Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INFLAMMATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1986

An assessment of inflammation in the reservoir after restorative proctocolectomy with ileoanal ileal reservoir.

The significance of inflammation of the mucosa of the ileal reservoir after restorative proctocolectomy is not known although in some cases it appears to be associated with symptoms when the condition has been referred to as pouchitis. This investigation has aimed to determined the prevalence of inflammation, to define pouchitis and to examine some factors which might be related to inflammation. Mucosal biopsies from the ileal reservoir were studied in 90 patients at up to 62 months after closure of the ileostomy. A histological grading system (0-6) was used to assess the severity of inflammation. Some degree of chronic and acute inflammation was found in 87% and 30% of cases respectively. The prevalence of a grade of 4 or more was 23% and 3.5%. There was a correlation between severity of chronic and acute inflammation. Severe histological acute inflammation (grade 4-6) was associated with sigmoidoscopic features of inflammation and with increased frequency of defaecation. Of 55 patients sigmoidoscoped by one clinician, 6 (11%) had pouchitis which was characterised by macroscopic inflammation of the reservoir, diarrhoea and a histological grade of 4 or more. The severity of chronic inflammation was not related to frequency of defaecation. Histological inflammation could not be correlated with the type of reservoir, residual volume after evacuation of a known volume of stool substitute introduced per anum into the reservoir or compliance of the reservoir. Acute inflammation was significantly more severe in patients with ulcerative colitis than in those with familial adenomatous polyposis.

Adenomatous Polyposis Coli↗
PubMed2001

Clinical significance of intra-amniotic inflammation in patients with preterm labor and intact membranes.

OBJECTIVE: The purpose of this study was to determine the frequency and clinical significance of intraamniotic inflammation in patients with preterm labor and intact membranes. STUDY DESIGN: Amniocentesis was performed in 206 patients with preterm labor and intact membranes. Amniotic fluid was cultured for aerobic and anaerobic bacteria and mycoplasmas. The diagnosis of intraamniotic inflammation was made in patients with a negative amniotic fluid culture on the basis of amniotic fluid concentrations of interleukin-6 (>2.6 ng/mL, derived from receiver operating characteristic curve analysis). Statistical analysis was conducted with contingency tables and survival techniques. RESULTS: Intra-amniotic inflammation (negative amniotic fluid culture but elevated amniotic fluid interleukin-6) was more common than intra-amniotic infection (positive amniotic fluid culture regardless of amniotic fluid interleukin-6 concentration; 21% [44/206 women] vs 10% [21/206 women]; P <.001). The amniocentesisto-delivery interval was significantly shorter in patients with intra-amniotic inflammation than in patients with a negative culture and without an inflammation (median, 20 hours [range, 0.1-2328 hours] vs median, 701 hours [range, 0.1-3252 hours], respectively; P <.0001). Spontaneous preterm delivery of <37 weeks was more frequent in patients with intra-amniotic inflammation than in those with a negative culture and without inflammation (98% vs 35%; P <.001). Patients with intra-amniotic inflammation had a significantly higher rate of adverse outcome than patients with a negative culture and without intra-amniotic inflammation. Adverse outcomes included clinical and histologic chorioamnionitis, funisitis, early preterm birth, and significant neonatal morbidity. There were no significant differences in the rate of adverse outcomes between patients with a negative culture but with intra-amniotic inflammation and patients with intra-amniotic infection (positive culture regardless of amniotic fluid interleukin-6 concentration). CONCLUSION: Intra-amniotic inflammation/infection complicates one third of the patients with preterm labor (32%; 65/206 women), and its presence is a risk factor for adverse outcome. The outcome of patients with microbiologically proven intra-amniotic infection is similar to that of patients with intra-amniotic inflammation and a negative amniotic fluid culture. We propose that the treatment of patients in preterm labor be based on the operational diagnosis of intra-amniotic inflammation rather than the diagnosis of intra-amniotic infection because the latter diagnosis cannot be undertaken rapidly.

Amniocentesis↗
PubMed1997

Effect of inflammation on the proliferation of human gingival epithelial cells in vitro.

