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PubMed1979

Patterns of inflammation in prostatic hyperplasia: a histologic and bacteriologic study.

In a series of 162 cases of surgically resected hyperplastic prostates the incidence of inflammation is 98.1%. Six morphologic patterns of inflammation are described: 1) segregated glandular inflammation, 2) periglandular inflammation, 3) diffuse stromal inflammation, 4) isolated stromal lymphoid nodules, 5) acute necrotizing inflammation and 6) focal granulomatous inflammation. The most common pattern, segregated glandular inflammation, is characterized by intraluminal neutrophils and foamy macrophages and by chronic inflammatory cells in the surrounding stroma. No significant morphological differences are found among groups of cases with positive and negative evidence by culture of bacterial prostatic infection. Quantitative but not qualitative morphologic differences are found between cases of gram-negative infections and infection by gram-positive organisms that often are considered non-pathogens.

Bacterial Infections↗

PubMed1996

Idiopathic granulomatous orbital inflammation.

PURPOSE: Granulomatous orbital inflammation may occur as an isolated condition of unknown origin. These idiopathic granulomatous lesions are believed to belong to the orbital pseudotumor group by some authors, whereas others consider them sarcoidosis limited to the orbit. The aim of this study is to define the clinicotherapeutic aspects of these lesions. METHODS: The records of all patients with diagnosis of orbital pseudotumor and orbital sarcoidosis from the Orbital Center Amsterdam in the period between 1976 and 1994 were reviewed to define those with idiopathic granulomatous orbital inflammation. The authors studied the clinicotherapeutic aspects and histopathology of idiopathic granulomatous orbital inflammation by analysis of their own series and the literature. RESULTS: Their study group encompassed seven patients with idiopathic granulomatous orbital inflammation. The mean follow-up was 9.5 years (range, 3.5-16.0 years). All had unilateral orbital presentation, with localization in the lacrimal gland in three patients. The lesions clinically presented with signs of mass effect or inflammation or both and were treated successfully with surgery, systemic corticosteroids, a combination of surgery and systemic corticosteroids, or systemic corticosteroids followed by irradiation. Histopathologic analysis showed a spectrum of granulomatous inflammation, admixed with nongranulomatous inflammation and fibrosis. There have been 30 similar cases described in the literature with comparable clinicotherapeutic characteristics. CONCLUSIONS: Based on this study and the literature, it appears that idiopathic granulomatous orbital inflammation is more related to orbital pseudotumor than to orbital sarcoidosis.

Acute Disease↗

PubMed1997

Reciprocal IFN-gamma and TGF-beta responses regulate the occurrence of mucosal inflammation.

