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At least 1,261 records · Page 70Linked to original sources
PubMed2002

Glutamine decreases interleukin-8 and interleukin-6 but not nitric oxide and prostaglandins e(2) production by human gut in-vitro.

BACKGROUND: Glutamine modulates cytokine production in various tissues but its effects on the production of other inflammatory mediators such as eicosanoids and nitric oxide have not been investigated in human gut. AIM: To evaluate the influence of glutamine on interleukin (IL)-8, IL-6, nitric oxide and prostaglandin E(2) production by human gut. METHODS: Ten fasted volunteers received either enteral glutamine or isonitrogenous amino acids over 6 h in a cross-over design. Series of duodenal biopsies were frozen or cultured for 24 h with 0.5 or 5 mM of glutamine or amino acids. IL-6, IL-8 and PGE(2) were measured in culture media by ELISA and nitrites by Griess assay. mRNA levels for IL-6, IL-8, Cyclooxygenase-2 and NO synthase-2 were assessed in biopsies by RT-PCR. Results in percent, (median [range]) were compared by Wilcoxon test. RESULTS: Glutamine decreased IL-8 and IL-6 in-vitro production: 63 [2-173] vs 100 [19-177] and 37 [5-489] vs 100 [33-431], both P<0.05. IL-8 mRNA level also decreased in biopsies cultured with 5 mM glutamine: 26 [13-142] vs 92 [34-215], P<0.05. Nitrites and PGE(2) concentrations were not significantly affected by glutamine. CONCLUSION: Glutamine has a specific inhibitory effect on pro-inflammatory cytokine production in the gut and may contribution to the modulation of intestinal inflammation.

Adult↗
PubMed2005

Cannabinoids and the digestive tract.

In the digestive tract there is evidence for the presence of high levels of endocannabinoids (anandamide and 2-arachidonoylglycerol) and enzymes involved in the synthesis and metabolism of endocannabinoids. Immunohistochemical studies have shown the presence of CB1 receptors on myenteric and submucosal nerve plexuses along the alimentary tract. Pharmacological studies have shown that activation of CB1 receptors produces relaxation of the lower oesophageal sphincter, inhibition of gastric motility and acid secretion, as well as intestinal motility and secretion. In general, CB1-induced inhibition of intestinal motility and secretion is due to reduced acetylcholine release from enteric nerves. Conversely, endocannabinoids stimulate intestinal primary sensory neurons via the vanilloid VR1 receptor, resulting in enteritis and enhanced motility. The endogenous cannabinoid system has been found to be involved in the physiological control of colonic motility and in some pathophysiological states, including paralytic ileus, intestinal inflammation and cholera toxin-induced diarrhoea. Cannabinoids also possess antiemetic effects mediated by activation of central and peripheral CB1 receptors. Pharmacological modulation of the endogenous cannabinoid system could provide a new therapeutic target for the treatment of a number of gastrointestinal diseases, including nausea and vomiting, gastric ulcers, secretory diarrhoea, paralytic ileus, inflammatory bowel disease, colon cancer and gastro-oesophageal reflux conditions.

Animals↗
PubMed1987

Intestinal accumulation of 111In-granulocytes in patients studied because of occult infection.

111In-granulocyte scintigraphy was performed on 245 patients in whom a localized infection was suspected. In 123 patients scintigraphy was positive and of these 35 (28%) had intestinal accumulations of 111In-granulocytes. Specific local causes for the intestinal uptake of radioactivity were antibiotic associated colitis (eight patients), local pyogenic bowel infection (four patients), systemic disease (two patients), bowel necrosis (two patients), colonic cancer (one patient) and Stevens-Johnson's syndrome (one patient). Nonspecific mechanisms of bowel accumulation were desquamation of labelled granulocytes (12 patients) and bleeding (two patients). In three cases the mechanism of colonic accumulation of granulocytes was not revealed. These results show that unexpected accumulations of labelled granulocytes in the gut is not a rare phenomenon and is often due to clinically significant intestinal inflammation or other disease, especially in patients who do not have signs of respiratory, pancreatic or oesophageal inflammation causing desquamated granulocytes to accumulate in the gut.

Adolescent↗
PubMed1996

Abdominal scintigraphy using 99mTc-HMPAO-labelled leucocytes in patients with seronegative spondylarthropathies without clinical evidence of inflammatory bowel disease.

