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PubMed2006

Relation between acute urinary retention, chronic prostatic inflammation and accompanying elevated prostate-specific antigen.

OBJECTIVE: To determine if there is a relationship between acute urinary retention (AUR), the prostate-specific antigen (PSA) level and chronic inflammation of the prostate. We therefore studied patients with benign prostatic obstruction (BPO) with (n = 64) or without (n = 168) acute urinary retention (AUR) who underwent transurethral resection of the prostate (TURP) in a retrospective case control study. MATERIAL AND METHODS: Between 2001 and 2004, a total of 232 patients underwent TURP due to BPO with or without AUR. The mean values of age, prostate volume, weight of resected prostate and PSA level and the histopathologic results of patients with and without AUR were compared. Chi(2) analysis was used to examine the relationship between prostatic inflammation and AUR. The contribution of each variable to AUR was assessed by means of multiple linear regression. RESULTS: A total of 64 patients (28%) were operated on for AUR due to BPO. There were no statistical differences between patients with or without AUR with respect to the mean values of PSA, percent free PSA, prostate size or weight of the resected prostate tissue. Elevated PSA values (>or=4.0 ng/ml) were detected in 64% and 38% of the patients in the AUR and non-AUR groups, respectively (p = 0.01). Histopathological re-evaluation demonstrated that chronic prostatic inflammation was present in 56% and 37% of the specimens in the AUR and non-AUR groups, respectively (p = 0.014). In the AUR group, the mean PSA level was significantly higher in patients with than without prostatic inflammation (7.75+/-5.26 vs 5.07+/-3.21 ng/ml; p = 0.022). The odds ratio of AUR for patients with chronic prostatic inflammation and elevated PSA was determined as 4.14 (95% CI 1.65-10.41). Multiple linear regression revealed that prostatic inflammation made a significant contribution to AUR. CONCLUSIONS: Chronic prostatic inflammation may be histopathological evidence of both elevated PSA level and AUR; hence it may play a role in the pathophysiology of AUR.

Aged↗
PubMed1998

A low molar ratio of retinol binding protein to transthyretin indicates vitamin A deficiency during inflammation: studies in rats and a posterior analysis of vitamin A-supplemented children with measles.

To assess whether the molar ratio of retinol-binding protein (RBP) to transthyretin (TTR) is of utility in detecting vitamin A (VA) deficiency during inflammation, we analyzed data from a rat model of endotoxin-induced inflammation and from a previously reported randomized, placebo-controlled trial of VA supplementation in children with acute measles. In rats, both marginal VA deficiency and inflammation were independent causes of low plasma RBP (two-way ANOVA, P < 0.001), whereas plasma TTR concentration was reduced only by inflammation (P < 0.001). The molar ratio of plasma RBP to TTR was reduced (by approximately 50%) only in rats with marginal VA deficiency and inflammation (two-way ANOVA interaction, P < 0.01). Serum retinol concentration, C-reactive protein (CRP, an indicator of inflammation) and the RBP:TTR molar ratio were determined in children with acute measles at baseline and 2 wk after subgroups received a placebo or a 210 micromol VA supplement. The ratio of RBP:TTR was selectively reduced in children in the placebo group with low plasma retinol (<0.35 micromol/L) and elevated CRP (>40 mg/L). In children with a low RBP:TTR molar ratio (<0.30) at baseline, the RBP:TTR ratio increased significantly 2 wk later only in the VA-treated subgroup. These analyses provide evidence that, because RBP is differentially reduced in comparison to TTR during VA deficiency, the combined determination of the concentrations of serum RBP and TTR may provide a promising means of detecting VA deficiency during inflammation.

Analysis of Variance↗
PubMed2004

Osteoarthritis, angiogenesis and inflammation.

