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PubMed1980

Comparative study between steroidal and nonsteroidal anti-inflammatory drugs on the mode of their actions on vascular permeability in rat carrageenin-air-pouch inflammation.

In an attempt to clarify mechanisms of anti-inflammatory actions of steroidal and nonsteroidal anti-inflammatory drugs with special reference to the possible role of E type prostaglandins in the inflammatory process, mode of actions of these drugs was investigated by using acute exudative stage and chronic proliferative stage of carrageenin-air-pouch inflammation in rats. This inflammation was induced on the back of rats by subcutaneous injection with air and carrageenin solution. Plasma exudation in the inflammation locus was determined with the aid of radioiodinated serum albumin. In the acute exudative stage of this inflammation, a single oral administration of dexamethasone, indomethacin, phenylbutazone or aspirin all exerted potent anti-exudative effect, while in the chronic proliferative stage, only dexamethasone was effective in inhibiting the exudation of the labeled albumin. Prostaglandin E level in the exudate of the acute stage inflammation was suppressed by either dexamethasone or indomethacin in accordance with the inhibition of the vascular permeability. These results suggest (1) significant role of prostaglandin E in the acute exudative inflammation, (2) similarity between steroidal and nonsteroidal anti-inflammatory drugs in the mechanism of their anti-exudative actions in the acute inflammation, (3) independency of the exudative process in the chronic proliferative inflammation from prostaglandins and (4) role of extra-prostaglandin mechanism(s) for the anti-exudative action of the anti-inflammatory steroids.

Animals↗
PubMed2005

Prostaglandins and cyclooxygenases in glial cells during brain inflammation.

Many brain disorders such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Huntington, stroke, head trauma, and infection, are associated with inflammation that is involved in neuropathologenesis and hyperalgesis. Microglia and astrocytes act as immune cells in the inflamed brain. Both cell types, but especially microglia, are thought to contribute to the onset of inflammation in many brain diseases by producing deleterious proinflammatory mediators. Prostaglandins (PGs), which are critical mediators of physiologic processes and inflammation, are largely produced by activated microglia and reactive astrocytes during brain inflammation. These compounds are converted from arachnoidic acid (AA) by two isoforms of the cyclooxygenase (COX) enzyme, namely COX-1 and COX-2. In particular, the action of COX-2 and PGs in CNS inflammation has gained much attention recently. PGs have been found to act neuroprotectively by elevating intracellular cAMP levels in neurons. These molecules also function as anti-inflammatory molecules to reduce the production of nitric oxide and proinflammatory cytokines, and to increase the expression of anti-inflammatory cytokines. However, accumulating evidence also shows that COX inhibitors alleviate various types of brain damage via suppressing inflammatory reactions. Accordingly, the roles of two COX enzymes in mediating inflammation and anti-inflammation have recently been debated. We provide here a review of recent findings indicating that the reciprocal interaction of glial cell activation, COX enzymes and PGs mediates neurodegeneration and neuroprotection during brain inflammation. In addition, the mechanism by which PGs mediate signaling is discussed.

Animals↗
PubMed2006

Transcutaneous electrical nerve stimulation at both high and low frequencies reduces primary hyperalgesia in rats with joint inflammation in a time-dependent manner.

BACKGROUND AND PURPOSE: Clinical studies of transcutaneous electrical nerve stimulation (TENS) have used a variety of outcome measures to assess its effectiveness, with conflicting results. It is possible that TENS is effective on some measures of pain and not on others. The purpose of this study was to test the hypothesis that TENS reduces primary hyperalgesia of the knee induced by joint inflammation. SUBJECTS: Male Sprague-Dawley rats were used in this study. METHODS: Inflammation of the knee joint was induced by intra-articular injection of a mixture of 3% kaolin and 3% carrageenan. Primary hyperalgesia was measured as the compression withdrawal threshold of the knee joint before and after the induction of inflammation (4 hours, 24 hours, and 2 weeks) and after sham TENS treatment, treatment with high-frequency TENS (100 Hz), or treatment with low-frequency TENS (4 Hz). RESULTS: The compression withdrawal threshold was significantly reduced at 4 hours, 24 hours, and 2 weeks after the induction of inflammation. Either high-frequency TENS or low-frequency TENS completely reversed the compression withdrawal threshold when applied at 24 hours or 2 weeks after the induction of inflammation but not when applied at 4 hours after the induction of inflammation. DISCUSSION AND CONCLUSION: These data suggest that TENS inhibits primary hyperalgesia associated with inflammation in a time-dependent manner after inflammation has already developed during both acute and chronic stages.

