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PubMed1997

[Nutrition and Crohn's disease].

The relationships between non-specific inflammatory bowel disease and nutrition is considered. One of the hypotheses holds that environmental factors, especially those in dietary intake, can be the initiators of intestinal inflammation. In this connection authors examined a group of patients suffering from Crohns disease and ulcerative colitis. Results observed in patients with Crohns disease indicate: preferred consumption of flour products, decreased intake of vegetables and fruit, lowered tolerance to milk and milk products, increased sugar consumption, increased proportion of smokers, no differences in diet regimen between nick and healthy subjects. (Tab. 3, Ref. 16.)

Crohn Disease↗
PubMed1998

[Probiotics in childhood].

The Probiotics (Lactic acid bacteria) represent a nutritional live microbial supplement that positively affects host by enhancing the microbial balance. A survey is made of the most relevant studies concerning the use of probiotics in the prevention and treatment of infantile acute diarrhoea (by rotavirus or other agents), pseudomembranous colitis, hospital-acquired and antibiotic-associated diarrhoeas. Although the probiotics mechanism of action is not yet completely understood, it has been hypothesized that they exert an inhibitory effect on the intestinal inflammation by immune response modulation. Due to this property, the use of probiotics has therefore been suggested in other severe diseases such as chronic inflammatory bowel diseases, rheumatoid arthritis, food allergy, atopic dermatitis and as immunoadjuvant for oral vaccines.

Child↗
PubMed1998

Antitumor necrosis factor therapy in rat chronic granulomatous colitis: critical dose-timing effects on outcome.

Inhibition of tumor necrosis fact (TNFalpha) is of potential benefit in the treatment of chronic inflammatory conditions. However, TNFalpha plays an important role in host defenses against infection, and blocking TNFalpha production may also have adverse effects. We tested the efficacy and safety of anti-TNFalpha therapy in experimental colitis induced by trinitrobenzenesulfonic acid. We cultured colonic wall specimens for bacterial growth and measured native TNFalpha protein synthesis in colonic tissue at days 0, 1, 4, 10 and 18 after induction of colitis. Anti-TNFalpha therapy (monoclonal g1 immunoglobulin, 15 mg/kg i.p., every third day) was started on either day 4 or day 10 after induction of colitis. On day 18, we measured the release of inflammatory mediators and scored colonic lesions. In acute lesions, several species of the common flora were grown, including Streptococcus, Staphylococcus, Bacteroides, clostridia and enterobacteria. In chronic lesions, only enterobacteria, clostridia and lactobacilli were isolated. TNFalpha production by inflamed colonic tissue was increased in both acute and chronic lesions. Anti-TNFalpha therapy induced a significant decrease in the release of inflammatory mediators and histopathological remission when treatment started on day 10. However, anti-TNFalpha therapy increased eicosanoid release and lesion scores when treatment started on day 4. In conclusion, acute colonic lesions showed polymicrobial infection. Anti-TNFalpha therapy induced remission of chronic intestinal inflammation, but early treatment did not prove effective.

Animals↗
PubMed1999

Clonal expansion of CD4+ TCRbetabeta+ T cells in TCR alpha-chain- deficient mice by gut-derived antigens.

A population of CD4+ alpha-beta+ T cells increases in the mucosal and peripheral lymphoid tissues of TCRalpha-chain-deficient mice with inflammatory bowel disease. The alpha-beta+ T cells, which produce predominantly IL-4, mediate the proliferation of colonic epithelial crypts and the infiltration of large numbers of IgA-producing plasma cells into the lamina propria of the colon. To examine whether enteric Ags were recognized by a population of monoclonal alpha-beta+ T cells leading to the intestinal inflammation, we examined the usage and clonotypes of TCR expressed by the alpha-beta+ T cells in TCRalpha-chain-deficient mice with inflammatory bowel disease. Analyses of immunoprecipitates by two dimensional electrophoresis and single-cell RT-PCR revealed that TCR of the alpha-beta+ T cells was a homodimer of beta-chains that was capable of recognizing luminal bacterial Ags. PCR single-strand conformation polymorphism analysis of TCR Vbeta transcripts revealed monoclonal accumulation of the alpha-beta+ T cells in the colonic lamina propria of the diseased mice. DNA sequencing revealed the accumulation of the alpha-beta+ T cells with the same CDR3 sequences in the colon. These findings suggest that the pathogenic CD4+ alpha-beta+ T cells expressing a homodimeric form of the TCRbeta-chains can be clonally expanded upon the stimulation with gut-derived Ags.