Abdominal scintigraphy with technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO)-labelled leucocytes is an excellent tool for evaluating disease extent and activity of intestinal lesions in patients with inflammatory bowel disease (IBD). In some cases of seronegative spondylarthropathies (SSp), IBD may remain subclinical. The aim of this study was to evaluate the presence of positive abdominal scintigraphy in patients with SSp and without clinical symptoms or signs of IBD. To this end we studied 32 patients with active SSp (European Spondylarthropathy Study Group 1991 criteria) without clinical evidence of IBD (eight had ankylosing spondylitis, four psoriatic arthritis, three reactive arthritis an 17 undifferentiated SSp) and 11 controls without SSp. All SSp and control patients received similar doses of non-steroidal anti-inflammatory drugs (NSAIDs). Abdominal scintigraphic images were obtained at 30 and 120 min after re-injection of 99mTc-HMPAO-labelled leucocytes. The 99mTc-HMPAO-labelled leucocyte scan was positive in 17 patients with SSp (53.1%) (six with ankylosing spondylitis, three with psoriatic arthritis, two with reactive arthritis and six with undifferentiated SSp). Fourteen patients scored from 2 to 4 on the intensity of uptake scale. The colon and terminal ileum were predominantly involved. Axial involvement was more frequent in patients with a positive scan than in patients with negative results (P<0.05) (64.7% vs 26.6%; odds ratio: 5). No control patient showed a positive scan. It is concluded that 99mTc-HMPAO-labelled leucocyte scan shows increased uptake among patients with SSp without evidence of IBD. These findings provide new evidence linking SSp with intestinal inflammation and suggest that in some cases a bowel-related process could contribute to the development of SSp. Long-term follow-up studies with more patients are necessary to evaluate the diagnostic and therapeutic implications of these results.

Abdomen↗
PubMed1986

111In-oxine-labelled white blood cells in the diagnosis and follow-up of Crohn's disease.

Prospectively, 43 patients with Crohn's disease (41 clinically active, 2 clinically inactive) and 7 patients with irritable bowel syndrome were examined by 111In-oxine-labelled leukocytes ('mixed' leukocyte preparations, n = 8; 'pure' granulocyte preparations, n = 42). The number of scintigraphically diagnosed inflamed bowel segments correlated significantly (r = 0.95, p less than 0.001) with the number of radiologically and endoscopically diagnosed segments. The exact localization of the diseased ileum may be difficult by scintigraphy. One complicating abscess and two fistulas were correctly diagnosed. The percentage of fecal excretion of radiolabelled leukocytes is highly specific for intestinal inflammations. It correlates significantly with the erythrocyte sedimentation rate (r = +0.69, p less than 0.001), serum albumin (r = -0.54, p less than 0.001), orosomucoid (r = +0.65, p less than 0.001), and with the A.I. (van Hees) (r = +0.67, p less than 0.001). In the follow-up of 9 patients, the percentage of fecal excretion decreased or increased more rapidly, but in correlation with the CDAI, A.I., or ESR. The authors conclude that this method is an alternative to common methods and that it is superior in primary diagnosis in patients with severe disease, bowel stenosis, abscesses, and after surgery. After clinical and biopsy-proven diagnosis of Crohn's disease, the special value of the leukocyte scan lies in the noninvasive follow-up of patients and its potential of localizing inflamed bowel segments and assessing disease activity.

Colon↗
PubMed1994

Analysis of T-lymphocyte subpopulations in inflammatory bowel diseases by three-color flow cytometry.

In order to better define changes in the relative proportion of peripheral blood T-lymphocyte subpopulations in patients with inflammatory diseases of the bowel, we performed simultaneous three-color fluorescence-activated cytometric (FACS) analysis using fluorophore-conjugated monoclonal antibodies with specificity for CD4, CD8, Leu 8, and CD45RA on 22 normal control subjects, 28 patients with Crohn's disease (CD), 15 patients with ulcerative colitis (UC), and 11 patients with intestinal inflammation secondary to etiologies other than inflammatory bowel disease (NIBD). This staining combination allowed enumeration of distinct T-cell subpopulations as follows: virgin CD4+, recall antigen helper T cells, nonspecific B-cell helper T cell, virgin CD8+, cytotoxic effector and suppressor effector and recall antigen cytotoxic T cells based on a synthesis of published functional analyses. No differences in the proportion of CD4+ or CD8+ cells or in the CD4+/CD8+ ratios were evident when UC and NIBD patients were compared to normal subjects. A significant reduction in the proportion of CD4+ cells and an increase in CD8+ cells was observed, however, in the CD group. When two-color analysis was performed, several significant differences in the proportions of circulating lymphocytes were seen. Specifically, these included significant increases in the number of CD4+, Leu 8- (P < 0.01) cells in all disease groups and an increase in CD4+, CD45RA+ cells in the NIBD group. Conversely, significant decreases in the proportions of CD8+, Leu 8+ (P < 0.01) cells were evident in the Crohn's disease group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Pericholangitis in a rabbit colitis model induced by injection of muramyl dipeptide emulsified with a long-chain fatty acid.