Animals↗
PubMed1995

NIH conference. Airway inflammation.

Diseases characterized by airway inflammation, excessive airway secretion, and airway obstruction affect a substantial proportion of the population. These diseases include asthma, chronic bronchitis, bronchiectasis, and cystic fibrosis. Asthma and chronic bronchitis may affect 25 million persons in the United States. Much progress has been made in the last decade toward an understanding of the mechanisms underlying chronic airway inflammation; recent work has resulted in several new concepts of the initiation and maintenance of airway inflammation. Airway production of chemokines, cytokines, and growth factors in response to irritants, infectious agents, and inflammatory mediators may play an important role in the modulation of acute and chronic airway inflammation. Lipid mediators may be produced by resident airway cells and by inflammatory cells; production of these mediators may also be altered by inflammatory cytokines. Increased airway obstruction may be related to intercurrent viral respiratory infection and to the induction of airway inflammation and airway hyperreactivity that results from such infection. Furthermore, several models exist to explain the processes by which airway inflammation is perpetuated in diseases such as asthma and chronic bronchitis. These include neurogenic inflammation, the perpetuation of the acute inflammatory response, and cycles of airway epithelial cell-mediated and inflammatory cell-mediated recruitment and activation of inflammatory cells. An understanding of these mechanisms of airway inflammation may provide the clinician with new therapeutic approaches to the treatment of these common and chronic diseases.

Bronchi↗
PubMedDate not supplied

The role of small airway inflammation in asthma.

Although inflammation in the large central airways has been the subject of numerous asthma studies, inflammation in the small distal airways remained largely unexamined because of the relative inaccessibility of these structures. However, fiberoptic bronchoscopy, combining endobronchial and transbronchial biopsy, now allows specimens to be obtained from both proximal and distal areas of the lung. Newly refined morphometric and immunocytochemical techniques have been applied to both autopsy and lung biopsy specimens. Together, these technological changes have had a profound impact on the study of small airway inflammation. Now, it is understood that the asthma-associated inflammation evident in the large airways occurs in the distal airways as well. The inflammatory process in the two regions has related features: infiltrates contain activated T lymphocytes and eosinophils, increased mucus plugging, and smooth muscle hyperplasia can be observed. Although the similarities are pronounced, inflammation in the small airways differs in important ways from large airway inflammation. The eosinophilic infiltration that occurs throughout the asthmatic lung also is active in the small airways. The contribution of small airway inflammation to deficits in pulmonary function has been clarified by thoracic high-resolution computed tomography imaging. Results of such imaging suggest that the distal airways are a major site of airway obstruction in patients with asthma and may play a significant role in airway hyperresponsiveness; both disorders are cardinal features of asthma. In addition, functional bronchoscopic studies of the small airways in asthma patients have found high peripheral airflow resistance, even when lung function appears normal. Current formulations of inhaled anti-inflammatory medications, particularly corticosteroids administered by metered dose inhalers using chlorofluorocarbon propellants, treat the proximal airways more effectively than the distal airways. However, some new formulations of inhaled steroids that utilize hydrofluoroalkane propellants produce aerosols of smaller average particle size, with greater penetration into the peripheral airways. Their potential to treat inflammation at peripheral sites may account for the significant improvements in asthma outcomes that have been reported in clinical trials of these new formulations.