Amino Acid Sequence↗
PubMed1991

The effect of elemental diet on intestinal permeability and inflammation in Crohn's disease.

This study examines whether treatment of acute Crohn's disease with an elemental diet improves intestinal integrity and inflammation as assessed by a 51Cr-labeled ethylenediaminetetraacetatic acid (EDTA) permeability test and the fecal excretion of 111In-labeled autologous leukocytes, respectively. Thirty-four patients with active Crohn's disease completed a 4-week treatment course with an elemental diet. Active disease was characterized by increased intestinal permeability [24-hour urine excretion of orally administered 51Cr-EDTA, 6.4% +/- 0.6% (mean +/- SE); normal, less than 3.0%] and by high fecal excretion of 111In-labeled leukocytes (14.2% +/- 1.1%; normal, less than 1.0%). Twenty-seven (80%) went into clinical remission, usually within a week of starting treatment. After 4 weeks of treatment, there was a significant decrease in both the urine excretion of 51Cr-EDTA (to 3.4% +/- 0.5%; P less than 0.01) and the fecal excretion of 111In (to 5.7% +/- 1.0%; P less than 0.001), indicating that such treatment is not just symptomatic. A framework for the mechanism by which elemental diet works, centering around the importance of the integrity of the intestinal barrier function, is proposed, and also appears to provide a logical explanation for some relapses of the disease.

Acute Disease↗
PubMed2003

Cholera toxin protects against action by Clostridium difficile toxin A. The role of antisecretory factor in intestinal secretion and inflammation in rat.

UNLABELLED: The protein antisecretory factor (AF) inhibits intestinal fluid secretion induced by the cholera toxin (CT) and Clostridium difficile toxin A (CDA). The present work investigated whether CT-induced AF protects against the enterotoxin action by CDA. Rats were pretreated perorally with CT or buffer as control, whereafter CDA-induced fluid secretion and cytotoxicity was tested in vivo in ligated intestinal loops; the mucosal level of AF was estimated using the Western blot technique. Rats given repeated peroral doses of CT became tolerant to CDA, the inhibition of fluid secretion and of cytotoxicity being 79% in eight out of nine animals. The repeated CT-treatment also induced long-lasting rise of AF in the mucosal epithelium. Recombinant AF given either perorally or intravenously inhibited both fluid secretion and cytotoxicity by CDA; similar results were obtained with a truncated 16-mer AF peptide. IN CONCLUSION: peroral CT-treatment induced tolerance to CDA in rat small intestine. The tolerance was probably mediated by AF induced via action of cholera toxin on the enteric nervous and immune system.

Animals↗
PubMed2006

[Comparison of effects of two kinds of fluid for resuscitation on bacterial translocation and inflammation of small intestine in rats with hemorrhagic shock].

OBJECTIVE: To investigate the effects of Ringer's solution (RS) or 6% hydroxyethyl saline (HES) on bacterial translocation and inflammation of the small intestine in rats with hemorrhagic shock. METHODS: Fifty healthy male SD rats were randomly divided into the sham group (SHA group, n=10), the Ringer's solution group (RS group, n=20) and 6% hydroxyethyl saline group (HES group, n=20). Controlled hemorrhagic shock model was reproduced in RS and HES groups. Bacterial translocation to the liver, the content of tumor necrosis factor-alpha (TNF-alpha) in intestinal tissue, and the myeloperoxidase (MPO) activity in the intestinal tissue were determined and compared among the groups, and the pathologic changes in the small intestine were observed. RESULTS: The mortality rate, bleeding volume and Chiu's scores were same in HES and RS groups (all P>0.05). Compared to SHA group, bacterial count and TNF-alpha level were increased significantly in HES and RS groups, and they were higher at 1 hour and lower at 24 hours in HES group than those in RS group. Compared to the SHA group, MPO activity increased at 1 hour in RS and HES groups, but no significant difference between the groups was found at 24 hours. CONCLUSION: RS prevents compromise of the intestinal barrier function better than the HES at 1 hour after fluid resuscitation. However, HES seems to be better in protecting the intestinal barrier function compared with RS at 24 hours after fluid resuscitation.