The above new findings concerning the immunological mechanisms governing mucosa, immune responses and oral tolerance in TCR-transgenic mice, as well as those operative in mice with experimental colitis, greatly expand our understanding of the processes that normally control mucosal inflammation and possibly other types of inflammation as well (Fig. 1). They indicate that, in the nondiseased mouse, ingested proteins evoke a Th1-cell (IFN-gamma) response in the mucosal follicles that is quickly counter-regulated by induction of T-cell anergy/deletion, if this Th1-cell response is inhibited (experimentally by anti-IL-12), TGF beta-producing cells appear, and these are capable of active immune suppression. This reciprocal relationship between IFN-gamma production and TGF-beta production is further supported in mouse models of mucosal inflammation. Thus, in the TNBS-colitis model, there is direct stimulation of the immune cells in the lamina propria as a result of diffuse haptenization of mucosal proteins, which leads to a massive Th1-cell response capable of overwhelming any suppressive counter-regulatory mechanisms normally generated in the PPs. This highly polarized Th1-cell response is controlled only by direct abrogation of IL-12 production with exogenous administration of anti-IL-12, or with indirect inhibition of this response via induction of oral tolerance and accompanying production of TGF-beta (Refs 6-8). The data obtained from this model are consistent with those obtained with another model of intestinal inflammation--inflammation in severe combined immunodeficiency (SCID) mice following lymphoid repletion with CD45Rbhi (naive) T cells. In this model, inflammation is again mediated by Th1 cells and is prevented by co-repletion with CD45Rbhi (memory) T cells, which appear to work by secreting TGF-beta (Refs 9, 10). Thus, a common feature of the various experimental models of intestinal inflammation studied to date is the Yin-Yang relationship of IFN-gamma and TGF-beta, with the former being proinflammatory and the latter anti-inflammatory. Is the IFN-gamma TGF-beta dichotomy that is evident both in the normal state and in models of inflammation simply a reflection of an underlying Th1 Th2 dichotomy? The answer to this important question is not yet known. Thus, while it is clear from the in vitro studies already discussed that IL-12 and/or IFN-gamma inhibit TGF-beta production, the role of IL-4 in this process is more elusive. These in vitro studies indicate that IL-4 is not required for TGF-beta production, a finding that is consistent with studies in which the transfer of CD45Rbhi, T cells from IL-4-/- mice protected SCID mice from colitis induced by CD45Rbhi T cells. However, the addition of IL-4 to in vitro cultures containing anti-IL-12 augmented TGF-beta production, most probably by IL-4 acting as a growth factor for TGF-beta-producing cells rather than as an inducing factor (T. Marth et al., unpublished). Obviously, more work will be necessary to resolve this issue. Finally, it should be noted that the above considerations apply to human inflammatory diseases of the gastrointestinal tract, such as Crohn's disease. Recently, it has been shown that T cells extracted from Crohn's disease tissues manifest skewed Th1-cell responses. The hypothesis can therefore be put forward that this disease results from a dysregulated Th1-cell response to ubiquitous mucosal antigens that is not appropriately controlled by normal counter-regulatory mechanisms. Interventions that artificially bring the excessive Th1-cell response back into balance, such as administration of IL-12 antagonists, should therefore find a central place in the treatment of the disease.

Animals↗

PubMed1998

Secondary closure of posterior continuous curvilinear capsulorhexis in normal eyes and eyes at risk for postoperative inflammation.

PURPOSE: To observe the posterior continuous curvilinear capsulorhexis (PCCC) after cataract surgery in control eyes and eyes with an increased risk for postoperative inflammation. SETTING: Department of Ophthalmology, University Hospital Antwerp, Belgium. METHODS: After phacoemulsification, a PCCC was performed before intraocular lens (IOL) implantation in 20 eyes of 18 patients with ocular or systemic conditions that predisposed them for increased postoperative inflammation; e.g., diabetes, uveitis, retinitis pigmentosa (inflammation group). These eyes were compared with 20 eyes of 16 patients who had the same surgical procedure but did not present a history of medical or ocular pathology (control group). The postoperative follow-up was 6 months to 3 years. Reclosure of the PCCC was evaluated by anterior segment photographs. The reclosure was classified as partial when newly formed tissue was present at the PCCC margin and total when the proliferation covered the entire PCCC area. RESULTS: Three types of PCCC reclosure were found: fibrotic, Elschnig pearl or multilayer, and monolayer. All 3 were seen within or at the margin of the PCCC area. Reclosure (total and partial) occurred in 8 eyes (40%) in the control group and 10 (50%) in the inflammation group. Total reclosure was more frequent in the inflammation group (4 eyes [20%]) than in the control group (1 eye [5%]). Monolayered or multilayered cellular proliferation was present in 8 eyes (40%) in the control group and 4 eyes (20%) in the inflammation group; fibrotic proliferation was found in the inflammation group only (7 eyes [35%]). CONCLUSION: Reclosure of the PCCC occurred in both groups, although the frequency of reclosure was slightly higher in the inflammation group. Although PCCC does not prevent posterior capsule opacification in all cases, it is useful in specific situations.

Adolescent↗

PubMed1996

Course of gut inflammation in spondylarthropathies and therapeutic consequences.

