impra and Gore-Tex ePTFE, Meadox weavenit and woven Dacron, Hemashield microvel and woven Dacron, and Golaski microknit Dacron were implanted as 6-mm diameter disks within rat subcutaneous and adipose tissue. Following 5 weeks of implantation samples were evaluated by histological and immunocytochemical analysis. Sections were stained using hematoxylin and eosin or reacted with ED1 antibody and GS1 lectin to quantify inflammation and neovascularization. respectively. The extent of inflammation and neovascularization were influenced by both tissue site of implantation and polymer characteristics. For subcutaneous implants, inflammation was graded as follows: Meadox weavenit > Hemashield woven > Meadox woven > Gore-Tex ePTFE > Hemashield microvel > ImpraePTFE > Golaski microknit, while only the Golaski microknit neovascularized. Inflammation was graded as follows for adipose implants: Hemashield woven > Hemashield microvel > Meadox weavenit > Meadox woven > Gore-Tex ePTFE > Golaski microknit > Imnpra ePTFE, while the following order of neovascularization was observed: Impra ePTFE > Gore-Tex ePTFE > Golaski microknit. The degree of inflammation following biomnaterial implantation has a profound effect on implant neovascularization. These data suggest an inverse relationship exists between inflammation and neovascularization.

Adipose Tissue↗
PubMed1999

Heme and acute inflammation role in vivo of heme in the hepatic expression of positive acute-phase reactants in rats.

Acute-phase protein synthesis in the liver during inflammation is regulated via cytokines and glucocorticoids. Using quantitative reverse transcription (RT)-PCR analysis and immunoassay, we explored, in the rat, the response of the acute-phase protein, alpha-2 macroglobulin (A2M), after systemic inflammation induced by lipopolysaccharide (LPS) or localized inflammation induced by turpentine oil (TO). The results indicate that synthesis of A2M is higher following TO-induced inflammation than LPS-induced inflammation and is not correlated with interleukin (IL)-6 or glucocorticoid levels. We studied the putative role of heme in this differential A2M expression following localized vs. systemic inflammation; addition of heme during LPS-induced inflammation can boost the expression of A2M, whereas blocking heme synthesis (by succinyl acetone) or enhancing its consumption in parallel biosynthetic pathways (cytochrome P450 induction by phenobarbital) decreases A2M expression. This decrease was abolished by exogenous heme supplementation. Finally, we demonstrate that heme supplementation is also able to increase the A2M response in female rats to a level similar to that in male rats providing a new insight into the puzzling sexual dimorphism observed previously during localized inflammation. We propose that heme should be considered a new regulatory element in controlling liver A2M expression during inflammation.

Acute-Phase Proteins↗
PubMed2007

Childhood maltreatment predicts adult inflammation in a life-course study.

Stress in early life has been associated with insufficient glucocorticoid signaling in adulthood, possibly affecting inflammation processes. Childhood maltreatment has been linked to increased risk of adult disease with potential inflammatory origin. However, the impact of early life stress on adult inflammation is not known in humans. We tested the life-course association between childhood maltreatment and adult inflammation in a birth cohort followed to age 32 years as part of the Dunedin Multidisciplinary Health and Development Study. Regression models were used to estimate the effect of maltreatment on inflammation, adjusting for co-occurring risk factors and potential mediating variables. Maltreated children showed a significant and graded increase in the risk for clinically relevant C-reactive protein levels 20 years later, in adulthood [risk ratio (RR)=1.80, 95% confidence interval (CI)=1.26-2.58]. The effect of childhood maltreatment on adult inflammation was independent of the influence of co-occurring early life risks (RR=1.58, 95% CI=1.08-2.31), stress in adulthood (RR=1.64, 95% CI=1.12-2.39), and adult health and health behavior (RR=1.76, 95% CI=1.23-2.51). More than 10% of cases of low-grade inflammation in the population, as indexed by high C-reactive protein, may be attributable to childhood maltreatment. The association between maltreatment and adult inflammation also generalizes to fibrinogen and white blood cell count. Childhood maltreatment is a previously undescribed, independent, and preventable risk factor for inflammation in adulthood. Inflammation may be an important developmental mediator linking adverse experiences in early life to poor adult health.

Adult↗
PubMed2006

Acute effect of standard heparin versus low molecular weight heparin on oxidative stress and inflammation in hemodialysis patients.