Airway Resistance↗
PubMed2003

[Effect of chronic Chlamydia infection with non-specific inflammation on cardiovascular complications in acute myocardial infarct].

It is known that local and systemic inflammatory processes play an important role in the genesis and development of atheroclerotic lesions and in the pathophysiology of acute coronary syndromes. This hypothesis is supported by findings of elevated parameters of the "inflammatory" reaction in the affected blood vessels but also in the blood of atherosclerotic patients. Known risk factors do not explain quite satisfactorily epidemiological cardiovascular phenomena and different manifestations of coronary heart disease. It is very probable that also Chlamydia pneumoniae is a risk factor. This assumption is based on evaluation of seroepidemiological data, examination of atherosclerotic plaques not only in humans but also in animal models with chlamydial infection. Based on retrospective and prospective evaluation of case-records the authors analyzed the incidence of cardiovascular complications in 83 patients with acute myocardial infarction (AIM), incl. 51 patients (31 men and 20 women, mean age 64.4 +/- 3.4 years who had a non-specific inflammation and chlamydial infection, and 32 patients (24 men and 8 women, mean age 64.7 +/- 3.6 years) who had chlamydial infections but no non-specific inflammation (in the blood). These patients were selected from all patients hospitalized during 1998-2001. When diagnosing acute myocardial infarction we applied WHO criteria, and the presence of at least two of three criteria was necessary: a history of prolonged (more than 20 min). stenocardia, electrocardiographic changes typical for ischaemia and/or necrosis and elevation of myocardial enzymes in serum, Non-specific inflammatory activity was present in patients (i.e. positive) if the following laboratory parameters were recorded: C-reactive protein > 5 mg/l assessed by the radial immunodiffusion method; fibrinogen > 4 mg/l assessed by the coagulation method according to Claus; leukocytes > 9.6 x 10(3)/microliter, leukocytes were counted automatically in a Coulter chamber; lymphocytes > 3.4 x 10(3)/microliter. Red cell sedimentation rate > 20 mm/hour. The activity was evaluated as positive when all parameters were elevated. The presence of chronic infection with Chlamydia pneumoniae was assessed qualitatively by antibody positivity (IgG) in serum using the microimmunoflurescent method (using a set from Labsystems Co.). The incidence of associated risk factors (obesity, smoking, diabetes, hyperlipidaemia and hypertension) is higher in the sub-group of patients with Chlamydia infections without inflammation, however, the difference is not statistically significant. The incidence of cardiovascular attacks was higher in the sub-group of patients with chlamydial infection and concurrent inflammation as compared with the sub-group of patients with chlamydial infection without inflammation. In case of re-infarction of the myocardium, a sudden cerebrovascular attack, death and arrhythmia the difference was statistically significant, while in case of cardiac failure and cardiogenic shock the difference was not significant. Patients with acute myocardial infarction with chlamydial infection and a concurrent non-specific inflammation had to be treated more often by combined (i.e. more intense) treatment, thrombolytic treatment, PTCA and surgery (bypass) of the coronary vessels as compared with patients with Chlamydia infections but without inflammation. The authors assume therefore that not only different risk factors but also the effect of non-specific inflammation and Chlamydia infection contribute towards the increased number of cardiovascular postinfarction complications. Therefore a therapeutic approach involving eradication of infection and suppression of the inflammatory reaction should be considered.

Arteriosclerosis↗
PubMed2003

[Malnutrition -- inflammation -- atherosclerosis (MIA syndrome) in patients with renal failure].