The adaptive or pathologic responses of epithelial cells to inflammation are poorly characterized. The purpose of this study was to determine if epithelial cells cultured from clinically healthy and inflamed human gingival tissues express differences in proliferation rate and viability. Briefly, the inflammation status of individual donor sites from 101 patients was visually assessed at the time of periodontal surgery and categorized as either non-to-slightly inflamed, moderately inflamed, or severely inflamed. Discarded gingival tissues were then processed to obtain primary cell cultures, for which proliferation rates were determined by calculating the ratio of mean population doublings to the number of days required for cultures to become confluent. In general, the cells in the minimally inflamed group exhibited characteristics different than cells in the moderately and severely inflamed groups. Specifically, the cells obtained from clinical sites which exhibited no-to-slight inflammation had a significantly higher mean proliferation rate than cells in either the moderate inflammation group or the severe inflammation group. Based on trypan blue exclusion, the cells obtained from clinical sites which exhibited no-to-slight inflammation also were more viable than cells obtained from sites with moderate inflammation or severe inflammation. Microscopic evaluation showed morphological changes associated with increased inflammation. Cell cycle analysis by fluorescent-activated cell sorting (FACS) revealed a directly proportional relationship between the degree of inflammation and apoptosis, and a strong inversely proportional trend between the degree of inflammation and the numbers of cells undergoing mitosis. Taken together, these data suggest that epithelial cell proliferation and viability are inversely associated with the degree of gingival inflammation, once a putative "adaptive threshold" is exceeded. Elucidation of the underlying mechanisms will likely lead to improvements in clinical diagnosis and treatment.

Adult↗
PubMed1990

[Localization of inflammation of tympanic cavity in human temporal bone pathology].

When we treat patients of otitis media, it is important to know the pathogenesis of otitis media. Therefore histopathological change of epithelium and bone in each site of tympanic cavity was observed using human temporal bones. Histopathological change of epithelium was classified as: acute, subacute and chronic in eighteen sites of tympanic cavity. Histopathological change of bone was observed in thirteen sites of tympanic cavity. And the frequency of histopathological change of epithelium and bone in each site was compared. A review of 350 temporal bones collected from autopsy cases revealed 171 (49.1%) to have otitis media, and a review of 170 temporal bones of otitis media cases revealed 165 (97.1%) to have bone changes. Differences in frequency of histopathological change of epithelium and bone existed in each site. Histopathological change in inferior portion of mastoid cells, round window niche and tympanic sinus was more frequent than in the other sites. Change of epithelium: in acute inflammation, no differences in frequency of histopathological change existed; in subacute inflammation and chronic inflammation, differences in frequency of histopathological change existed in each site. Change of bone: most changes were bone formation and bone reconstruction, but there was no clear finding that bone formation narrowed tympanic cavity without mastoid cells. Osseous destruction was found in mastoidectomy cases and cholesteatoma cases. It is thought that the frequency of inflammation is related to structure of cavity, aeration, immunologic activity or structure of the epithelium, and that the pathogenesis of otitis media, especially in chronic otitis media, is different in each site of tympanic cavity. It is thought that because the subjects of this study were not operated cases but autopsy cases, slight bone change was very frequent, but severe bone change, was rare. And we examined the pathogenesis of tympanic cavity of each case of acute inflammation and chronic inflammation of pars tensa and cases where there were no findings of inflammation in the pars tensa. In most cases of acute inflammation of pars tensa, inflammation of tympanic cavity was acute; in chronic inflammation of pars tensa, chronic. It was interesting that, in cases of normal pars tensa, inflammation was frequently found in tympanic cavity. Therefore, it is important to pay attention to the possibility of inflammation in tympanic cavity, even if the tympanic membrane appears normal.

Adolescent↗
PubMed1992

99Tcm-labelled IgG scanning does not predict the distribution of intestinal inflammation in patients with inflammatory bowel disease.