Angiogenesis and inflammation are closely integrated processes in osteoarthritis (OA) and may affect disease progression and pain. Inflammation can stimulate angiogenesis, and angiogenesis can facilitate inflammation. Angiogenesis can also promote chondrocyte hypertrophy and endochondral ossification, contributing to radiographic changes in the joint. Inflammation sensitizes nerves, leading to increased pain. Innervation can also accompany vascularization of the articular cartilage, where compressive forces and hypoxia may stimulate these new nerves, causing pain even after inflammation has subsided. Inhibition of inflammation and angiogenesis may provide effective therapeutics for the treatment of OA by improving symptoms and retarding joint damage. This review aims to summarize (i) the evidence that angiogenesis and inflammation play an important role in the pathophysiology of OA and (ii) possible directions for future research into therapeutics that could effectively treat this disease.

Chronic Disease↗
PubMed2002

Inflammation at the insertion site is not predictive of catheter-related bloodstream infection with short-term, noncuffed central venous catheters.

BACKGROUND: Noncuffed, percutaneously inserted central venous catheters (CVCs) are widely used and cause at least 250,000 bloodstream infections (BSIs) in U.S. hospitals each year. We report a prospective study to determine whether inflammation at the insertion site is predictive of CVC-related BSI. METHODS: Percutaneously inserted, noncuffed CVCs inserted into the subclavian, internal jugular, or femoral vein in two randomized trials during 1998-2000 were prospectively studied; most patients were in an intensive care unit. The condition of the insertion site was evaluated daily by research nurses, quantifying pain (0, 1), erythema (0-2), swelling (0, 1), and purulence (0, 1); the lowest possible overall inflammation score was 0 and the highest was 5. CVC-related BSI was confirmed in each case by demonstrating concordance between isolates from the catheter segment and from blood cultures by restriction-fragment DNA subtyping. RESULTS: Among 1,263 CVCs prospectively studied, 333 (26.3%) were colonized at removal; of these, 35 catheters (2.7%) caused BSIs (5.9 per 1000 CVC days). BSIs were caused by coagulase-negative staphylococci (n = 27), enterococci (n = 4), enteric Gram-negative bacilli (n = 3), or (n = 1). Most insertion sites showed little or no inflammation at the time of removal. There were no significant differences among mean scores for each inflammatory variable examined or overall score among colonized CVCs (0.1 +/- 0.1), catheters causing CVC-related BSI (0.2 +/- 0.4), and noncolonized CVCs (0.1 +/- 0.1). The sensitivity of local inflammation for diagnosis of CVC-related BSI was dismal (0-3%). CONCLUSION: Local inflammation is uncommon with infected CVCs, probably because most catheter-associated infections are currently caused by coagulase-negative staphylococci, a pathogen that incites little local or systemic inflammation. Whereas overt inflammation of the insertion site should raise suspicion of CVC-related BSI caused by or Gram-negative bacilli, especially if the patient has fever or other signs of sepsis, in general, site appearance cannot be relied on to identify catheter colonization or CVC-related BSI.

Catheterization, Central Venous↗
PubMed2004

High density lipoproteins in the intersection of diabetes mellitus, inflammation and cardiovascular disease.

PURPOSE OF REVIEW: Low HDL-cholesterol, diabetes mellitus and elevated C-reactive protein as well as various inflammatory diseases are risk factors for coronary heart disease. Both diabetes mellitus and inflammation decrease HDL-cholesterol. We summarize recent findings on the mechanisms underlying low HDL-cholesterol in diabetes and inflammation, as well as on novel functions of HDL that may protect not only from atherosclerosis but also from diabetes mellitus and inflammation-induced organ damage. RECENT FINDINGS: Elevated levels of non-esterified fatty acids and disturbed insulin action contribute to low HDL-cholesterol in diabetes mellitus by modifying lipolysis, apolipoprotein A-I production, as well as the activities of adenosine triphosphate-binding cassette transporter A1 and lipid transfer. Inflammation causes low HDL-cholesterol by increasing the activities of endothelial lipase and soluble phospholipase A2 and by replacing apolipoprotein A-I in HDL with serum amyloid A. HDL and lysosphingolipids therein have been identified as activators of the protein kinase Akt, which in turn is a regulator of apoptosis in beta-cells, endothelial cells, and smooth muscle cells, as well as a regulator of nitric oxide production and adhesion molecule expression in endothelial cells. SUMMARY: The protective properties of HDL in cytokine production, lipid oxidation, cholesterol efflux and reverse cholesterol transport make HDL a protective agent in inflammation-induced organ damage including diabetes mellitus. However, inflammation and diabetes cause a decrease in HDL-cholesterol concentrations and impair HDL function, placing HDL into the centre of a vicious cycle that may escalate into diabetes mellitus, inflammation-induced organ damage and atherosclerosis.