Gut inflammation plays a crucial role in the pathogenesis of spondylarthropathies (SpA) since ileocolonoscopic studies have demonstrated the presence of gut inflammation in different forms of this concept: in ankylosing spondylitis (AS) (60%), in enterogenic (90%) and urogenital reactive arthritis (20%), in undifferentiated SpA (65%), in the pauciarticular and axial forms of psoriatic arthritis (16%), in late onset pauciarticular juvenile chronic arthritis (80%) and in acute anterior uveitis (66%). The strong relationship between gut and joint inflammation was demonstrated by performing a second ileocolonoscopy: remission of the joint inflammation was always connected with a disappearance of gut inflammation, whereas persistence of locomotor inflammation was mostly associated with the persistence of gut inflammation. During further evolution 20% of the non-ankylosing spondylitis SpA patients can develop AS. About 6% of the total group SpA patients, in whom inflammatory bowel disease (IBD) was excluded, developed Crohn's disease 5 to 9 years later. All these patients initially presented with gut inflammation, which indicates that this finding has prognostic value. The high prevalence of evolution to IBD in SpA patients confirms the thesis that both disease entities bear common pathogenic mechanisms, and confirms the place of IBD in the concept of SPA. Sulphasalazine (SASP), a successful drug in the treatment of IBD, has demonstrated its effectiveness in the treatment of SpA. The beneficial effect of the drug in this disease entity could be due to its anti-inflammatory effect on the gut wall, by normalizing its permeability and by preventing the entrance of antigens through the defective gut wall. However, SASP could not prevent the evolution to IBD.

Arthritis, Rheumatoid↗

PubMed1999

Milk cytokines and subclinical breast inflammation in Tanzanian women: effects of dietary red palm oil or sunflower oil supplementation.

Previously, we have found that subclinical breast inflammation, as indicated by raised breastmilk concentrations of sodium and the inflammatory cytokine, interleukin-8 (IL-8), was highly prevalent in Bangladesh and associated with poor infant growth. In order to investigate further the prevalence of subclinical breast inflammation and to assess the impact of dietary intervention, we studied rural Tanzanian women taking part in a study of dietary sunflower or red palm oil supplementation during late pregnancy and lactation. We measured breastmilk concentrations of IL-8, the anti-inflammatory cytokine, transforming growth factor-beta2 (TGF-beta) and the ratio of sodium to potassium. We also estimated systemic inflammation by plasma concentrations of the acute phase proteins, alpha1-acid glycoprotein and C-reactive protein. There were highly significant intercorrelations among milk Na/K ratio and concentrations of IL-8 and TGF-beta, the last only after treatment with bile salts which also improved TGF-beta recovery in the enzyme-linked immunosorbent assay (ELISA). Plasma acute phase protein concentrations tended to correlate with milk Na/K ratio and IL-8, suggesting that subclinical breast inflammation was related to systemic inflammation. Dietary supplementation with vitamin E-rich sunflower oil but not provitamin A-containing red palm oil decreased milk Na/K, IL-8 and TGF-beta at 3 months postpartum; however, the effect was significant only for Na/K ratio. The results suggest that milk Na/K ratio, IL-8, and TGF-beta all measure the same phenomenon of subclinical breast inflammation but that Na/K ratio, having the lowest assay variability, is the most useful. Subclinical breast inflammation may result in part from systemic inflammation and may be improved by increased dietary intake of vitamin E-rich sunflower oil.

Acute-Phase Proteins↗

PubMed2002

[Neurogenic inflammation. II. pathophysiology and clinical implications].

Neurogenic inflammation is elicited by activation of unmyelinated sensory neurons through noxious stimuli and subsequent release of neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) from peripheral nerve endings. The nerve-mediated inflammatory responses in the tissue consist of hyperaemia and oedema which under some circumstances may be accompanied by pain. Neurogenic inflammation has been implicated in the pathophysiology of various human diseases with uncertain etiology. Signs of inflammation and hyperalgesia associated with chronic pain syndromes such as migraine, arthritis and complex regional pain syndrome resemble the characteristics of neurogenic inflammation. By extrapolation of convincing evidence obtained in rodent models, neurogenic inflammation is assumed to contribute to diseases of the respiratory system, gastrointestinal tract, urogenital tract, and skin in humans. Since, however, highly selective substance P receptor antagonists, found to be effective against inflammation in rodents, failed to inhibit inflammatory processes in clinical trials, the hypothesis of an involvement of neurogenic inflammation in human diseases is discussed critically in this review. Beyond its primarily inflammatory character neurogenic inflammation can be regarded as a mechanism that activates protective responses, thus bringing about a first line of defence to maintain the integrity of the tissue and to contribute to tissue repair.

Animals↗

PubMed2001

Relationship between airway inflammation, hyperresponsiveness, and obstruction in asthma.