Animals↗
PubMedDate not supplied

The role of plasma high molecular weight kininogen in experimental intestinal and systemic inflammation.

Inflammation is accompanied by activation of the plasma kallikrein-kinin system (KKS). KKS activation has been demonstrated in a variety of inflammatory human diseases. To further explore the participation of KKS in arthritis and inflammatory bowel disease, we used two experimental animal models in arthritis and enterocolitis. We found that activation of KKS is associated with arthritis induced by intraperitoneal injection of peptidoglycan-polysaccharide polymers (PG-PS) as well as the enterocolitis and systemic inflammation induced also by PG-PS when injected into the intestinal wall of genetically susceptible Lewis rats. We postulated that KKS participates in the pathogenesis of inflammatory reactions involved in cellular injury, coagulation, fibrinolysis, kinin formation, complement activation, cytokine secretion, and release of proteases. We demonstrated that therapy with a specific plasma kallikrein inhibitor modulated the experimental enterocolitis, arthritis, and systemic inflammation. The fact that deficiency of plasma high molecular weight kininogen in the genetically susceptible Lewis rat results in decreased chronic enterocolitis and systemic inflammation also supports our hypothesis. We suggest that KKS plays a similar role in idiopathic human intestinal inflammatory disease and arthritis, making kallikrein-kinin system proteins appealing targets for drug therapy in chronic inflammatory diseases such as rheumatoid arthritis and Crohn's disease.

Amino Acid Sequence↗
PubMed1999

Characteristics of inflammation-induced hypertrophy of rat intestinal smooth muscle cell.

Inflammation of the human intestine causes thickening of the smooth muscle layers, and studies in rats infected with Trichinella spiralis (Tsp) have shown hyperplasia of the intestinal smooth muscle cells (ISMC). We have shown that Tsp-induced inflammation caused a fivefold increase in total protein per ISMC over control, while ISMC from the noninflamed distal ileum also showed a threefold increase. The amount of alpha-smooth muscle (SM) actin per ISMC increased nearly 500% over control by postinfection (PI) day 6. The proportion of alpha-SM actin in the total cellular protein increased 200% by day 6 PI, indicating a higher density of alpha-SM actin in the hypertrophied ISMC. Gamma-SM actin mRNA increased sharply and was matched by an increased fractional content of gamma-SM actin protein. These increases in the smooth muscle-specific actins may affect force production and further demonstrate the plasticity of smooth muscle in the inflamed intestine.

Actins↗
PubMed1999

Relationship between persistence of Helicobacter pylori and dysplasia, intestinal metaplasia, atrophy, inflammation, and cell proliferation following partial gastrectomy.

Helicobacter pylori and partial gastric resection are risk factors for gastric cancer. Our aims were to investigate the presence of H. pylori in postgastrectomy patients and to correlate that with alterations in mucosal architecture and cell proliferation. One hundred fifty-one endoscopic biopsies from 22 patients, (15-47 years of age, mean 29.2 years) following partial gastrectomy with Billroth II reconstruction for peptic ulcer disease, were examined for the presence of H. pylori using Giemsa staining. Sections were scored for grade of hyperplasia, intestinal metaplasia, dysplasia, inflammation, and atrophy. Immunohistochemistry for proliferative cell nuclear antigen (PCNA) was used to characterize cell proliferation. H. pylori was observed in 17/22 (77.3%) of patients or in 57/151 (37.7%) of biopsies. Metaplasia was seen in 18/22, chronic atrophic gastritis in 20/22, and cystic glandular dilation in 21/22 patients. The highest type of metaplasia in each patient was: four Type I, five Type IIA and nine Type IIB. Dysplasia was present in 16 biopsies from nine patients. H. pylori was more prevalent in intestinal metaplasia type I (44.8% of biopsies), than in type IIA (32.7%) or type IIB (25%). No H. pylori was detected in regions showing dysplasia or cystic glandular dilation. H. pylori colonization was associated with degree of inflammation (P = 0.00001) and cell proliferation (P = 0.0001). In conclusion, H. pylori is commonly seen many years after gastrectomy, it is associated with an increased epithelial cell proliferation, and it is not present in areas of histologic markers of premalignancy (type IIB metaplasia and dysplasia).