Rabbit colitis has been induced by injection of muramyl dipeptide emulsified with a long-chain fatty acid. The muramyl dipeptide emulsion was injected submucosally at six portions of the rectum and colon, 10 cm proximal to the anus, using a flexible endoscope. Six rabbits were injected six times every 2 weeks and subsequently killed 2 weeks after the last injection. The histological changes of the colon that occurred in all 6 rabbits were mononuclear cell and histiocyte infiltration with sporadic eosinophils, transmural infiltration, and well-maintained goblet cell populations. These changes were different in degree. In 4 of 6 rabbits histological examination of the liver showed pericholangitis and periductal fibrosis mimicking the pericholangitis frequently seen in patients with inflammatory bowel disease. Fibrosis bridging between the portal and portal veins occurred in 2 rabbits, and noncaseating granuloma was seen in 1 rabbit. These histological changes in our model have led to the suggestion that continuous stimulation with bacterial cell wall fragments may be involved in chronic intestinal inflammation and extraintestinal manifestations such as pericholangitis.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1996

Extraintestinal manifestations of granulomatous enterocolitis induced in rabbits by long-term submucosal administration of muramyl dipeptide emulsified with Freund's incomplete adjuvant.

We examined whether extraintestinal manifestations of granulomatous enterocolitis in rabbits might be produced by the long-term administration of muramyl dipeptide which represents the basic fragment of the bacterial cell wall, emulsified with Freund's incomplete adjuvant. Muramyl dipeptide emulsion was injected submucosally at six sites in the rectum and colon, 10 cm proximal to the anus, each time with a flexible endoscope. Seven rabbits were injected nine times or more every month, and all were sacrificed 1 month after the last injection. The histological changes in the colon in the seven rabbits were mononuclear cell infiltration, epithelioid granulomas, granulomatous lesion, and denuded and regenerative epithelia, although the changes differed in degree. In five of the seven rabbits, histological examination of the liver showed pericholangitis and periductal fibrosis, findings analogous to sclerosing cholangitis in patients with inflammatory bowel disease. In four of the seven rabbits, fibrosis bridging mainly between portal and portal veins, and, in places, between portal and central veins, was seen. Two of the seven rabbits developed polyarthritis. The histological changes in our model suggest that continuous stimulation with bacterial cell wall fragments may be involved in the extraintestinal manifestations of chronic intestinal inflammation such as that seen in inflammatory bowel disease.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1999

Management of urinary complications in Crohn's disease.

Among the 127 patients who underwent surgical treatment for Crohn's disease at Tohoku University Hospital, urinary complications were noted in 13 patients (10.2%), including urolithiasis in 6 patients (4.7%), a ureteral obstruction in 4 (3.1%), and urinary fistula in 3 (2.4%). In patients with urolithiasis, conservative therapy was effective. An ureteral obstruction was detected on the right side in all 4 of these cases because of the inflamed terminal ileum. In 2 of the 4 cases, the symptoms improved by either preoperative total parenteral nutrition or elemental diet therapy. A resection of the inflamed intestine was necessary in all cases. In patients with urinary fistulas, a resection of the inflamed intestine combined with a reconstruction of the urinary tract was carried out after total parenteral nutrition. In conclusion, conservative therapy with preoperative total parenteral nutrition or elemental diet therapy proved to be effective for a ureteral obstruction since it improved the intestinal inflammation. As a definitive treatment, surgery is still necessary for the management of urinary fistulas and ureteral obstruction. Based on our findings, patients with urolithiasis in Crohn's disease should thus be treated conservatively in the same way as patients without Crohn's disease.

Adolescent↗
PubMedDate not supplied

Is the rectum usually empty?--A quantitative study in subjects with and without diarrhea.