BACKGROUND: Although the role of eosinophils in airway inflammation in chronic asthma has been extensively studied, a role for neutrophils has not been well characterized. Furthermore, prior studies have not systematically sought or controlled for factors that might confound the relationship between cellular markers of inflammation and physiologic measures of airway function. OBJECTIVE: The purpose of this study was to determine whether eosinophilic and neutrophilic inflammation independently contribute to abnormalities of airway function in asthma. METHODS: Multivariate analysis of data collected during screening and enrollment of 205 asthmatic adults for clinical trials was conducted to examine the relationships between cellular inflammation in induced sputum and FEV(1) and methacholine responsiveness (PC(20)) while confounding factors were controlled for. RESULTS: We found that age, sex, ethnicity, and use of inhaled corticosteroids were important confounding factors of the relationship between cellular inflammation and airway function. When these factors were controlled for, multivariate analysis showed that eosinophil percentage in induced sputum is independently associated with lower FEV(1) and lower PC(20) (P = .005 and P = .005, respectively). In the same models, increased sputum neutrophil percentage is independently associated with lower FEV(1) (P = .038) but not with PC(20) (P = .49). CONCLUSIONS: These results suggest that both eosinophilic inflammation and neutrophilic inflammation independently contribute to abnormalities of FEV(1) in asthma. Therapies directed specifically at control of neutrophilic inflammation might be useful in improving airway caliber in patients with chronic asthma.

Adult↗

PubMed2005

Skip inflammation of the appendiceal orifice: a prospective endoscopic study.

OBJECTIVE: The purpose of the study was to evaluate the incidence of discontinuous inflammation of the appendiceal orifice in patients undergoing colonoscopy for diagnosis or surveillance of colonic disease. MATERIAL AND METHODS: Consecutive and unselected patients subjected to colonoscopy over a 3-year period were included in a prospective study. Biopsies were taken within 2 cm of the orifice of the appendix, from the caecum and from predefined colonic segments. Discontinuous inflammation of the appendiceal orifice was defined as an area of macroscopic inflammatory changes distinct from a normal caecum of ascending colon. The biopsies were graded histologically for the presence and severity of inflammation by a pathologist without knowledge of the endoscopic findings. RESULTS: A total of 271 patients were included. The final diagnoses were: ulcerative colitis (UC) (83 patients), Crohn's disease (CD) (54), indeterminate colitis (12), irritable bowel syndrome (IBS) (54), microscopic colitis (15) and other disease (53). Endoscopic discontinuous inflammation of the appendiceal orifice was found in 27% (95% CI: 17-38%) of patients with UC, 24% (95% CI: 13-39%) with CD, 40% (95% CI: 12-74%) with indeterminate colitis, 8% (95% CI: 0-36%) with microscopic colitis, 10% (95% CI: 3-24%) of patients with IBS and in 9% (95% CI: 2-021%) of other diseases (p<0.05). A correlation was found for endoscopic and histological discrimination between normal and inflamed mucosa (p<0.001). However, in 24% of patients, endoscopic inflammation was without histological signs of inflammation, primarily in an otherwise normal colon. CONCLUSIONS: Discontinuous inflammation of the appendiceal orifice is common in patients with IBD irrespective of clinical activity. However, patients with otherwise normal colon may also show congestion of this area without or with minimal microscopic inflammation.

Adult↗

PubMed2002

Time course of quartz and TiO(2) particle-induced pulmonary inflammation and neutrophil apoptotic responses in rats.