Cardiovascular disease (CVD) is the major cause of death in end-stage renal disease (ESRD). Malnutrition may worsen patient outcome by aggravating existing inflammation and heart failure, accelerating atherosclerosis and increasing susceptibility to infection. Available data demonstrate that chronic inflammation, a non-traditional risk factor which is observed commonly in uremic patients, play a key role in the genesis of both malnutrition and CVD in ESRD. Moreover, inflammation is associated with congestive heart failure. Pro-inflammatory cytokines are pivotal to the inflammation. There is evidence that a chronic inflammation with activation of C-reactive protein, interleukin-6, tumour necrosis factor alpha and other cytokines is associated with increased oxidative stress and endothelial dysfunction in ESRD patients. Strong relations between malnutrition, inflammation and atherosclerosis in ESRD patients suggest the presence of a MIA (malnutrition, inflammation, and atherosclerosis) syndrome, which is associated with high mortality rate. Thus, it could be speculated that suppression of the vicious cycle of malnutrition, inflammation and atherosclerosis (MIA) would improve survival in ESRD patients. Therefore, the early stage of chronic renal failure is the ideal time to start therapeutic interventions.

Arteriosclerosis↗
PubMed2004

Hyperhomocysteinemia in relation to plasma free amino acids, biomarkers of inflammation and mortality in patients with chronic kidney disease starting dialysis therapy.

BACKGROUND: Plasma levels of total homocysteine (tHcy) and free amino acids (AAs) are influenced by nutritional status in patients with chronic kidney disease (CKD), whereas the role of chronic inflammation is not clear. METHODS: In a cross-sectional analysis, fasting levels of plasma tHcy, total cysteine (tCys), AA, serum albumin (Alb), and several inflammation markers, including C-reactive protein (CRP), were analyzed in a cohort of 250 patients with CKD starting renal replacement therapy. Patients were followed up during a 4-year period to assess overall mortality in relation to basal tHcy level. RESULTS: Ninety-three patients (37%) with signs of inflammation (CRP > or = 1 mg/dL) had significantly lower levels of tHcy, tCys, and serum Alb than 157 noninflamed patients. tHcy and tCys levels correlated positively with serum Alb levels and negatively with CRP levels (rho = -0.24; P < 0.0001; rho = -0.15; P < 0.05, respectively) and other inflammation markers. tHcy and tCys correlated significantly with levels of several AAs. The presence of both inflammation and malnutrition was associated with lower tHcy levels than when malnutrition was present without inflammation. Multivariate analysis showed that serum Alb, CRP, plasma folate, and vitamin B12 levels were independently associated with tHcy levels after adjustment for other variables. tHcy, but not tCys, level was significantly greater in survivors than nonsurvivors, and Kaplan-Meier analysis showed that greater tHcy level was associated with better survival. CONCLUSION: Plasma tHcy and tCys levels are interrelated to plasma AA levels and were lower in patients with inflammation. Thus, inflammation may contribute to the reverse association between tHcy level and mortality in patients with CKD starting renal replacement therapy.

Amino Acids↗
PubMed1988

Suppression of acute inflammation by 15 methyl prostaglandin E1.

Prostaglandins are important regulators of inflammatory responses. The rat subcutaneous air pouch, a model for synovial inflammation, was used to study the effect of systemic injections of prostaglandin E1 (PGE1) and its stable analog 15S,15 methyl prostaglandin E1 (15M PGE1) on nonimmunologically induced acute inflammation. The 15M PGE1 analog was a more effective longer-lasting antiinflammatory agent. Acute inflammatory responses were induced with three diverse stimuli including monosodium urate crystals, leukotriene B4 and formylmethionylleucyl-phenylalanine. Animals were treated with 15 M PGE1 for 2 days before induction of inflammation. Analysis of pouch fluid 6 hours after injection of the inflammatory stimulus indicates that 15M PGE1 treatment suppressed exudate volume and protein concentration, polymorphonuclear leucocyte accumulation and activity of the lysosomal enzyme beta-galactosidase. Treatment with 15M PGE1 was least effective in preventing the fluid phase of inflammation (exudate volume and protein concentration) when leukotriene B4 was used to induce inflammation. Direct observation (dissecting microscope) of pouch lining vessels indicated that 15M PGE1 reduced markedly the intense vascular reactivity (increased number of dilated vessels and filamentous, corkscrew-shaped vessels) usually seen in an acute inflammatory response. The antiinflammatory effect of 15M PGE1 was also documented by histopathology of pouch lining tissue. Treatment with 15M PGE1 reduced substantially the invasion of pouch tissue by polymorphonuclear leucocytes which was induced by all three stimuli of inflammation. Results of these experiments show that systemic administration of 15M PGE1 is capable of suppressing acute inflammation induced by monosodium urate crystals, by the potent soluble naturally occurring mediator of inflammation leukotriene B4, and by the synthetic chemotactic peptide, formylmethionylleucylphenylalanine.