In order to assess the value of 99Tcm-labelled-immunoglobulin G(99Tcm-IgG) in the assessment of the activity and distribution of intestinal inflammation in patients with inflammatory bowel disease (IBD), 99Tcm-IgG scans were performed in 18 patients. Patients were divided clinically into two groups, those with (ten patients) and those without (eight patients), intestinal inflammation. Disease activity and distribution were assessed by 111In-oxine granulocyte scanning and/or histological extent of inflammation at endoscopy or surgery in all patients with IBD and most of those without intestinal inflammation. In the assessment of the presence or absence of inflammation, a sensitivity of 80% and specificity of 87% were achieved. However, when the localization of intestinal inflammation was evaluated, only five of eight true positive scans were concordant with the distribution of intestinal inflammation as determined by other methods. Thus, significant areas of inflammation were missed in five of ten patients with IBD (two false negative, three incorrect localization of inflammation). Although 99Tcm-IgG scanning appears to have moderate sensitivity and acceptable specificity in the detection of intestinal inflammation, it performs poorly in assessing the distribution of inflammation and is, therefore, of little value in the assessment of patients with suspected or proven IBD.

Australia↗
PubMed2006

Role of substance P in hydrogen sulfide-induced pulmonary inflammation in mice.

We have shown earlier that H(2)S acts as a mediator of inflammation. In this study, we have investigated the involvement of substance P and neurogenic inflammation in H(2)S-induced lung inflammation. Intraperitoneal administration of NaHS (1-10 mg/kg), an H(2)S donor, to mice caused a significant increase in circulating levels of substance P in a dose-dependent manner. H(2)S alone could also cause lung inflammation, as evidenced by a significant increase in lung myeloperoxidase activity and histological evidence of lung injury. The maximum effect of H(2)S on substance P levels and on lung inflammation was observed 1 h after NaHS administration. At this time, a significant increase in lung levels of TNF-alpha and IL-1beta was also observed. In substance P-deficient mice, the preprotachykinin-A knockout mice, H(2)S did not cause any lung inflammation. Furthermore, pretreatment of mice with CP-96345 (2.5 mg/kg ip), an antagonist of the neurokinin-1 (NK(1)) receptor, protected mice against lung inflammation caused by H(2)S. However, treatment with antagonists of NK(2), NK(3), and CGRP receptors did not have any effect on H(2)S-induced lung inflammation. Depleting neuropeptide from sensory neurons by capsaicin (50 mg/kg sc) significantly reduced the lung inflammation caused by H(2)S. In addition, pretreatment of mice with capsazepine (15 mg/kg sc), an antagonist of the transient receptor potential vanilloid-1, protected mice against H(2)S-induced lung inflammation. These results demonstrate a key role of substance P and neurogenic inflammation in H(2)S-induced lung injury in mice.

Air Pollutants↗
PubMed2002

Changes in gene expression and neuronal phenotype in brain stem pain modulatory circuitry after inflammation.

Recent studies indicate that descending pain modulatory pathways undergo time-dependent changes in excitability following inflammation involving both facilitation and inhibition. The cellular and molecular mechanisms of these phenomena are unclear. In the present study, we examined N-methyl-D-aspartate (NMDA) receptor gene expression and neuronal activity in the rostral ventromedial medulla (RVM), a pivotal structure in pain modulatory circuitry, after complete Freund's adjuvant (CFA)-induced hindpaw inflammation. The reverse transcription polymerase chain reaction analysis indicated that there was an upregulation of mRNAs encoding NMDA receptor subunits in the RVM after inflammation. The increase in the NR1, NR2A, and NR2B receptor mRNAs started at 5 h, maintained for 1-7 days (P < 0.05-0.001) and returned to the control level at 14 days after inflammation. Western blot analysis indicated that the protein translation products of the NR2A subunit were also increased (P < 0.01). In single-unit extracellular recordings, we correlated RVM neuronal activity with the paw withdrawal response in rats with inflammation. We describe these RVM cells as on-, off-, and neutral-like cells because of their similarity to previous studies in which neuronal responses were correlated with tail-flick nocifensive behavior in the absence of inflammation. In contrast to previous studies in the absence of inflammation, using tail flick as a behavioral correlate, fewer off-like cells in naïve animals exhibited a complete pause before the paw withdrawal to a noxious thermal stimulus. The percentage of cells showing a pause of activity after noxious stimulation was further reduced after inflammation (chi(2) P < 0.0001 vs. naïve rats). Continuous neuronal recordings (3-6.5 h) revealed a phenotypic switch of RVM neurons during the development of inflammation: 11/15 neutral-like cells initially unresponsive to noxious stimuli exhibited and maintained response profiles characteristic of pain modulatory neurons (became off-like: n = 5; became on-like: n = 6). Neutral-like cells recorded in noninflamed animals did not show response profile changes during continuous recordings (5-5.5 h, n = 7). A population study (n = 165) confirmed an increase in on- and off-like cells and a decrease in neutral-like cells at 24 h after inflammation as compared with naïve rats (P < 0.001). These results suggest that enhanced NMDA receptor activation mediates time-dependent changes in excitability of RVM pain modulatory circuitry. The functional phenotypic switch of RVM neurons provides a novel mechanism underlying activity-dependent plasticity and enhanced net descending inhibition after inflammation.