Apoptosis, or programmed cell death, has been reported to play an important role in the resolution of pulmonary inflammation. This study was undertaken to investigate the role of apoptosis in resolving particle-induced lung inflammatory responses in exposed rats, using a dose-response / time course experimental design. Groups of rats were exposed via intratracheal instillation to 0, 0.5, 1, 5, 10, or 50 mg/kg body weight of quartz (i.e., crystalline silica) particles or to 0, 0.5, 1, 5, 10, 20, or 50 mg/kg of pigment-grade titanium dioxide (TiO(2)) particles and evaluated for lung inflammation parameters and evidence of apoptosis of inflammatory cells at 24, 48, 72, or 168 hours post exposure. At each post exposure evaluation period, bronchoalveolar lavage (BAL)-recovered cells from control and particle-exposed rats were assessed for apoptosis using 4 different techniques. The results in silica-exposed rats demonstrated a significant dose-related increase in inflammation concomitant with apoptosis of pulmonary inflammatory cells at 24 to 48 hours post exposure. At later postexposure time points, both the silica-induced inflammatory responses and apoptotic levels of inflammatory cells at higher doses (i.e., >or= 5 mg/kg) were reduced but persisted through 1 week. TUNEL (TdT-mediated dUTP nick end-labeling) assay studies confirmed that the vast majority of apoptotic cells were neutrophils. In contrast, titanium dioxide particle exposures produced transient pulmonary inflammation but only small measurable and nonsignificant apoptotic responses at higher exposure concentrations. These results suggest that the sustained lung inflammatory response in rats exposed to >or= 5 mg/kg silica may be related to the ineffectiveness of the normal apoptotic mechanisms associated with resolution of inflammation. However, because quartz particles are known to be cytotoxic to alveolar macrophages and other lung cells, normal apoptotic mechanisms may have limited utility for resolving particle-induced inflammation, particularly because silica may not be representative of other particle-types. Alternatively, it seems unlikely that apoptosis served to promote silica-induced lung inflammatory responses because the initial increase of apoptosis in inflammatory cells was subsequently correlated with a reduction of the pulmonary inflammatory response in silica-exposed rats. The findings from this in vivo study demonstrate that the neutrophil, and not the alveolar macrophage, is the primary inflammatory cell-type that undergoes apoptosis in response to particles. Furthermore, at doses causing similar degrees of inflammation at 24 hours post exposure, the magnitude of apoptosis induced by silica is significantly larger than that induced by TiO(2), indicating that there are potency differences in lung inflammation as well as apoptotic responses among different particle-types.

Animals↗

PubMed2003

Assessing the role of neutrophil apoptosis in the resolution of particle-induced pulmonary inflammation.

Following inflammatory-cell recruitment in the lung, neutrophil apoptosis and subsequent engulfment by macrophages are regarded as important components in the resolution of pulmonary inflammation. The goal of this study was to further investigate the role of apoptosis and its influence, if any, on the pulmonary inflammatory process following exposures to the following particulate types: amorphous (AMO) or crystalline silica (Si), lipopolysaccharide (LPS), or pigment-grade titanium dioxide (TiO2). Rats were intratracheally instilled either with TiO2, AMO, or Si particles at doses of 1 or 5 mg/kg or 6 microg LPS. Following exposures, bronchoalveolar lavage fluids and lung tissues were collected and evaluated at 12, 24, 48, or 168 h (i.e., 1 wk). At the 1 mg/kg dose, AMO instillation produced the highest pulmonary inflammatory response, concomitant with a rise in apoptotic cells that mirrored temporally the transient nature of the inflammatory response. At 5 mg/kg, amorphous silica and crystalline silica particles induced substantial pulmonary inflammation [approximately 50-60% neutrophils (PMNs)] at 12 h postexposure (pe). A fundamental difference between the two inflammatory patterns, however, was the subsequent reversibility of inflammation in the AMO-exposed rats at 168 h postexposure and the sustained inflammatory effect in the Si-exposed animals measured through 168 h pe (approximately 40% PMNs). Pulmonary apoptotic responses in AMO-exposed rats mirrored temporally and correlated with the time-course reduction of inflammatory responses, leading to resolution. In the Si-exposed rats, apoptotic levels remained elevated, concomitant with sustained inflammation measured through 168 h pe. High doses of TiO2 particles produced transient lung inflammation, but with low levels of apoptosis. In addition, instillation of LPS produced a transient inflammatory response which mirrored the time course of apoptosis levels and was resolved by 168 h pe. cDNA microarray methods demonstrated that gene expression was altered for several apoptosis-related genes in AMO-, Si-, and LPS-exposed animals at 24 h pe. The results of these studies demonstrate that, following exposures, the resolution of lung inflammation correlated temporally with apoptotic levels of neutrophils in AMO- and LPS-exposed rats. Alternatively, instillation of crystalline silica resulted in sustained pulmonary inflammation and measurable apoptosis at 1 wk postexposure, but the apoptotic cell processes were not effective in resolving the inflammatory response. The findings suggest that the coordination between the resolution of inflammation and inflammatory cell apoptosis in the lung is dependent on the particle-type and that other factors, such as particle cytotoxicity, may also be important.