Acute Disease↗
PubMed1987

A microbiologic and clinical study of placental inflammation at term.

This study describes the relationships between histologically evident inflammation of the placenta, membranes, and umbilical cords, and correlates these lesions with clinical outcome and with amniotic fluid and amniotic membrane cultures in pregnancies at risk for clinical infection. The overall frequency of inflammation in 123 placentas was 85.45%. There were good interrelationships between inflammatory lesions at various sites. Membrane infiltrates of 3+ were seen in 90.9% of intra-amniotic infection cases, but in only 18.4% of asymptomatic patients (P less than .001). Conversely, 76.9% of patients with 3+ inflammation had intra-amniotic infection, whereas only 7% with lesser degrees of inflammation had intra-amniotic infection. Inflammation of any degree (1-3+) had a low specificity (28%) for febrile maternal outcome. Bacteria were recovered in 117 (95.1%) of the amniotic fluids. The grade of histologic lesions was associated with total colony count of bacteria in amniotic fluid (P less than .05) and with high-virulence bacteria in amniotic fluid (P less than .05), and Mycoplasma hominis in amniotic fluid (P less than .05). Bacteria were found in 67.6% and mycoplasmas in 18.6% of amniotic membrane cultures. Chlamydia trachomatis was not recovered in any of 35 amniotic membrane cultures. No significant correlation was seen between organisms in the amniotic membrane and histologic inflammation. Thus, positive amniotic fluid culture results are associated with histologic inflammation, and may cause the inflammatory response. A logistic regression model revealed that predictors of histologic inflammation include maternal diagnosis, amniotic fluid colony count, and M hominis in amniotic fluid.

Adult↗
PubMed2006

Targeting of angiogenic endothelial cells at sites of inflammation by dexamethasone phosphate-containing RGD peptide liposomes inhibits experimental arthritis.

OBJECTIVE: To investigate whether RGD peptide-exposing long circulating polyethylene glycol (PEG) liposomes (RGD-PEG-L) targeted to alphavbeta3 integrins expressed on angiogenic vascular endothelial cells (VECs) are able to bind VECs at sites of inflammation and whether such liposomes containing dexamethasone phosphate (DEXP) can be used as carriers to interfere with the development of experimental arthritis. METHODS: Binding and internalization of RGD-PEG-L were studied by fluorescence-activated cell sorting and confocal microscopy using fluorescently labeled liposomes. Radiolabeled liposomes were used to test in vivo pharmacokinetics and inflammation site targeting in lipopolysaccharide (LPS)-induced inflammation and adjuvant-induced arthritis (AIA) in rats. In vivo inflammation targeting was visualized by intravital microscopy using fluorescently labeled RGD-PEG-L. Therapeutic efficacy of DEXP-encapsulating RGD-PEG-L compared with nontargeted liposomes was evaluated in rats with AIA. RESULTS: RGD-PEG-L bound to and were taken up by proliferating human VECs in vitro. In vivo, increased targeting of radiolabeled RGD-PEG-L to areas of LPS-induced inflammation in rats was observed. Specific association with the blood vessel wall at the site of inflammation was confirmed by intravital microscopy. One single intravenous injection of DEXP encapsulated in RGD-PEG-L resulted in a strong and long-lasting antiarthritic effect in rat AIA. CONCLUSION: RGD-targeted PEG liposomes represent an endothelial cell-specific drug delivery system that targets VECs at sites of inflammation. Use of these liposomes to deliver DEXP to VECs at arthritis-affected sites proved efficacious in rat adjuvant arthritis. These data indicate that VECs have an essential role in the inflammation process and suggest the possibility of using VEC targeting for therapeutic intervention in inflammatory processes such as arthritis.