Adolescent↗
PubMed2001

The role of probiotics in the treatment of intestinal infections and inflammation.

Clinical studies have established that certain probiotics are useful in a variety of intestinal disorders, including viral diarrhea, antibiotic-associated diarrhea, Clostridium difficile-associated diarrhea, and traveler's diarrhea. Evolving data suggest that probiotics might be useful in the control of inflammatory diseases, treatment and prevention of allergic diseases, cancer prevention, and stimulation of the immune system, which may result in the reduction in respiratory disease. A review of current data regarding the most common probiotics is presented. It is important that probiotic use be directed by well-designed, placebo-controlled clinical studies published in peer-reviewed journals.

Journal Article↗
PubMed1997

Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease.

OBJECTIVE: The purpose of the study was to test the hypothesis that cardiac mucosa, carditis, and specialized intestinal metaplasia at an endoscopically normal-appearing cardia are manifestations of gastroesophageal reflux disease. SUMMARY BACKGROUND DATA: In the absence of esophageal mucosal injury, the diagnosis of gastroesophageal reflux disease currently rests on 24-hour pH monitoring. Histologic examination of the esophagus is not useful. The recent identification of specialized intestinal metaplasia at the cardia, along with the observation that it occurs in inflamed cardiac mucosa, led the authors to focus on the type and condition of the mucosa at the gastroesophageal junction and its relation to gastroesophageal reflux disease. METHODS: Three hundred thirty-four consecutive patients with symptoms of foregut disease, no evidence of columnar-lined esophagus, and no history of gastric or esophageal surgery were evaluated by 1) endoscopic biopsies above, at, and below the gastroesophageal junction; 2) esophageal motility; and 3) 24-hour esophageal pH monitoring. The patients were divided into groups depending on the histologic presence of cardiac epithelium with and without inflammation or associated intestinal metaplasia. Markers of gastroesophageal reflux disease were compared between groups (i.e., lower esophageal sphincter characteristics, esophageal acid exposure, the presence of endoscopic erosive esophagitis, and hiatal hernia). RESULTS: When cardiac epithelium was found, it was inflamed in 96% of the patients. The presence of cardiac epithelium and carditis was associated with deterioration of lower esophageal sphincter characteristics and increased esophageal acid exposure. Esophagitis occurred more commonly in patients with carditis whose sphincter, on manometry, was structurally defective. Specialized intestinal metaplasia at the cardia was only seen in inflamed cardiac mucosa, and its prevalence increased both with increasing acid exposure and with the presence of esophagitis. CONCLUSION: The findings of cardiac mucosa, carditis, and intestinal metaplasia in an endoscopically normal-appearing gastroesophageal junction are histologic indicators of gastroesophageal reflux disease. These findings may be among the earliest signs of gastroesophageal reflux and contribute to the authors understanding of the pathophysiology of the disease process.

Adolescent↗
PubMed2002

Modulation of inflammation by vasoactive intestinal peptide and bombesin: lack of effects on neutrophil apoptosis.

Inhibition of neutrophil apoptosis has been identified as a prominent feature in chronic inflammation, parenchymal damage, and unresolved organ dysfunction. Lung injury animal models suggest that the neuropeptides vasoactive intestinal peptide and bombesin are protective. Therefore, in vitro effects of VIP and bombesin on apoptosis of normal human neutrophils were tested. For measuring effects on cell survival and apoptosis, trypan dye exclusion, colorimetric MTT assay to assess cell survival, and caspase-3 assay and annexin-V binding for analysing apoptosis rates were used. Foetal calf serum, Fas ligand, and tumour necrosis factor-alpha served as modulatory control agents; survival-promoting and apoptosis-inducing activities of the respective agents were confirmed. Vasoactive intestinal peptide and bombesin, however, failed to significantly affect cell death in neutrophils. Data suggest that direct regulation of neutrophil apoptosis is unlikely to be among the mechanisms of lung-protective actions of VIP and bombesin.

Apoptosis↗
PubMed1998

Subtherapeutic corticosteroids potentiate the ability of interleukin 10 to prevent chronic inflammation in rats.