Animals↗
PubMed2003

Vascular inflammation: a role in vascular disease in hypertension?

PURPOSE OF REVIEW: In this review, we summarize the more recent clinical evidence highlighting the importance of vascular inflammation in terms of clinical risk prediction, and the mechanisms mediating the upregulation of inflammatory mediators in cardiovascular disease and hypertension. RECENT FINDINGS: Markers of inflammation have been shown to be upregulated in different forms of cardiovascular disease, and to correlate with vascular risk. Atherosclerosis is characterized by chronic inflammation of the vascular wall. The I-kappaB/nuclear factor-kappaB system is considered a major intracellular inflammatory pathway, mediating most of the vascular inflammatory responses. Increasing evidence indicates that hypertension, through the vasoactive peptides angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies proinflammatory properties of angiotensin II have been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. The angiotensin II receptors involved in the inflammatory process and the interaction between angiotensin II and nitric oxide in mediating vascular inflammation have been identified. In addition, recent advances concerning the role of endothelin-1 as another important mediator of chronic inflammation in the vascular wall has been documented, and the relationship between endothelin-1 and angiotensin II on vascular inflammation demonstrated. SUMMARY: Inflammatory mechanisms are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of useful markers of inflammation, of new therapeutic targets to interfere with these mechanisms, and the evaluation of the efficacy of antiinflammatory treatments will allow progress in our ability to combat cardiovascular disease and the complications of hypertension.

Angiotensin II↗
PubMed1999

Placental membrane inflammation and risks of maternal-to-child transmission of HIV-1 in Uganda.

UNLABELLED: Prospective follow-up of 172 HIV-infected pregnant women and their infants was conducted at Mulago Hospital, Kampala, Uganda during 1990 to 1992. Information was collected on maternal immune status (CD4 counts or clinical AIDS), and concurrent infections with sexually transmitted diseases. Infants were observed on a follow-up basis to determine HIV infection, using polymerase chain reaction (PCR) under 15 months of age and enzyme immunoassay/Western blot for those older than 15 months. Placental membrane inflammation (chorioamnionitis and funisitis), and placental villous inflammation (villitis, intervillitis, and deciduitis) were diagnosed by histopathology. Mother-to-child HIV transmission rates were assessed, and adjusted odds ratios (OR) and 95% confidence intervals (95% CI) of transmission were estimated using women with no placental pathology or evidence of immune suppression as a reference group. RESULTS: The overall mother-to-child HIV transmission rate was 23.3%. Women with no placental membrane inflammation or immune suppression had a transmission rate of 11.3%; compared with 25.5% in women with placental inflammation and no immunosuppression (adjusted OR, 2.87; 95% CI, 1.04-7.90), and 37.0% in immunosuppressed women (OR, 3.07; 95% CI, 1.42-6.67). We estimate that 34% of HIV transmission could be prevented by treatment of placental membrane inflammation in nonimmunocompromised women. Transmission rates were 40.9% with genital ulcer disease (OR, 3.57; 95% CI, 1.28-9.66). Placental villous inflammation and artificial rupture of membranes did not increase transmission rates and cesarean section was associated with a nonsignificant reduction of risk (OR, 0.70; 95% CI 0.24-2.06). CONCLUSION: Placental membrane inflammation increases the rate of mother-to-child HIV transmission.

Blotting, Western↗
PubMed2005

Kidney insufficiency and nutrient-based modulation of inflammation.