Action Potentials↗
PubMed1999

Systemic inflammatory response syndrome without systemic inflammation in acutely ill patients admitted to hospital in a medical emergency.

Criteria of the systemic inflammatory response syndrome (SIRS) are known to include patients without systemic inflammation. Our aim was to explore additional markers of inflammation that would distinguish SIRS patients with systemic inflammation from patients without inflammation. The study included 100 acutely ill patients with SIRS. Peripheral blood neutrophil and monocyte CD11b expression, serum interleukin-6, interleukin-1beta, tumour necrosis factor-alpha and C-reactive protein were determined, and severity of inflammation was evaluated by systemic inflammation composite score based on CD11b expression, C-reactive protein and cytokine levels. Levels of CD11b expression, C-reactive protein and interleukin-6 were higher in sepsis patients than in SIRS patients who met two criteria (SIRS2 group) or three criteria of SIRS (SIRS3 group). The systemic inflammation composite score of SIRS2 patients (median 1.5; range 0-8, n=56) was lower than that of SIRS3 patients (3.5; range 0-9, n=14, P=0.013) and that of sepsis patients (5.0; range 3-10, n=19, P<0.001). The systemic inflammation composite score was 0 in 13/94 patients. In 81 patients in whom systemic inflammation composite scores exceeded 1, interleukin-6 was increased in 64 (79.0%), C-reactive protein in 59 (72.8%) and CD11b in 50 (61.7%). None of these markers, when used alone, identified all patients but at least one marker was positive in each patient. Quantifying phagocyte CD11b expression and serum interleukin-6 and C-reactive protein concurrently provides a means to discriminate SIRS patients with systemic inflammation from patients without systemic inflammation.

Acute Disease↗
PubMed1993

Quantitative determination of pentane in exhaled air correlates with colonic inflammation in the rat colitis model.

Oxygen radicals play a key role in inflammation and inflammatory tissue damage. Quantitative determination of pentane, a hydrocarbon generated by membrane lipid peroxidation initiated by oxygen radicals, in expired air has been used as a noninvasive determinant or index of inflammation in various conditions. Herein we report the first examination of the relationship between exhaled pentane and colonic inflammation in a rodent model of colitis. Colitis was induced in rats (n = 33) using the trinitrobenzene-sulfonic acid (TNB) model of colitis. Exhaled air was collected in a closed chamber on randomly selected animals on days 1, 2, 4, 7, 11, 13, 15, 20, and 25 post-TNB treatment, and pentane was assayed by means of gas chromatography. Gross and microscopic evidence of inflammation was compared with exhaled pentane levels. Pentane levels varied from 0.0 to 14.6 nmol/l of air and were significantly increased in TNB-treated rats compared with control rats only on days 7 to 15 after treatment (P < 0.05). Gross inspection showed severe colonic inflammation through the first week (mean score = 4.7 out of a possible 5), persistent inflammation on days 7 to 15 (3.2), and healing and fibrosis from the end of week two until day 25 (1.9 to 0). Histologic evaluation confirmed a progression of inflammation from acute ulceration to chronic inflammation to fibrosis and scarring. We have demonstrated that pentane exhalation is increased after the induction of colonic inflammation, with a seven-day lag time, and returns rapidly to normal as acute inflammation resolves. This suggests that pentane exhalation can be used as a noninvasive measure of colonic inflammation in rodent models of colitis and perhaps clinically in humans.