BACKGROUND & AIMS: Interleukin (IL)-10, which inhibits macrophages and T-helper lymphocyte type 1 (TH1) lymphocytes, attenuates chronic granulomatous inflammation induced by bacterial cell wall polymers. This study determines whether corticosteroids enhance the protective effects of IL-10 in cultured peripheral blood mononuclear cells (PBMNCs) and in vivo when started before or after the onset of experimental chronic granulomatous inflammation. METHODS: Intestines of Lewis rats were injected intramurally with streptococcal peptidoglycan-polysaccharide (PG-APS) polymers. Daily murine recombinant IL-10 and/or dexamethasone (DEX) therapy was started 12 hours before or at several intervals after PG-APS injection. RESULTS: IL-10 plus corticosteroids additively inhibited IL-1beta secretion in human PBMNCs but preserved the beneficial IL-1RA/IL-1beta ratio induced by IL-10. IL-10 started before PG-APS injection significantly attenuated intestinal and extraintestinal inflammation, with even more pronounced effects in combination with subtherapeutic doses of DEX. The combination of DEX decreased the effective dose of IL-10 by at least one half. After onset of systemic inflammation using doses effective for prevention, IL-10 monotherapy had nearly no benefit and DEX plus IL-10 was similar to the mild therapeutic effect of DEX alone. CONCLUSIONS: The combination of IL-10 and corticosteroids allows lower doses of both agents in preventing chronic intestinal and systemic inflammation. However, timing of IL-10 administration is a critical variable in regulating inflammation.

Animals↗
PubMed1988

Changes in intestinal permeability and epithelial differentiation during inflammation in the rat.

We examined changes in gut permeability in a controlled model of inflammation produced in rats after infection with the nematode parasite, Nippostrongylus brasiliensis. The probe, 51Cr-EDTA, was injected into ligated loops of jejunum in vivo and recovery of radioactivity was measured in urine, kidney, and intact loop at five hours. Urinary recovery was significantly increased during the early (day 7) and acute (day 10) stages of the infection compared with values in control rats but subsequently returned to normal. Urinary clearance of the probe after iv injection was unaltered during infection. Villus atrophy occurred only at the stage, whereas crypt hyperplasia was evident at both the early and acute stages. The terminal ileum appeared normal and showed normal permeability when compared with controls. We conclude that permeability changes are local to the site of inflammation, are reversible after healing and may be related to an increase in the proportion of relatively undifferentiated epithelium.

Animals↗
PubMed2000

Recombinant human interleukin-11 modulates ion transport and mucosal inflammation in the small intestine and colon.

Human recombinant interleukin 11 (rhIL-11) is a cytokine that suppresses the clinical signs of colitis in animal models of inflammatory bowel disease (IBD) and may be an effective therapeutic agent in the treatment of IBD. The objective of the current study was to investigate whether rhIL-11 was capable of reversing abnormalities in secretomotor function associated with gut inflammation. We investigated the effects of rhIL-11 on epithelial electrogenic ion transport in the jejunum and colon. Application of rhIL-11 (10 to 10,000 ng/ml) at either the luminal or serosal side of mucosal sheets isolated from control rats induced a concentration-dependent reduction of transmural potential difference (PD) in the jejunum and decreased the short-circuit current (Isc), representative of active electrogenic transport, in the colon. To investigate the effect of rhIL-11 on an inflamed gut, we isolated jejunal and colonic tissue from HLA-B27 transgenic rats with active inflammation of the bowel that represents an animal model of IBD. In jejunum and colon isolated from HLA-B27 transgenic rats, basal electrogenic ion transport was significantly attenuated and, under these conditions, rhIL-11 caused no changes in either transmural PD or Isc. However, in HLA-B27 rats, pretreatment with subcutaneous doses of rhIL-11 suppressed the symptoms of diarrhea, normalized myeloperoxidase activity in the jejunum and colon and healed mucosal injury. In the jejunum from HLA-B27 rats, healing of the intestinal inflammatory response enhanced basal transmural PD and the rhIL-11-duced changes in mucosal ion transport resembled those seen in uninflamed controls. Conversely, in the colon, healing of the mucosa did not normalize basal active ion transport nor did it reverse the inhibition of rhIL-11-induced changes in colonic Isc. Our results suggest that endogenous IL-11 may act as a modulator of epithelial transport under physiologic conditions and may act as a potent anti-inflammatory cytokine during active intestinal inflammation.