PURPOSE OF REVIEW: Patients with chronic kidney disease have a high cardiovascular mortality rate. Despite recent advances in dialysis techniques, over 20% of US dialysis patients die every year. Protein-energy malnutrition and inflammation are common and usually concurrent in chronic kidney disease patients, and have been implicated as the main cause of high mortality. We reviewed the pathophysiology of the malnutrition-inflammation complex syndrome and its potential modulation by dietary and other nutritional interventions in chronic kidney disease patients. RECENT FINDINGS: The malnutrition-inflammation complex syndrome is a main cause of the atherosclerotic cardiovascular disease epidemic in chronic kidney disease. This may be by virtue of the syndrome's inflammatory components. Malnutrition and inflammation lead to weight loss over time, i.e. cachexia in slow motion, and result in decreased serum cholesterol and homocysteine levels. A 'reverse epidemiology' of cardiovascular risk factors is observed in chronic kidney disease, in that obesity, hypercholesterolemia and hyperhomocysteinemia are paradoxically associated with better survival. Among the possible etiologies of the malnutrition-inflammation complex syndrome, anorexia, low nutrient intake and oxidative stress are theoretically amenable to dietary modulation; however, the bulk of findings are epidemiological. SUMMARY: There is no consensus as to how to correct the malnutrition-inflammation complex syndrome in chronic kidney disease patients. Because the malnutrition-inflammation complex syndrome is multifactorial, its correction probably requires a battery of simultaneous interventions, rather than one single modality. Clinical trials focusing on the syndrome are currently non-existent and are therefore urgently required to improve poor clinical outcome in chronic kidney disease patients.

Humans↗
PubMedDate not supplied

Linking oxidative stress and inflammation in kidney disease: which is the chicken and which is the egg?

For end-stage renal disease (ESRD) patients, cardiovascular disease remains the single most common cause of excess morbidity and mortality. Furthermore, although the prevalence of traditional cardiovascular risk factors is high in the dialysis population, the extent and severity of associated cardiovascular morbidity and mortality remain disproportionate to traditional risk factor profiles. Consequently, considerable effort has been focused on "nontraditional" risk factors for cardiovascular events in this patient population. Among the examined nontraditional risk factors, increased oxidative stress as well as increased acute phase inflammation are postulated to be important contributors to uremic cardiovascular risk. Additional important uremic cardiovascular risk factors include malnutrition and endothelial dysfunction, both of which may be directly linked to the processes that cause increased oxidative stress and inflammation in uremia. In this context I review available data linking the pathogenesis of oxidative stress to acute phase inflammation and uremia. I also review data suggesting that oxidative stress in uremia directly contributes to the development of acute phase inflammation and that patients with higher levels of inflammation have higher levels of oxidative stress biomarkers. Similarly I review emerging data on the potential effects of antioxidant therapy on inflammatory biomarkers, as well as data suggesting that strategies to lower acute phase inflammation may also improve biomarkers of oxidative stress. Theoretical constructs evaluating the linkage of oxidative stress and inflammation in uremia and their contribution to the pathogenesis of atherosclerosis are suggested.

Antioxidants↗
PubMed1992

The role of intercellular adhesion molecule-1 in chronic airway inflammation.

We have examined the role of intercellular adhesion molecule-1 (ICAM-1) in chronic airway inflammation and airway hyperresponsiveness in a primate model of asthma. Airway cellular composition was assessed by bronchoalveolar lavage (BAL) and airway responsiveness was measured as the bronchoconstrictor response to inhaled methacholine. In animals with chronic airway inflammation (increased BAL eosinophils) and sustained airway hyperresponsiveness, a 7 day dosing scheme with a murine anti-human ICAM-1 monoclonal antibody (R6.5, 2 mg/kg/day; i.v.) did not reduce the existing airway inflammation or airway hyperresponsiveness. In contrast, a similar dosing scheme with dexamethasone (0.2 mg/kg/day, i.m.) was found to significantly reduce both the airway eosinophilia and hyperresponsiveness. However, one week after cessation of dexamethasone treatment, the airway inflammation and hyperresponsiveness returned to pre-treatment levels. In further experiments where animals were first treated with dexamethasone (7 days) followed by a 7 day treatment with R6.5, the reoccurrence of airway inflammation and subsequent increase in airway responsiveness was prevented. We conclude that the efficacy of ICAM-1 is primarily associated with inhibition of the influx of inflammatory cells into the airways and subsequent reduction in airway responsiveness. These data suggest that in lungs with pre-existing inflammation the modulation of ICAM-1 following treatment with glucocorticoids may be a novel and more selective long-term treatment for control of the chronic airway inflammation and hyperresponsiveness associated with bronchial asthma.