Air↗
PubMed1998

Intrathecal NSAIDS attenuate inflammation-induced neuropeptide release from rat spinal cord slices.

Inflammation enhances release of neuropeptides from sensory nerve terminals in the spinal cord, and this may contribute to the development of hyperalgesia. In a similar manner, proinflammatory prostaglandins also augment peptide release from sensory neurons. To ascertain whether the inflammation-induced increase in peptide release from spinal cord slices is mediated by production of these eicosanoids, we examined whether intrathecal administration of nonsteroidal antiinflammatory drugs (NSAIDS) could attenuate the effects of inflammation. Unilateral injection of 150 microl of complete Freund's adjuvant (CFA) into the hindpaw of adult Sprague-Dawley rats resulted in a lower threshold for paw withdrawal (hyperalgesia) on 1, 4, and 5 days after injection. Five days after the induction of inflammation, capsaicin-evoked release of immunoreactive substance P (iSP) and immunoreactive calcitonin gene-related peptide (iCGRP) was increased approximately 2-fold in slices of cord tissue from the side ipsilateral to CFA injection, compared to spinal cord slices from the non-inflamed side. Intrathecal administration of 1 microl/h of 10 nmol/microl solution of the NSAID, ketorolac, for 1 day prior to and throughout the inflammation significantly attenuated the inflammation-induced increase in capsaicin-evoked release of both peptides without altering release in cord tissue from the non-inflamed side. Systemic administration of the same amount of ketorolac did not attenuate the effect of inflammation on peptide release. Intrathecal administration of 16 nmol/h (S)-ibuprofen, before and throughout the inflammation, also significantly attenuated the increase in evoked neuropeptide release associated with inflammation, whereas (R)-ibuprofen was ineffective. These results suggest that inhibition of cyclooxygenase at the level of the spinal cord attenuates the augmentation of neuropeptide release induced by peripheral inflammation, and provide further evidence for an action of prostaglandins at central terminals of sensory neurons during inflammation.

Animals↗
PubMed1996

The relationship of gingival crevicular fluid short chain carboxylic acid concentration to gingival inflammation.

Short-chain carboxylic acids (SCCA; C < or = 5; e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and exhibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentrations, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingival inflammatory agents, gingival inflammation should increase with increasing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an objective quantitative assessment of gingival inflammation used. To accomplish these tasks, sites within subjects were stratified by location and pocket depth, and the following quantified: bacterial presence; SCCA concentration; and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and canines (all r > or = 0.47; all p < or = 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation did not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of these pathogens (-0.31 < or = r < or = 0.39; 0.08 < or = p < or = 0.75) for any of the locations. Finally, the SCCA concentration did not correlate with the level of individual or groups of pathogens. These data, together with historical work and other preliminary data, support the hypothesis that SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, begin to explain the apparent lack of a direct relationship between current gingival inflammation and the prediction of bacterially mediated periodontal attachment loss.

Aggregatibacter actinomycetemcomitans↗
PubMed1986

Effect of dexamethasone, indomethacin, ibuprofen, and probenecid on carrageenan-induced brain inflammation.