The authors have investigated the frequency with which the rectum contains feces by recording the presence or absence of fecal contamination of the membrane or of discoloration by feces of the contents of dialysis bags placed in the unprepared rectum for one hour. Feces were present in the rectum in 31 per cent of 32 studies in normal control subjects, in 49 per cent of 80 studies in obese subjects (P less than 0.05 from controls), in 36 per cent of 28 studies in patients with the irritable bowel syndrome, and in 31 per cent of 103 studies in patients with ulcerative proctocolitis, whether or not they had diarrhea. Fecal staining of the bag and its contents occurred much more frequently in 27 studies in subjects with various other diarrheal diseases (67 per cent, P less than 0.02 from controls), including eight with steatorrhea (87 per cent, P less than 0.02 from controls). The frequency with which feces were present was unaffected by age, sex, or time of day of the study. These results provide quantitative support for the assertion that in subjects without diarrhea the rectum is usually empty. In patients with diarrhea or steatorrhea and no distal large intestinal inflammation, however, the rectum usually does contain fecal material.

Adolescent↗
PubMed2004

Experimental colitis does not increase the prevalence of ANKENT, a spontaneous joint disease in mice.

A possible relationship between intestinal inflammation and joint disease development was investigated. Clinical symptoms of colitis--diarrhea and rectal bleeding--were confirmed by findings of inflammatory processes in the colon in dextran sodium sulfate-treated mice and joint ankylosing enthesopathy (ANKENT) developed in 12.8 % mice with chronic colitis and 13.6 % mice in the control group. Consequently no significant difference in ANKENT frequency was found between mice with and without chronic colitis and the occurrence of ANKENT in both groups was typical for conventional conditions. ANKENT cannot be triggered solely a generalized inflammatory process in the gut.

Animals↗
PubMed2005

Treatment of Crohn's disease with anti-IL-6 receptor antibody.

We have demonstrated, by using a T-cell transfer murine colitis model, that blocking interleukin 6 (IL-6) signaling with monoclonal antibody (mAb) to IL-6 receptor (IL-6R) abrogated apoptosis resistance of lamina propria T cells, suppressed the expression of vascular adhesion molecules, and successfully prevented and treated intestinal inflammation. Based on these results, we carried out an exploratory clinical trial to investigate the safety and efficacy of humanized anti-IL-6R mAb, MRA, in patients with Crohn's disease (CD). The results were promising, with 80% of the patients given every-2-week MRA infusions for 12 weeks showing a significantly higher clinical response rate as compared to 31% of the placebo-treated patients. Twenty percent of the patients on this regimen went into remission as compared to 0% of the placebo group. The acute-phase responses were normalized by a single MRA infusion, which strongly suggests IL-6 is the major cytokine responsible for their production in CD.

Animals↗
PubMed2002

Enhanced macrophage responsiveness to lipopolysaccharide and CD40 stimulation in a murine model of inflammatory bowel disease: IL-10-deficient mice.

OBJECTIVE: To elucidate the role of macrophages in the pathogenesis of inflammatory bowel disease, proinflammatory characteristics of macrophages were estimated in a murine model of spontaneous intestinal inflammation. MATERIALS AND METHODS: Peritoneal macrophages from IL-10deficient mice were stimulated with lipopolysaccharide (LPS) or an anti-CD40 monoclonal antibody (mAb). Cytokine release was assessed by enzyme-linked immunosorbent assay. CD40 expression was examined by two-color flow cytometric analysis. Induction of suppressor of cytokine signaling 3 (SOCS3) mRNA was evaluated by real-time quantitative RT-PCR. RESULTS: In the presence of LPS or anti-CD40 mAb, TNF-alpha and IL-12p70 release from macrophages of mutant mice was significantly higher than that from macrophages of wild-type mice. This may be due to the difference in IL-10 production by macrophages, since activated macrophages of wild-type mice produced IL-10 in amounts sufficient to suppress an increased release of cytokines from activated macrophages of mutant mice. LPS and CD40 stimulation induced significantly high level of SOCS3 expression in macrophages of mutant mice in comparison to those of wild-type mice. CONCLUSIONS: Macrophages from a murine model of inflammatory bowel disease demonstrated enhanced responsiveness to immunological and bacterial stimuli. This suggests significant roles of macrophages in the pathogenesis of inflammatory bowel disease.

Animals↗
PubMed2001

Calcium-dependent interleukin-8 gene expression in T84 human colonic epithelial cells.