Airway Resistance↗
PubMed2006

Airway inflammation in subjects with gastro-oesophageal reflux and gastro-oesophageal reflux-related asthma.

STUDY OBJECTIVES: Asthma and gastro-oesophageal reflux (GER) are both characterized by airway inflammation. DESIGN: The purposes of this work were (i) to study airway inflammation in patients troubled by gastro-oesophageal reflux (GER) and GER associated with asthma, (ii) to ascertain whether GER can aggravate asthma by exacerbating the pre-existing airway inflammation and oxidative stress and (iii) to establish the validity of analysing breath condensate and induced sputum when studying the airways of subjects affected by GER. PATIENT S AND METHODS: We enrolled 14 patients affected by mild asthma associated with GER (40 +/-12 years), nine with mild but persistent asthma (39 +/- 13 years), eight with GER (35 +/- 11 years) and 17 healthy subjects (37 +/- 9 years). Sputum cell counts and concentrations of interleukin-4 (IL-4), IL-6 and 8-isoprostane were measured in breath condensate and supernatant. MEASUREMENTS AND RESULTS: GER-related asthma is characterized by an eosinophilic inflammation, as determined by elevated concentrations of IL-4 in breath condensate and sputum supernatant, and by sputum cell analysis. GER alone presents a neutrophilic pattern of inflammation when determined by elevated concentrations of IL-6 in sputum cell analysis. A concomitant increase has been found in 8-isoprostane in GER associated (or not associated) with asthma. CONCLUSIONS: We conclude that GER is characterized by a neutrophilic airway inflammation and by increased oxidative stress. GER does not however aggravate pre-existing airway inflammation in asthma patients. Determinations of inflammatory and oxidant markers in the breath condensate of subjects with GER reflect these measured in the induced sputum.

Adult↗
PubMed2005

Role of granulocyte elastase and interleukin-6 in the diagnosis of male genital tract inflammation.

Chronic genital tract inflammations are a frequent cause or at least a concomitant factor of male fertility disturbances. The diagnosis is difficult because of the mostly asymptomatic course of the disease. Therefore, determination of biochemical markers of inflammation in addition to the number of leucocytes in the seminal plasma has been recommended. The aim of the study was to find out whether determination of granulocyte elastase and interleukin-6 provide comparable and reliable results with regard to diagnosis of genital tract inflammation; in addition, the association between genital tract inflammation and semen quality should be evaluated with special focus on potentially disturbed sperm functions like sperm motility and DNA integrity. In a prospective study, the concentrations of interleukin-6 (IL-6) and granulocyte elastase were determined in seminal plasma samples from 340 patients to investigate the relationship with other parameters of genital tract inflammation such as the number of peroxidase-positive cells and conventional semen parameters. Microbiological investigations were included. As post-testicular inflammatory influences may cause sperm DNA damage, the correlation between IL-6 and elastase and DNA integrity was evaluated by the sperm chromatin structure assay. IL-6 and elastase were significantly correlated both with each other (P < 0.01) and the number of peroxidase-positive cells (P < 0.01). IL-6 showed a highly significant negative correlation with sperm vitality (P < 0.01) and a significant negative correlation with sperm motility (P < 0.05). Elastase concentrations were highly significantly associated with the number of peroxidase-positive cells (P < 0.01) and negatively correlated with sperm vitality (P < 0.01). Moreover, there were significantly negative correlations with sperm motility (P < 0.05), progressive motility according to WHO a quality (P < 0.05) as well as sperm morphology (P < 0.05). In addition, a significant negative correlation was observed between elastase concentrations and percentage of spermatozoa with intact DNA, which may suggest the use of anti-inflammatory treatment. It can be concluded that both IL-6 and granulocyte elastase are useful and suitable as markers for silent genital tract inflammation; in contrast to previous contributions there were clear correlations of IL-6 and granulocyte elastase with sperm parameters, the relationship of elastase with semen quality being more marked. Moreover, the results of the study confirm the need for a change of the threshold value of peroxidase-positive cells according to WHO definition to lower levels for definition of silent genital tract inflammation.