Animals↗
PubMed1993

Inverse regulation of alpha- and beta-adrenoceptors during trinitrobenzenesulfonic acid (TNB)-induced inflammation in guinea-pig small intestine.

The hypothesis has been raised that intestinal motor disturbances induced by inflammation of the digestive tract may reflect alterations in intestinal cell-membrane receptors. This question has been addressed herein for adrenoceptors by performing [3H]prazosin, [3H]rauwolscine and [3H]DHA binding studies on guinea-pig jejunal smooth-muscle membrane preparations from both healthy controls and 3, 6, and 10 days after TNB-induced intestinal inflammation. Each of the adrenoceptor subtype-selective radioligands used bound selectively to a single saturable class of sites, with no significant (p < 0.05) variation of dissociation constant (KD) values along the inflammatory process. In contrast maximal binding capacities (Bmax) for the different radioligands varied moderately but significantly (p < 0.05 and p < 0.01) according to the time after TNB injection. The alpha-adrenoceptors were significantly upregulated, respectively from (mean +/- SE in fmoles/mg of proteins) 27 +/- 3.8 (controls) to 91 +/- 3.1 (day 10) for the alpha 1-subtype, and from 26 +/- 2.7 (controls) to 102 +/- 5.9 (day 10) for the alpha 2-subtype. In contrast beta-adrenoceptors were down-regulated from 384 +/- 34.6 (controls) to 158 +/- 17.2 (day 10). These findings highlighted an apparently inverse pathological regulation of intestinal alpha- and beta- adrenoceptor densities. They suggest that changes in intestinal adrenoceptors, probably resulting from functional denervation of the inflamed bowel tissue, may contribute to the altered intestinal motility observed in inflammatory bowel diseases.

Animals↗
PubMed2002

Faecal calprotectin: a marker of inflammation throughout the intestinal tract.

OBJECTIVE: To assess the potential of measuring the calcium-binding protein calprotectin in faeces as a method of screening for alimentary inflammation and neoplasia. SETTING: Hospital day services unit for endoscopy and faecal analysis in the clinical biochemistry department. PARTICIPANTS: Consented patients attending for routine endoscopy were requested to provide faeces. Seventeen of the initial 30 patients provided faeces before and 1 week after endoscopy. After this, 116 patients for planned endoscopy provided faeces before endoscopy. The group comprised 43 patients with upper-gastrointestinal lesions, seven patients with inflammatory bowel disease, seven patients with irritable bowel syndrome, 31 patients with colonic disorders, and 28 normal people. A final 18 patients with known inflammatory bowel disease (seven patients), gastric carcinoma (one patient), colorectal cancer (eight patients) and colorectal adenoma (two patients) had faeces analysed. METHOD: Faeces were analysed by the Nycotest PhiCal enzyme-linked immunosorbent assay (ELISA) (Nycomed, Oslo, Norway), and the final 18 patients were analysed by the newer version marketed as Calprest. RESULTS: No definite differences between pre- and post-endoscopy calprotectin were found, but it was considered preferable in the subsequent patients to analyse pre-endoscopy faeces. Upper-gastrointestinal disorders showed little difference in calprotectin levels, Barrett's oesophagus (median 6.8 mg/l), gastric ulcer (median 6.5 mg/l) or gastritis/duodenitis (median 5.2 mg/l), but these levels were all higher than the median calprotectin level of normal subjects (4.5 mg/l). The oesophageal and gastric carcinoma median was elevated significantly at 30 mg/l. Inflammatory bowel disease was also associated with marked elevation (Crohn's disease, 31.2 mg/l; ulcerative colitis, 116.2 mg/l). Colorectal polyps (median 3.7 mg/l) and adenoma (median 3.8 mg/l) showed no elevated levels in contrast to colorectal carcinoma (median 53.4 mg/l). The elevated calprotectin in inflammatory bowel disease and colorectal carcinoma combined gave a sensitivity of 81.8% and a specificity of 73.2%. CONCLUSIONS: Calprotectin levels are elevated in inflammation and cancer but are not helpful in differentiating between these disorders. In our series, calprotectin was not elevated in colonic polyps or adenomata. Calprotectin could be helpful as a screening method in a general gastroenterology population for inflammatory bowel disease and those with carcinoma, as well as assessing and monitoring disease activity in inflammatory bowel disease.

Adult↗