Animals↗
PubMed2000

Assessment of ileal pouch inflammation by single-stool calprotectin assay.

PURPOSE: Assessment of inflammation within the ileal pouch to establish a diagnosis of "pouchitis" requires both pouch endoscopy and biopsy because there can be a poor correlation between macroscopic and histologic assessments of inflammation. A simplified diagnostic test would be of clinical advantage. Calprotectin is a stable myelomonocytic protein, measurable in feces. It quantitatively relates to inflammation within the gastrointestinal tract. This study was designed to compare single and 24-hour stool measurements of calprotectin in patients with and without evidence of ileal pouch inflammation with endoscopic, histologic, and immunohistochemical indices. METHODS: Twenty-four-hour stool collections were made in ileal pouch patients, 9 with and 15 without (7 with ulcerative colitis and 8 with familial polyposis coli) evidence of pouch inflammation. First-morning stool concentration and total 24-hour calprotectin were quantified by use of a single step enzyme-linked immunosorbent assay. Biopsies from the reservoir were taken for conventional histology and scoring of intraepithelial neutrophil infiltrate. Cells positive for CD3, CD45RO, CD14, and CD15 within the lamina propria were quantified by use of immunohistochemistry. RESULTS: The mean first-morning stool calprotectin concentration correlated with the 24-hour level (r = 0.91; P = <0.0001). The median single-stool calprotectin concentrations were 39 mg/l, 4 mg/l, and 8.5 mg/l (normal range, 0.2-10 mg/l) in patients with inflamed, noninflamed ulcerative colitis, and familial adenomatous polyposis, respectively. All nine patients with endoscopic and histologic evidence of pouch inflammation had raised stool calprotectin. Two of 15 patients without evidence of pouch inflammation had abnormal stool calprotectin. Single-stool calprotectin concentration correlated with the percentage of mature granulocytes (CD15; r = 0.46; P = 0.04) and activated macrophages (CD14; r = 0.65; P = 0.006), but not memory T cells (CD45RO; r = -0.05; P = 0.4) within the lamina propria. CONCLUSION: Single first-morning stool calprotectin levels provide a quantitative measure of pouch inflammation, which may be helpful in the diagnosis and assessment of pouchitis.

Biomarkers↗
PubMed1992

Vitamin A deficiency and inflammation: the pivotal role of secretory cells in the development of atrophic, hyperplastic and metaplastic change in the tracheal epithelium in vivo.