Adolescent↗
PubMed2006

Risk factors for prostatic inflammation extent and infection in benign prostatic hyperplasia.

AIM: To investigate the risk factors for prostatic inflammation extent and infection in patients with benign prostatic hyperplasia (BPH) so as to manage prostatic inflammation more efficiently. METHODS: Sixty patients with BPH undergoing TURP between September 2005 and December 2005 in West China Hospital of Sichuan University were studied. Prostate fluid (PF) was collected for the measurement of secretory IgA (SIgA) and complement 3 (C3). Prostate tissue were collected for testing bacterial 16S rDNA by real-time PCR, examining SIgA in the tissue and examining the inflammation. The possible clinical and immune risk factors for prostatic inflammation or infection were analyzed by using the logistic regression method. RESULTS: Abnormal white blood cell count in urinalysis, prostatic infection and a high concentration of C3 in PF are the risk factors for prostatic inflammation extent (P = 0.025, 0.034 and 0.035, respectively and odds ratio [OR] = 18.269, 8.284 and 1.508, respectively). Risk factors for prostatic infection include the C3 concentration and the concentration of SIgA in PF (P = 0.003 and 0.013, respectively, and OR=1.645 and 0.993, respectively). CONCLUSION: The present study suggests that prostatic inflammation is associated with urinary tract infection, prostatic infection and the activated complement and that prostatic infection is associated with the activated complement and downregulated mucosal immunity in prostates of the patients with BPH. It is also suggested that individual immune regulation should be considered in the treatment of prostatic inflammation and infection of patients with BPH.

Bacteria↗
PubMed2003

Painful inflammation-induced increase in mu-opioid receptor binding and G-protein coupling in primary afferent neurons.

Opioids mediate their analgesic effects by activating mu-opioid receptors (MOR) not only within the central nervous system but also on peripheral sensory neurons. The peripheral analgesic effects of opioids are best described under inflammatory conditions (e.g., arthritis). The present study investigated the effects of inflammation on MOR binding and G-protein coupling of full versus partial MOR agonists in dorsal root ganglia (DRG) of primary afferent neurons. Our results show that Freund's complete adjuvant (FCA) unilateral hindpaw inflammation induces a significant up-regulation of MOR binding sites (25 to 47 fmol/mg of protein) on DRG membranes without affecting the affinity of either full or partial MOR agonists. In our immunohistochemical studies, the number of MOR-immunoreactive neurons consistently increased. This increase was mostly caused by small-diameter nociceptive DRG neurons. The full agonist DAMGO induced MOR G-protein coupling in DRG of animals without FCA inflammation (EC50 = 56 nM; relative Emax = 100%). FCA inflammation resulted in significant increases in DAMGO-induced MOR G-protein coupling (EC50 = 29 nM; relative Emax = 145%). The partial agonist buprenorphine hydrochloride (BUP) showed no detectable G-protein coupling in DRG of animals without FCA inflammation; however, partial agonist activity of BUP-induced MOR G-protein coupling was detectable in animals with FCA inflammation (EC50 = 1.6 nM; relative Emax = 82%). In behavioral studies, administration of BUP produced significant antinociception only in inflamed but not in noninflamed paws. These findings show that inflammation causes changes in MOR binding and G-protein coupling in primary afferent neurons. They further underscore the important differences in clinical studies testing peripherally active opioids in inflammatory painful conditions.