OBJECTIVE: Atherosclerotic cardiovascular diseases caused by traditional and non-traditional risk factors are the most common cause of morbidity and mortality in hemodialysis patients. Recently, much interest has been focused on non-traditional factors, such as oxidative stress, inflammation, and endothelial dysfunction. Hemodialysis patients are not only exposed to oxidative stress but also to inflammation. Although anticoagulants are the most frequently used drugs in hemodialysis patients, their effect upon oxidative stress and inflammation in dialysis patients are still unknown. METHODS: Thirty-three hemodialysis patients were randomized into three groups. Group 1 received standard heparin while group 2 received low molecular weight heparin during the dialysis therapy. Group 3 (control group) did not receive any anticoagulant agent. Investigators were blinded to the therapy. Serum concentrations of oxidative stress and inflammation markers, including C-reactive protein, tumor necrosis factor alpha, superoxide dismutase, and malondialdehyde, were measured before and after dialysis session. RESULTS: The oxidative stress and inflammation markers were significantly increased in groups 1 and 3 (p < 0.05 for each) compared to their baseline values. In contrast, baseline and end-treatment values of the oxidative stress and inflammation markers were comparable in the group 2 (p > 0.05). CONCLUSION: These findings indicate that the type of anticoagulants may take a role in the acute effect of hemodialysis upon oxidative stress and inflammation markers. A comparison of the groups revealed that low molecular weight heparin decreased the oxidative stress and inflammation, whereas standard heparin increased the oxidative stress and inflammation. Low molecular weight heparin appears to have an additive benefit for hemodialysis patients.

Adult↗
PubMed2004

Epidemiology of inflammation and prostate cancer.

PURPOSE: We provide an overview of some of the basic, clinical and epidemiological research that has been conducted to investigate the potential role of chronic inflammation in prostate carcinogenesis and to provide direction for future research on this hypothesis. MATERIALS AND METHODS: We reviewed the literature on this topic. RESULTS: Chronic inflammation has long been linked to cancers with an infectious etiology, such as stomach, liver and colon cancer, in patients with inflammatory bowel disease. Whether intraprostatic inflammation contributes to prostate carcinogenesis is unknown. Inflammation is frequently present in prostate biopsies, radical prostatectomy specimens and tissue resected for treatment of benign prostatic hyperplasia. Also, inflammatory infiltrates are often found in and around foci of atrophy that are characterized by an increased proliferative index. These foci, called proliferative inflammatory atrophy, may be precursors of early prostate cancer or may indicate an intraprostatic environment favorable to cancer development. Epidemiological studies have indirectly examined the role of chronic inflammation in prostate carcinogenesis through studies of pro-inflammatory and anti-inflammatory factors. When taken together studies of sexually transmitted infections, clinical prostatitis, and genetic and circulating markers of inflammation and response to infection hint at a link between chronic intraprostatic inflammation and prostate cancer. CONCLUSIONS: Additional well-designed basic, clinical and epidemiological studies are needed to resolve questions about the role of chronic inflammation in prostate carcinogenesis and to determine if intraprostatic inflammation is a rational target for chemoprevention.

Acute-Phase Proteins↗
PubMed1995

Influence of acute inflammation on iron and nutritional status indexes in older inpatients.

OBJECTIVE: To investigate the relations between acute inflammation, as shown by high C-reactive protein (CRP) serum levels, and laboratory indexes of iron and nutritional status and to ascertain whether the presence of acute inflammation affects the diagnostic reliability of these indexes. DESIGN: Cross-sectional study. SETTING: Geriatric ward for rehabilitation. PARTICIPANTS: A total of 163 patients, 77 men and 86 women aged 60 years or older. MEASUREMENTS: CRP values > 1 mg/dL were considered to indicate the presence of acute inflammation. Iron status was explored by measuring erythrocyte mean cell volume (MCV), hemoglobin (Hb), serum iron (Fe), TIBC, percent transferrin saturation (% TS) and ferritin (SF). Nutritional status was determined by albumin (Alb) and prealbumin (pre-Alb) serum levels. MAIN RESULTS: In the whole series, CRP correlated significantly with all iron status variables except erythrocyte MCV (directly with SF, inversely with the others) and correlated inversely with Alb and pre-Alb. Mean values of iron status variables were significantly different in patients with inflammation and those without: SF was higher and the other variables lower. Patients with low % TS (< 16%) showed a pattern consistent with iron deficiency. Compared to the group with normal values, they had more severe anemia, lower MCV, Fe, and SF, and higher TIBC; mean Alb, pre-Alb, and CRP values were not significantly different. The prevalence of inflammation was 50% (39.5% in the group with normal % TS). A similar pattern was observed in patients with microcytosis (MCV < 84 fL) associated with low % TS; dividing this subgroup according to SF values (low, < 30 micrograms/L) did not provide more information because patients with acute inflammation were excluded. CONCLUSIONS: Patients with acute inflammation present altered iron status indexes that resemble those observed in the anemia of chronic disease. Fe, TIBC and SF lose diagnostic value. The concomitant presence of microcytosis and low % TS, and to a lesser extent the presence of one of these alterations, is suggestive of iron deficiency associated with inflammation and may warrant gastrointestinal tract investigations and ferrous salt treatment. Protein-calorie malnutrition seems to enhance the effects of inflammation on iron status indexes.