A model of brain inflammation has recently been developed in mice using intraventricular injection of carrageenan (CAR). This model is characterized by increased brain water and vascular permeability, by neutrophil extravasation, and by evidence of increased pro-inflammatory arachidonic acid metabolites. The purpose of the current experiments was to determine the mechanism(s) by which CAR induces brain inflammation and to determine the utility of the CAR model in testing systemically administered therapeutic agents for their capacity to inhibit brain inflammation. Dexamethasone inhibited the increased brain water but not the increased vascular permeability produced by CAR. Indomethacin, an inhibitor of prostaglandin formation, suppressed peripheral inflammation produced by local injection of CAR but not brain inflammation produced by intraventricular CAR injection. Subsequent studies with carbon-14-labeled indomethacin showed that indomethacin penetrates peripheral tissues but is excluded from normal brain or brains inflamed by injection of CAR. Ibuprofen, another prostaglandin synthesis inhibitor, also had no effect on brain inflammation. Probenecid, an organic acid transport inhibitor, completely inhibited CAR-induced brain inflammation and also slowed brain elimination of intraventricularly administered prostaglandins. These experiments suggest, but do not conclusively prove, that increased prostaglandin formation contributes to brain inflammation. Also, the results with indomethacin and CAR-induced brain inflammation indicate that CAR-induced inflammation may be a useful model for screening for the ability of anti-inflammatory agents to cross the blood-brain barrier and exert their effect on brain inflammation.

Animals↗
PubMed1992

Mitomycin C-induced colitis in rats: a new animal model of acute colonic inflammation implicating reactive oxygen species.

The mechanism of the tissue damage induced by colonic inflammation in ulcerative colitis is not established. We therefore developed and characterized a simple new rat model of acute colonic inflammation induced by a single systemic injection of mitomycin C. After an intraperitoneal injection of mitomycin-C, colon histologic examination revealed transient (3 to 14 days) diffuse, colonic inflammation and injury that, like human ulcerative colitis, was limited to the mucosal layer. The rest of the gastrointestinal tract was spared. Gut permeability, as measured by urinary excretion of orally administered lactulose and mannitol, was unchanged 3 days after injection, when inflammation was already present; permeability was increased at 7 days, when inflammation was maximal. Mitomycin C did not produce inflammation in experimentally bypassed segments of small bowel despite the presence of colonic-type bacteria, suggesting that lack of intraluminal bacteria was not responsible for the absence of inflammation in the small intestine. Chemiluminescence, a means of estimating levels of reactive oxygen species, was greater in the intact, inflamed colon of mitomycin C-treated rats than in bypassed segments. Moreover, inflamed mucosal scrapings produced more in vitro luminol-enhanced chemiluminescence. Furthermore, the reactive oxygen species scavengers allopurinol, catalase, and WR-2721 decreased inflammation severity. We therefore conclude: (1) the mitomycin C-treated rat is a novel, easy to prepare animal model of acute inflammation of colonic mucosa, with morphologic similarities to the acute phase of ulcerative colitis in human beings; (2) increased gut permeability in mitomycin C-treated rats is the result, not the cause, of the inflammation; and (3) reactive oxygen species play an important role in colonic inflammation and tissue injury in this model, and possibly in human ulcerative colitis.

Animals↗
PubMedDate not supplied

Acute systemic inflammation is associated with an increase in peritoneal solute transport rate in chronic peritoneal dialysis patients.

BACKGROUND: This study was performed to evaluate the effects of acute systemic inflammation on peritoneal solute transport rate (PSTR) in chronic peritoneal dialysis (CPD) patients. METHODS: A baseline standard peritoneal equilibration test (PET) was performed on each patient every 6 months, and blood concentration of high-sensitivity C-reactive protein (hs-CRP) was assayed every 2 months in our peritoneal dialysis clinic. Acute systemic inflammation was defined as a greater than 10-fold increase in hs-CRP concentration compared with baseline value, in the absence of peritonitis, and returning to baseline level in 2 months. In patients with acute systemic inflammation, PET and hs-CRP concentration assays were performed during inflammation and after recovery. Ten patients with acute systemic inflammation were enrolled in the inflammation group and 42 other patients served as controls. RESULTS: There were no significant changes in hs-CRP and dialysate-to-plasma ratio of creatinine (D/Pcreat) in the control group during the study period. In the inflammation group, median hs-CRP levels at baseline, during acute inflammation, and at recovery were 2.3 mg/L (range 0.3 - 4.5 mg/L), 39.2 mg/L (range 15.1 - 117.4 mg/L), and 3.7 mg/L (range 0.9 - 8.9 mg/L), respectively. Median D/Pcreat increased significantly from baseline (0.64; range 0.55 - 0.98) to time of acute inflammation (0.72; range 0.60 - 0.96) (p < 0.05). The D/Pcreat at recovery was 0.67 (range 0.52 - 0.94), which decreased significantly from time of acute inflammation (p < 0.05). There was no correlation between changes in log (hs-CRP) and changes in D/Pcreat. CONCLUSION: We have shown here that acute systemic inflammation is associated with a temporary increase in PSTR in CPD patients.