Animals↗
PubMed1991

Accumulation of plasma cells in inflamed sites: effects of antigen, nonspecific microbial activators, and chronic inflammation.

Plasma cells are common in chronically inflamed sites, including periodontal lesions. The aim of this study was to determine which factors contribute to this local accumulation of plasma cells. Specifically, we sought to evaluate the effects of specific antigen and nonspecific activators from an infectious agent associated with chronic inflammation (Fusobacterium nucleatum, an organism prominent in chronic periodontal lesions) and the effect of the chronic inflammation itself. Chronic inflammation (14 to 17 days) was induced in horseradish peroxidase (HRP)-immune rabbits by subcutaneous injection of 50 microliters of sterile alum in several sites in their backs. Controls included sites injected with saline or more acute sites examined after 3 days of alum inflammation. Sites were challenged with HRP (the antigen), sonicated F. nucleatum (the nonspecific activator), or both together to see whether F. nucleatum has an adjuvant effect. Three days after challenge, HRP-specific antibody-forming cells (AFC) were enumerated after peroxidase histochemistry. In noninflamed sites or sites with acute inflammation, virtually no HRP-specific AFC were evident. In contrast, chronic inflammation alone was sufficient to elicit a specific AFC response (congruent to 10 cells per mm2). Addition of either F. nucleatum or HRP to the chronic lesion about doubled the number of HRP-specific AFC. However, a dramatic 8- to 15-fold (80 to 150/mm2) increase was seen in chronically inflamed sites challenged with antigen and activator together. Interestingly, the activator did not have this adjuvant effect in the acute sites or in normal skin. In short, accumulation of plasma cells in inflamed sites is promoted by chronic inflammation, activators of microbial origin, and specific antigen. This milieu can be expected to develop in some periodontal lesions and could help explain why gingival crevicular fluid from some sites may contain extraordinary levels of locally produced specific antibodies for certain antigens.

Acute Disease↗
PubMed1997

Inflammation modulates in vitro colonic myoelectric and contractile activity and interstitial cells of Cajal.

Inflammation suppresses phasic contractile activity in vivo. We investigated whether inflammation also suppresses in vitro phasic contractile activity and, if so, whether this could in part be due to the alteration of specific slow wave characteristics and morphology of the interstitial cells of Cajal (ICC). Circular muscle strips were obtained from normal and inflamed distal canine colon. Inflammation was induced by mucosal exposure to ethanol and acetic acid. The amplitudes of spontaneous, methacholine-induced, substance P-induced, and electrical field stimulation-induced contractions were smaller in inflamed muscle strips than in normal muscle strips. Inflammation reduced the resting membrane potential and the amplitude and duration of slow waves in circular muscle cells. Inflammation did not affect the amplitude of inhibitory junction potentials but did decrease their duration. Ultrastructural studies showed expansion of the extracellular space between circular muscle cells, reduction in the density of ICC and associated neural structures, damage to ICC processes, vacuolization of their cytoplasm, and blebbings of the plasma membrane. We conclude that inflammation-induced alterations of slow wave characteristics contribute to the suppression of phasic contractions. These alterations may, in part, be due to the damage to ICC. Inflammation impairs both the myogenic and neural regulation of phasic contractions.

Acetic Acid↗
PubMed1999

Medullary dorsal horn neuronal activity in rats with persistent temporomandibular joint and perioral inflammation.