Acute Disease↗
PubMed1997

Angiogenesis and inflammation in invasive carcinoma of the breast.

AIM: To investigate the relation between angiogenesis and inflammation in invasive carcinoma of the breast. METHODS: Sections from 75 invasive carcinomas of the breast were stained using immunohistochemistry for von Willebrand factor, CD3, CD8, CD45RO, CD45RA, CD20, CD68, and c-erbB-2. Tumour vascularity was assessed by counting vessels in the three most vascular areas, and calculating the average (x 400 magnification, field 0.168 mm2). Each pattern of inflammation was scored semiquantitatively. RESULTS: The main pattern of inflammation was a diffuse infiltrate of macrophages, and to a lesser extent T cells. Perivascular and perilobular clusters of B and T cells were noted at the edge of the carcinomas, but were less prominent than the diffuse inflammation. Diffuse inflammation, particularly macrophages, was associated with high tumour grade, tumour necrosis, large tumour size, and c-erbB-2 expression. Perivascular and perilobular inflammation also increased with tumour grade. Tumour vascularity increased slightly with intensity of diffuse inflammation (Spearman's rank correlation coefficient rs = 0.17, p = 0.08), and was inversely related to perilobular inflammation (rs = -0.23, p = 0.03). CONCLUSIONS: The correlations between inflammation and vascularity were weak in this study (r2 about 0.04) and thus there was no evidence of an important relation. Discrepancies between this and other studies may be resolved by studying expression of angiogenic cytokines and proteolytic enzymes by tumour infiltrating inflammatory cells, and their relation to tumour vascularity.

Breast Neoplasms↗
PubMed2005

Systemic and upper and lower airway inflammation at exacerbation of chronic obstructive pulmonary disease.

RATIONALE: In addition to pulmonary involvement, stable chronic obstructive pulmonary disease (COPD) is associated with nasal and systemic inflammation. Although exacerbations of COPD are associated with increased pulmonary and systemic inflammation, determinants of the systemic response remain obscure, and nor is it known whether there is nasal involvement. OBJECTIVES: To investigate upper airway, lower airway, and systemic inflammation at exacerbation of COPD. METHODS: We sampled sputum, nasal wash, and serum from 41 exacerbations (East London cohort) for analysis of pathogenic microorganisms and inflammatory indices (sputum/nasal wash leukocytes, interleukin [IL]-6, IL-8, and myeloperoxidase; serum IL-6 and C-reactive protein). Values were compared with stable COPD. MEASUREMENTS AND MAIN RESULTS: Exacerbation of COPD is associated with greater nasal, sputum, and serum inflammation than the stable state. At exacerbation, inflammatory markers were highly correlated within nasal wash and serum (all r >/= 0.62, p < 0.001), but not sputum. The degree of upper airway inflammation correlated with the degree of lower airway inflammation (e.g., nasal wash/sputum myeloperoxidase; r = 0.50, p = 0.001). The degree of systemic inflammation correlated with the degree of lower airway inflammation (e.g., serum IL-6/sputum IL-8; r = 0.35, p = 0.026), and was greater in the presence of a sputum bacterial pathogen (29.0 g/dl C-reactive protein difference, p = 0.002). We did not find relationships between the upper airway and systemic compartments. CONCLUSIONS: Exacerbation of COPD is associated with pan-airway inflammation; the systemic inflammatory response is proportional to that occurring in the lower airway and greater in the presence of a bacterial pathogen.

Aged↗