Biological Transport↗
PubMed2005

Local and systemic inflammation in chronic obstructive pulmonary disease.

There is growing evidence for systemic inflammation in chronic obstructive pulmonary disease (COPD). Increased circulating levels of inflammatory cytokines and acute phase proteins occur in stable disease, and COPD exacerbations are notably associated with pulmonary and systemic inflammation. Although the course of inflammation is determined by the balance between pro- and antiinflammatory mediators, in COPD most attention has focused on the former. During exacerbation, however, upregulation of antiinflammatory markers occurs. The main causes of systemic inflammation in COPD remain to be elucidated, although systemic hypoxia is a candidate factor. Although a relationship between lung and systemic inflammation has been suggested, experimental evidence indicates no direct correlations in the regulation of inflammation in the pulmonary and systemic compartments. Longitudinal studies are needed to unravel the role of systemic inflammation in the course of COPD, to analyze the role of acute exacerbations on the chronicity of inflammation, and to evaluate the response of systemic inflammation to different interventions. Emphasis should be placed on the identification of signaling pathways induced and/or altered in skeletal muscle by inflammation, as muscle wasting is a prominent feature of chronic inflammatory disease conditions and contributes significantly to impaired physical functioning and health status in COPD.

Cytokines↗
PubMed2002

The roles of NMDA receptor activation and nucleus reticularis gigantocellularis in the time-dependent changes in descending inhibition after inflammation.

Previous studies indicate that descending modulation of nociception is progressively increased following persistent inflammation. The present study was designed to further examine the role of supraspinal neurons in descending modulation following persistent inflammation. Constant levels of paw withdrawal (PW) and tail flick (TF) latencies to noxious heat stimuli were achieved in lightly anesthetized rats (pentobarbital sodium 3-10 mg/kg/h, i.v.). Electrical stimulation (ES, 0.1 ms, 100 Hz, 20-200 A) was delivered to the rostral ventromedial medulla (RVM), mainly the nucleus raphe magnus (NRM). ES produced intensity-dependent inhibition of PW and TF. Following a unilateral hindpaw inflammation produced by injection of complete Freund's adjuvant (CFA), ES-produced inhibition underwent time-dependent changes. There was an initial decrease at 3 h after inflammation and a subsequent increase after inflammation in the excitability of RVM neurons and the inhibition of nocifensive responses. These changes were most robust after stimulation of the inflamed paw although similar findings were seen on the non-inflamed paw and tail. The inflammation-induced dynamic changes in descending modulation appeared to be correlated with changes in the activation of the N-methyl--aspartate (NMDA) excitatory amino acid receptor. Microinjection of an NMDA receptor antagonist, AP5 (1 pmol), resulted in an increase in the current intensity required for inhibition of the PW and TF. The effect of AP5 was less at 3 h after inflammation and significantly greater at 11-24 h after inflammation. In a subsequent experiment, ES-produced inhibition of nocifensive responses after inflammation was examined following selective chemical lesions of the nuclei reticularis gigantocellularis (NGC). Compared to vehicle-injected animals, microinjection of a soma-selective excitotoxin, ibotenic acid, enhanced ES-produced inhibition at 3 h but not at 24 h after inflammation. We propose that these time course changes reflect dynamic alterations in concomitant descending facilitation and inhibition. At early time points, NMDA receptor and NGC activation enhance descending facilitation; as time progresses, the dose-response curve of NMDA shifts to the left and descending inhibition dominates and masks any descending facilitation.