Studies at spinal levels indicate that peripheral tissue or nerve injury induces a state of hyperexcitability of spinal dorsal horn neurons that participates in the development of persistent pain and hyperalgesia. It has not been demonstrated that persistent injury in the orofacial region leads to a similar state of central hyperexcitability in the trigeminal system. The purpose of the present study was to conduct a parametric analysis of the response properties of nociceptive and nonnociceptive neurons in trigeminal nucleus caudalis (medullary dorsal horn, MDH) in a rat model of persistent orofacial inflammation. Neurons were recorded extracellularly and classified as low-threshold mechanoreceptive (LTM, n = 49), wide dynamic range (WDR, n = 82), and nociceptive-specific (NS, n = 11) neurons according to their response properties to mechanical stimuli applied to their cutaneous receptive fields (RFs). The inflammation was induced 24 h before the recordings by injecting complete Freund's adjuvant (CFA) into the temporomandibular joint (TMJ) capsule or the perioral (PO) skin. The mean areas of the high-threshold RFs of WDR neurons in TMJ (8.66 +/- 0.61 cm(2), n = 25) and PO (5.61 +/- 2.07 cm(2), n = 25) inflamed rats were significantly larger than those in naive rats (1.10 +/- 0. 16 cm(2), n = 32). The mean RF size in TMJ-inflamed rats also was significantly larger than that in PO-inflamed rats (P < 0.01). Furthermore the mean area of the RFs of NS neurons (3.74 +/- 1.44 cm(2), n = 5) was significantly larger in TMJ inflamed rats as compared with naive rats (0.4 +/- 0.09 cm(2), n = 3) (P < 0.05). The background activity in the TMJ- and PO-inflamed rats was generally greater in WDR and NS neurons, but less in LTM neurons, when compared with naive rats. The responses of WDR neurons to noxious mechanical stimuli were increased significantly in TMJ-inflamed rats (P < 0.05) as compared with naive rats. WDR neuronal responses to mechanical stimulation also were increased in PO-inflamed rats but to a lesser extent than in TMJ-inflamed rats. The injection of CFA into the TMJ or PO skin resulted in reduced responses of LTM neurons to mechanical stimuli. The responses of MDH nociceptive neurons to 48-55 degrees C heating were greater in inflamed rats as compared with naive rats. A subpopulation of WDR neurons recorded from TMJ (n = 4 of 10)- or PO (n = 3 of 13)-injected rats responded to cooling in addition to heating of the RFs but did not grade their responses with changes in stimulus intensity. These results indicate that persistent orofacial inflammation produced hyperexcitability of MDH nociceptive neurons. TMJ inflammation resulted in more robust changes in MDH nociceptive neurons as compared with PO inflammation, consistent with previous studies of increased inflammation, increased MDH Fos-protein expression, and increased MDH preprodynorphin mRNA expression in this deep tissue orofacial model of pain and hyperalgesia. The inflammation-induced MDH hyperexcitability may contribute to mechanisms of persistent pain associated with orofacial deep tissue painful conditions.

Animals↗
PubMed2001

Orofacial deep and cutaneous tissue inflammation and trigeminal neuronal activation. Implications for persistent temporomandibular pain.

A rat model has been developed to characterize the responses of brainstem trigeminal neurons to orofacial deep and cutaneous tissue inflammation and hyperalgesia. 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. The TMJ and PO inflammation resulted in orofacial behavioral hyperalgesia and allodynia that peaked within 4-24 h and persisted for at least 2 weeks. Compared to cutaneous CFA injection, the injection of CFA into the TMJ produced a significantly stronger inflammation associated with a selective upregulation of preprodynorphin mRNA in the trigeminal spinal complex, an enhanced medullary dorsal horn hyperexcitability, and a greater trigeminal Fos protein expression, a marker of neuronal activation. The Fos-LI induced by TMJ inflammation persisted longer, was more intense, particularly in the superficial laminae, and more widespread rostrocaudally. Thus, the inflammatory irritant produces a stronger effect in deep than in cutaneous orofacial tissue. As there is heavy innervation of the TMJ by unmyelinated nerve endings, a strong nociceptive primary afferent barrage is expected following inflammation. An increase in TMJ C-fiber input after inflammation and strong central neuronal activation may initiate central hyperexcitability and contribute to persistent pain associated with temporomandibular disorders. Since deep inputs may be more effective in inducing central neuronal excitation than cutaneous inputs, greater sensory disturbances may occur in pain conditions involving deep tissues than in those involving cutaneous tissues.

Animals↗