Animals↗

PubMed2004

Monocyte adhesion molecule expression in interstitial inflammation in patients with renal failure.

BACKGROUND: Patients with renal failure have an increased susceptibility to infections. We therefore studied the recruitment of monocytes and their expression of adhesion molecules CD11b and CD62L at the site of interstitial inflammation in patients with renal failure. Furthermore, we studied if the capacity of monocytes to up-regulate CD11b in interstitial inflammation was determined by the interstitial concentration of chemotactic factors. METHODS: Three intensities of interstitial inflammation (0, intermediate and intense) were established in skin blister chambers. Leukocyte count, CD11b/CD62L expression, monocyte chemotactic protein-1 (MCP-1) and blister activity in terms of CD11b mobilization were determined. RESULTS: The CD62L expression on monocytes was lower in the peripheral circulation in patients with renal failure compared with healthy subjects (P<0.005 and P<0.001). At the site of interstitial inflammation patients had a higher expression of CD62L (intermediate, P<0.05; intense, P<0.005). Furthermore, monocytes from patients had an impaired capacity to mobilize CD11b both in the peripheral circulation (P<0.005) and at the intermediate and intense sites of interstitial inflammation (P<0.005 and P<0.001, respectively) compared with cells collected from healthy subjects. We incubated monocytes in blister exudates, in order to explore whether this phenomenon is caused by cellular factors and/or to the interstitial concentration of chemotactic mediators. The expression of CD11b on monocytes from healthy blood donors incubated in blister exudates from either patients or healthy subjects in vitro was similar. The interstitial concentration of MCP-1 at the site of intermediate inflammation was significantly lower in patients with renal failure compared with the corresponding blister exudate collected from healthy subjects (P<0.05), but no differences were observed at the site of intense inflammation. Furthermore, neutralizing the action of MCP-1 in blister exudates with monoclonal antibodies did not have any impact on monocyte CD11b expression following incubation in blister exudates. CONCLUSION: These studies indicate that the impaired capacity of monocytes to mobilize CD11b at the site of inflammation in patients with renal failure is more dependent on constitutive cellular factors than the concentration of CD11b mobilizing factors in the interstitium.

Adult↗

PubMed2001

Fecal calprotectin: validation as a noninvasive measure of bowel inflammation in childhood inflammatory bowel disease.

BACKGROUND: Calprotectin is an abundant neutrophil protein, which is extremely stable in feces. This study aimed to validate fecal calprotectin as a marker of bowel inflammation against invasive measures in children with inflammatory bowel disease (IBD), including colitis and small bowel Crohn disease. METHODS: Fecal calprotectin was measured using a simple enzyme-linked immunosorbent assay in 36 spot stool samples from 22 children before colonoscopy and from 14 children before technetium-99 (99Tc) scanning. Using standard scoring systems, the severity of inflammation was assessed macroscopically and histologically at six standard sites in those who underwent colonoscopy and also at six standard sites in those who underwent 99Tc scanning. The subscores from each site were summated to give combined severity and extent scores for macroscopic and for histologic inflammation in the group undergoing colonoscopy and total inflammation in the group undergoing 99Tc scanning. RESULTS: In the 22 children who underwent colonoscopy, median fecal calprotectin was 4.9 mg/L (0.1-272.5 mg/L) (range). Disease groups included six normal cases, nine ulcerative colitis cases, two isolated Crohn colitis cases, two indeterminate colitis cases, and three allergic colitis cases. Fecal calprotectin correlated closely with colonic macroscopic inflammation (r = 0.75, P < 0.001) and histologic inflammation (r = 0.85, P < 0.001). Of the 14 children undergoing 99Tc scanning, 10 had Crohn disease, 3 had ulcerative colitis, and 1 had allergic colitis. Median fecal calprotectin was 9.1 mg/L (0.3-141.7 mg/L), and this correlated closely with the 99Tc scanning score (r = 0.80, P = 0.001). CONCLUSION: Fecal calprotectin correlates closely with the best invasive measures of colonic and small bowel inflammation in childhood inflammatory bowel disease. As a sensitive objective measure of bowel inflammation that is risk-free and noninvasive, fecal calprotectin lends itself particularly to the monitoring of and assessment of therapeutic interventions in children with inflammatory bowel disease.