We showed previously that the proliferation of hamster airway secretory cells decreases during vitamin A deficiency (VAD) but later increases when submucosal inflammation develops (Virchows Arch [B] 59:231-242, 1990). This observation has important biological implications since two morphological extremes (atrophy and quiescence versus hyperplasia and hyperproliferation) are reported in the literature for VAD tracheal epithelium in vivo. In the present study, histological slides of tracheal rings from 35-day-old control and VAD hamsters (Virchows Arch [B] 45:197-219, 1984) were reviewed again. Rings from VAD hamsters were selected based on the absence or presence of a florid submucosal inflammation. Quantitative analyses were made on the cartilaginous part of rings from the anterior third of the trachea. When inflammation was absent, a mucociliary pseudostratified epithelium was, for the most part, maintained. The mitotic rate (MR, 6 h colchicine blockade) of secretory cells was markedly reduced (29-fold) but that of basal cells was not changed significantly. Moreover, cell density was not changed by VAD but ciliated cells and secretory cells were decreased and basal cells were increased, proportionally. We call this "minimal morphological change." Thinning (atrophy) of the minimally changed epithelium was associated with focal cell sloughing. Small scattered foci of epidermoid metaplasia (multiple layers of highly keratinized cells which were extremely flat, so that the epithelium was thin and attenuated) were also seen. We call this "atrophic epidermoid metaplasia." When inflammation was present, hyperplastic changes (stratification and epidermoid metaplasia) predominated and cells were in mitosis at all epithelial levels (low, middle, superficial) except in the most superficial (terminally differentiated) squames. The tracheal epithelium was thickened and hypercellular. The cells were piled up at the stratified lesions, and epithelial height, cell density and epithelial MR were significantly increased compared with the non-inflamed VAD epithelium. The effects of VAD and inflammation on cell proliferation were analyzed further by studying 7 h bromodeoxyuridine (BrdU) labelling patterns of cells in VAD tracheal epithelium, with and without submucosal inflammation. In addition, inflammation was induced in "minimally changed epithelium" by mild mechanical injury. The BrdU labelling patterns confirmed that DNA synthesis by secretory cells is reduced markedly by VAD. However, this suppression is overidden by the influx of inflammatory cells (the nature of the stimulus is unknown). The results indicate that the morphological contrasts (atrophy and hyperplasia) seen in the trachea during VAD in vivo are related to extremes in proliferation rates of tracheal secretory cells, regulated by VAD alone (minimal replication) and by inflammation (maximal replication).

Animals↗
PubMed2006

Helicobacter pylori infection is the major risk factor for gastric inflammation in the cardia.

We attempted to clarify the pathogenesis of gastric inflammation in the cardia. Eighty Japanese participated in this study. Biopsy specimens of the gastric antrum, corpus, and cardia (1 cm from the squamocolumnar junction) were obtained, and histological gastritis was evaluated. Cardiac inflammation was also evaluated using magnifying gastroscopy. We examined Helicobacter pylori infection, gastric juice pH/bile acid (BA), serum pepsinogen and gastrin levels, gastroesophageal reflux disease (GERD), and habitual smoking and assessed the relations between these factors and cardiac inflammation. The prevalence of H. pylori infection was statistically higher in patients with cardiac inflammation than in those without inflammation (P < 0.05). The relationship was also demonstrated by magnifying gastroscopy. Cardiac inflammation was linked to low acid output but not linked to the BA concentration or habitual smoking. Cardiac inflammation was more pronounced in patients without GERD. These results suggest that H. pylori is a major risk factor for cardiac inflammation in the Japanese.

Adult↗
PubMed2006

Innate immunity in triggering and resolution of acute gouty inflammation.

Gout has long been recognized as a disease of recurrent bouts of acute inflammation that undergo self-resolution. This inflammation is triggered by the body's response to monosodium urate (MSU) crystals. In this paper, we focus on recent studies that describe how interactions of MSU crystals with the components of the innate immune system trigger acute gouty inflammation as well as mechanisms that are involved in the resolution of this inflammation. Specifically, we describe how toll-like receptors mediate the uptake of MSU crystals involved in the initiation and resolution of gouty inflammation. We also describe recent findings on the role of apoptotic clearance in the resolution of gouty inflammation. In addition, how therapies used to treat gout act on the innate immune system to inhibit MSU crystal-induced inflammation and promote the resolution of inflammation is discussed.

Acute Disease↗
PubMed2006

Correlation of dendritic cell infiltration with active crypt inflammation in ulcerative colitis.