2-Amino-5-phosphonovalerate↗
PubMed2003

Coeruleospinal inhibition of nociceptive processing in the dorsal horn during unilateral hindpaw inflammation in the rat.

Behavioral and neurochemical studies have shown that the coeruleospinal modulation system is activated by peripheral inflammation, and that this modulation system is active in only the dorsal horn ipsilateral, but not in the dorsal horn contralateral, to the site of inflammation; the present study was designed to confirm electrophysiologically this previous finding. Extracellular recordings from dorsal horn neurons were continued for at least 4 h after the induction of inflammation. Unilateral hindpaw inflammation was produced by a subcutaneous injection of carrageenan (2 mg in 0.15 ml saline). Background activity and responses to noxious heating were compared between rats receiving bilateral lesions in the locus coeruleus/subcoeruleus (LC/SC) and non-operated control rats. In neurons located in the dorsal horn ipsilateral to the inflamed paw, prior to inflammation, there was no significant difference in either the background activity or the heat-evoked response in neurons in LC/SC-lesioned compared to LC/SC-intact rats. Four hours after the induction of inflammation, there was a significant increase in both the background activity and heat-evoked response in neurons in LC/SC-lesioned compared to LC/SC-intact rats. In neurons located in the dorsal horn contralateral to the inflamed paw, 4 h after inflammation, no significant increase in either the background activity or the heat-evoked response in neurons in LC/SC-lesioned rats was observed, as well as in the case before inflammation. These results suggest that the coeruleospinal modulation system is active in only the dorsal horn ipsilateral, but not in the dorsal horn contralateral, to the site of inflammation during the development of unilateral hindpaw inflammation.

Action Potentials↗
PubMed2003

Inflammation and nutrition in renal insufficiency.

Protein-energy malnutrition (PEM) and inflammation are common in patients with chronic kidney disease (CKD) and worsen as the CKD progresses toward the end-stage renal disease (ESRD). These conditions are major predictors of poor clinical outcome in kidney failure, as reflected by a strong association between hypoalbuminemia and cardiovascular disease (CVD). It has been suggested that inflammation is the cause of both PEM and CVD and, hence, the main link among these conditions, but these hypotheses are not well established. Increased release or activation of inflammatory cytokines, such as interleukin-6 or tumor necrosis factor alpha, may suppress appetite, cause muscle proteolysis and hypoalbuminemia, and may be involved in atherogenesis. Increasing serum levels of proinflammatory cytokines caused by reduced renal function, volume overload, oxidative or carbonyl stress, decreased levels of antioxidants, increased susceptibility to infection in uremia, and the presence of comorbid conditions may lead to inflammation in CKD patients. In hemodialysis patients, the exposure to dialysis tubing and dialysis membranes, poor quality of dialysis water, back-filtration or back-diffusion of contaminants, and foreign bodies in dialysis access maybe additional causes of inflammation. Similarly, episodes of overt or latent peritonitis, peritoneal dialysis (PD) catheter and its related infections, and constant exposure to PD solution may contribute to inflammation in these patients. The degree to which PEM in dialysis patients is caused by inflammation is not clear. Because both PEM and inflammation are strongly associated with each other and can change many nutritional measures and outcome concurrently in the same direction, the terms malnutrition-inflammation complex syndrome (MICS) and/or malnutrition-inflammation-atherosclerosis (MIA) have been suggested to denote the important contribution of both of these conditions to poor clinical outcome. Maintenance dialysis patients who are underweight or who have low serum levels of cholesterol, creatinine, or homocysteine may be suffering from the MICS/MIA and its subsequent poor outcome. Consequently, obesity and hypercholesterolemia may appear protective, which is known as reverse epidemiology. Although MICS/MIA may have a significant contribution in reversing the traditional CVD risk factors in dialysis patients, it is not clear whether PEM or inflammation and their complications can be effectively managed in CKD and ESRD or whether their management improves clinical outcome.

Humans↗