Adolescent↗

PubMed2006

Different patterns of inflammation and prognosis in invasive carcinoma of the breast.

AIM: Inflammation in carcinoma of the breast may represent an immune response to the tumour, but there is evidence that this response is impaired. Inflammation may also stimulate tumour growth by releasing proteolytic enzymes and angiogenic factors. Prognostic studies have produced conflicting results, but most investigators have not evaluated the different patterns of inflammation. The aim of this study was to test the hypothesis that moderate or marked diffuse inflammation is associated with a better prognosis. We also tested the 'danger model', which suggests that necrosis is necessary for an effective immune response. METHODS AND RESULTS: On multivariate analysis of women with stage 1 and 2 tumours (n = 679, median follow-up of 9.8 years), survival was independently associated with diffuse inflammation (relative risk 0.43, 95% confidence interval 0.24, 0.77, P =0.005) in addition to histological grade, axillary lymph node status, tumour size and oestrogen receptor status. The presence or absence of tumour necrosis did not have a clear effect on the relationship between survival and diffuse inflammation. CONCLUSIONS: Moderate or marked diffuse inflammation in breast cancer is associated with a better prognosis, suggesting that the immune effects of the inflammation predominate over the protumour effects.

Adult↗

PubMed2005

Plasticity of the enteric nervous system during intestinal inflammation.

Inflammation of the bowel causes structural and functional changes to the enteric nervous system (ENS). While morphological alterations to the ENS are evident in some inflammatory conditions, it appears that relatively subtle modifications to the neurophysiology of enteric microcircuits may play a role in gastrointestinal (GI) dysfunction. These include changes to the excitability and synaptic properties of enteric neurones. The response of the ENS to inflammation varies according to the site and type of inflammation, with the functional consequences depending on the nature of the inflammatory stimulus. It has become clear that inflammation at one site can produce changes that occur at remotes sites in the GI tract. Immunohistochemical data from patients with inflammatory bowel disease (IBD) and animal models indicate that inflammation alters the neurochemical content of some functional classes of enteric neurones. A growing body of evidence supports an active role for enteric glia in neuronal and neuroimmune communication in the GI tract, particularly during inflammation. In conclusion, plasticity of the ENS is a feature of intestinal inflammation. Elucidation of the mechanisms whereby inflammation alters enteric neural control of GI functions may lead to novel treatments for IBD.

Animals↗

PubMed2006

Incidental acute prostatic inflammation is associated with a lower percentage of free prostate-specific antigen than other benign conditions of the prostate: a prospective screening study.

OBJECTIVE: To evaluate the performance of percentage free/total prostate-specific antigen (f/tPSA) as a screening tool for prostate cancer, and to assess the impact of prostatic inflammation on f/tPSA. PATIENTS AND METHODS: Men aged 50-65 years were invited for prostate cancer screening. Biopsies were taken from men with a tPSA of > or = 4 ng/mL, together with those with a tPSA of 1.1-3.99 ng/mL and a f/tPSA of < or = 20%. Histological evidence of prostate cancer, acute inflammation, chronic inflammation, and benign prostatic tissue were noted in biopsy cores, together with the associated f/tPSA values. RESULTS: The cancer detection rate was 4.3% (33/773). Evidence of inflammation was found in about half (87/175) of those biopsied. Men with acute inflammation (27/175, 15%) had significantly lower serum f/tPSA values (mean 13.4%) than those with chronic inflammation (mean 16.6%, P = 0.002) and benign prostatic tissue (mean 15.7%, P = 0.034), but were similar to men with prostate cancer (mean 15.3%, P = 0.315). CONCLUSIONS: In this prospectively screened cohort of men, there was a high incidence of asymptomatic inflammation on prostatic histology; f/tPSA values were significantly lower in men with acute inflammation. This might explain the variability of f/tPSA in improving specificity when used as a screening tool for prostate cancer, and might also reduce its effectiveness in differentiating tumours with more aggressive potential.