The aim of this study was to evaluate the histological localization and phenotypic characteristics of infiltrating dendritic cells (DCs) and to examine the relationship between the degree of DC infiltration and the severity of inflammation in the colonic mucosa in ulcerative colitis (UC). Also explored was the expression of macrophage inflammatory protein-3alpha (MIP-3alpha), and its receptor CC-chemokine receptor 6 (CCR6), to evaluate the significance of immature DCs in the crypt inflammation evident in UC. There was a significant positive correlation between the number of infiltrating DCs and the degree of crypt inflammation, mononuclear cell infiltration, crypt atrophy, and comprehensive active inflammation. No significant correlation between the number of S-100 protein(+) cells and the severity of crypt atrophy was found. S-100 protein(+), MIP-3alpha(+), and CCR6(+) cells were frequently localized in or around the crypt with inflammation. MIP-3alpha(+) neutrophils and S-100 protein(+) CCR6(+) cells with dendritic morphology were detected in or around the crypt inflammation. Both S-100 protein(+) DCs and CCR6(+) cells were frequently clustered in the surface mucosa beneath the surface epithelium when the crypt was not inflamed. CD1a(+) Langerhans-cell-type DCs were not found in any of the tissues examined. These data indicate that DCs participate not only in chronic inflammation but also in active crypt inflammation.

Acute Disease↗
PubMed1998

Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection.

BACKGROUND & AIMS: Whether inflammation of the cardia indicates gastroesophageal reflux disease (GERD) and/or is a manifestation of pangastritis caused by Helicobacter pylori infection is unknown. The aim of this study was to evaluate the relationship between cardia inflammation, H. pylori infection, and cardia intestinal metaplasia in patients with and without GERD. METHODS: Patients with GERD were compared with controls undergoing endoscopy for a variety of other conditions. Endoscopic biopsy specimens from the distal esophagus and cardia, fundus, and antrum were evaluated for inflammation, H. pylori infection, and intestinal metaplasia. RESULTS: Neither the prevalence of H. pylori infection (controls, 48%; GERD, 41%) nor cardia inflammation (controls, 41%; GERD, 40%) differed between groups. All 11 controls and 22 of 23 patients with GERD (96%) and cardia inflammation had H. pylori infection. Esophagitis was more common among GERD patients (33%) than controls (7%; P = 0.01). Cardia intestinal metaplasia was more common among controls (22%) than GERD patients (3%; P = 0.01); all had cardia inflammation, 7 had H. pylori infection, and 6 had metaplasia elsewhere in the stomach. CONCLUSIONS: The prevalence of cardia inflammation is similar in patients with and without GERD and is associated with H. pylori infection (P < 0.001). Cardia intestinal metaplasia is associated with H. pylori-related cardia inflammation (P = 0.01) and intestinal metaplasia elsewhere in the stomach, indicating that it is distinct from Barrett's esophagus.

Adult↗
PubMed1994

Prostatic fluid inflammation in prostatitis.

We studied expressed prostatic secretions from 106 patients with prostatitis to determine the longitudinal course of prostatic fluid inflammation. Prostatic fluid specimens were collected from 14 patients with acute bacterial, 13 with chronic bacterial and 79 with abacterial prostatitis. White blood cells per high power microscopic field of the expressed prostatic secretion were counted under a cover slip. Inflammation in the expressed prostatic secretion was considered to be consistent with prostatitis if there were 10 or more white blood cells per high power field. The 14 patients with acute bacterial prostatitis had a mean of 10 visits with a mean followup of 59 months. Inflammation resolved within 1 month in 9 patients with acute bacterial prostatitis but it recurred in 5 other patients in association with urinary tract infection. The 13 patients with chronic bacterial prostatitis had a mean of 10 visits with a mean followup of 58 months. Episodic inflammation in the expressed prostatic secretion associated with urinary tract infection was seen in all patients during followup. The 79 patients with abacterial prostatitis had a mean of 7 visits with a mean followup of 40 months. Resolution of inflammation in the expressed prostatic secretion occurred in 9 patients (11%). Inflammation in the expressed prostatic secretion at followup was seen in 70 patients (89%), and 27 of the 79 patients (34%) had 10 or more white blood cells per high power field of expressed prostatic secretion in all subsequent specimens. In cases of abacterial prostatitis, neither the initial expressed prostatic secretion white blood count nor the presence of symptoms reliably predicted subsequent inflammation. The data suggest that prostatic inflammation resolves in most patients with acute bacterial prostatitis and is episodic in patients with chronic bacterial or abacterial prostatitis.

Acute Disease↗