Acute Disease↗

PubMed2005

Proteomic biomarker analysis of amniotic fluid for identification of intra-amniotic inflammation.

BACKGROUND: Intra-amniotic inflammation is associated with poor neonatal outcome independent of prematurity. We applied proteomic technology (SELDI: surface-enhanced laser desorption ionisation) to identify the proteomic profile of intra-amniotic inflammation. DESIGN: One hundred and four samples of amniotic fluid were analysed. In stage 1, samples from patients with symptoms of preterm labour and known outcomes were tested to identify the characteristic profile for inflammation. We extracted the profile using a novel, stepwise logical approach comparing SELDI tracings from patients who delivered preterm and had intra-amniotic inflammation in response to infection to the tracings of patients who had symptoms of preterm labour but delivered at term. In stage 2, we applied the algorithm to samples from pregnancies whose outcomes were unknown to the investigators. SETTING: North-American university in collaboration with Ciphergen field demonstration laboratory. SAMPLE: One hundred and four samples of human amniotic fluid from transabdominal amniocentesis. METHODS: SELDI (surface-enhanced laser desorption ionisation) and Mass Restricted analysis, a novel algorithm for extraction of clinical and biological relevant biomarkers from proteomic SELDI tracings. MAIN OUTCOME MEASURE: Presence of intra-amniotic inflammation and/or infection leading to preterm birth. RESULTS: Patients with intra-amniotic inflammation that deliver preterm have a distinctive amniotic fluid proteomic profile of three or four of the following proteins: neutrophil defensins-1 and -2, and calgranulins A and C. Based on the presence or absence of these biomarkers, we devised the mass restricted (MR) score ranging from 0 (all biomarker peaks absent) to 4 (all biomarker peaks present). In stage 1, MR score > 2 had 92.9% sensitivity (95% CI 76.5-98.9) and 91.8% specificity (95% CI 80.4-97.7) for detection of intra-amniotic inflammation. In blind testing (stage 2), MR score > 2 provided 100% specificity and sensitivity (95% CI 100-100). A MR score > 2 was associated with imminent preterm delivery. CONCLUSION: Proteomic analysis of amniotic fluid reveals the presence of biomarkers characteristic of intrauterine inflammation. This methodology may identify the subgroup of patients that might benefit most from interventions to prevent fetal damage in utero.

Adult↗

PubMed1994

Long-term urethral catheterization increases risk of chronic pyelonephritis and renal inflammation.

OBJECTIVE: To determine the prevalences of chronic pyelonephritis and chronic renal inflammation in elderly nursing home patients at the time of death and to assess correlation with urethral catheterization and other putative risk factors. DESIGN: Prospective assessment of risk factors with the prevalences of chronic pyelonephritis and renal inflammation at autopsy. SETTING: A 240-bed long-term care facility. PARTICIPANTS: All residents > or = 65 years old who died and were autopsied during a 2-year period. MEASUREMENTS: Antemortem assessment of risk factors for renal inflammation, including a search for any urethral catheterization in the person's life. Prospective assessment of urethral catheterization, catheter obstruction, and use of anti-inflammatory medications and urine cultures. Urinary tract pathology was assessed for gross and microscopic evidence of inflammation and urinary tract stones. RESULTS: The duration of catheterization was significantly associated with increasing prevalence of bacteriuria, polymicrobial bacteriuria, chronic pyelonephritis, and chronic renal inflammation. The prevalence of chronic pyelonephritis at death was 10 percent (5/52) for patients catheterized > 90 days during their last year of life and zero (0/65) when catheterized < or = 90 days (P < 0.02; Fisher's exact test). Chronic pyelonephritis was significantly associated with renal stones and hydronephrosis. The prevalence of chronic renal inflammation without chronic pyelonephritis was significantly greater than that of chronic pyelonephritis: the prevalence was 43 percent (20/47) when catheterized > 90 days and 18 percent (12/65) when < or = 90 days (P < 0.05). Chronic renal inflammation was associated with hydronephrosis, ureteral dilatation, acute pyelonephritis and diastolic hypertension. CONCLUSION: Chronic pyelonephritis and chronic renal inflammation are associated with long-term catheterization.

Age Factors↗