OBJECTIVE AND DESIGN: IL-8 is a chemokine that activates and recruits neutrophils and plays a major role in intestinal inflammation. Signal transduction pathways mediated by protein kinases are central in regulating IL-8 gene expression, however, little is known about the role of Ca2+ in this event. In this study, we characterize the effect of intracellular Ca2+ on interleukin-8 gene expression in T84 human colonic epithelial cells. MATERIALS AND METHODS: Cells were stimulated with Ca2+ ionophore, A23187 or thapsigargin, a Ca2+-ATPase inhibitor. Semi-quantitative RT-PCR was used to examine IL-8 mRNA and ELISA for protein quantification. Reporter gene techniques were used to determine transcription rate. RESULTS: A23187 and thapsigargin caused a dose- and time-dependent accumulation of IL-8 mRNA and protein production which was dependent on the release of Ca2+ from intracellular stores. FK506, a specific inhibitor of calcineurin, inhibited A23187- and thapsigargin-induced IL-8 mRNA expression in a dose dependent manner. Reporter gene studies and actinomycin D chase experiments showed that A23187 and thapsigargin enhanced IL-8 gene transcription and stabilized IL-8 mRNA transcripts, respectively. CONCLUSION: Intracellular Ca2+ plays an important role in regulating IL-8 transcriptionally and posttranscriptionally through calcium/calmodulin-dependent calcineurin.

Adenocarcinoma↗
PubMed2002

Contractility in vitro and mitochondrial response in small and large rabbit bowel after anastomosis.

Leakage of a large bowel anastomosis remains the most serious postoperative complication in gastrointestinal surgery. In a recent experimental study we found that surgically induced hypoxia resulted in more derangement of a variety of biochemical markers in the large bowel (LB) than in the small bowel (SB). We explored the question of whether spontaneous and agonist-induced contractility of SB and LB muscle strips was influenced by surgical procedures and how contractility was related to energetic oxidative metabolism capacity in smooth muscle mitochondria. Sixty male New Zealand rabbits were operated on under general anesthesia. Segments of ileum and colon were resected from each rabbit, and an end-to-end anastomosis was constructed. A representative subset of segments from SB (n = 14) and LB (n = 14) at time 0 was used as controls. Tracts containing an anastomosis were resected at days 2, 7, and 14 after operation. At each time point, 20 segments adjacent to the anastomosis of both SB and LB were used for tensiometric and biochemical studies. Tensiometric studies demonstrated modifications in the smooth muscle function at both the acute and chronic stages with intestinal inflammation that may contribute to surgical stress-associated abnormal motility. Biochemical data showed that the respiratory capacity of the resected LB was more impaired than that of the SB. In both SB and LB, changes in respiratory activity preceded tensiometric changes. Thus abnormalities of contractility after surgical stress are more evident in LB than SB in segments adjacent to the anastomoses. This could be the consequence of abnormal biochemical changes, as adenosine triphosphate (ATP) is required for membrane potential maintenance, calcium homeostasis, and actin-myosin interactions.

Anastomosis, Surgical↗
PubMed2006

Suppression of proinflammatory cytokine production in macrophages by lansoprazole.

Macrophages (MPs) produce increased levels of proinflammatory cytokines in Crohn's disease; these cytokines are thought to play a central role in the occurrence of the disease. Biologics are currently available for anti-cytokine therapy, but treating intestinal inflammation through direct suppression of proinflammatory cytokine production could be more effective. P-ATPase inhibitors have been reported to be anti-inflammatory, and these inhibitors might suppress the production of MP proinflammatory cytokines. In this study, we examined the effect of two types of ATPase inhibitors on the expression patterns of typical proinflammatory cytokines. Peritoneal MPs from 6- to 8-week-old mice were cultured for 48 h in the presence of lansoprazole (P-ATPase inhibitor), bafilomycin A(1) (V-ATPase inhibitor), or the control solvent dimethylsulfoxide. The MPs were then examined for cytokine expression by quantitative real-time polymerase chain reaction (PCR), and culture supernatants were examined for cytokine production with a multiplex assay in a suspension array system. The possible existence of P-ATPase mRNA in MPs was explored using reverse-transcriptase PCR. P-ATPase mRNA was not detected in MP cells. However, all examined proinflammatory cytokines decreased significantly in their mRNA and protein expression in the lansoprazole-treated group. Conversely, bafilomycin A(1) increased the levels of these cytokines. Lansoprazole might be useful for the treatment of inflammatory bowel diseases (IBDs), including Crohn's disease, as it suppresses the production of relevant MP proinflammatory cytokines. However, because P-ATPase was not detected in MPs, the mechanism is unclear and remains to be studied further in an IBD animal model.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2002

Plasma levels of soluble CD40 ligand are elevated in inflammatory bowel diseases.

BACKGROUND AND AIMS: CD40/CD40 ligand (CD40L) interaction is important for induction of T cell dependent antibody production and cell-mediated immune responses. Overexpression of CD40/CD40L in the intestinal mucosa is likely to be involved in the pathogenesis of inflammatory bowel disease (IBD). A soluble form of CD40L (sCD40L) exists in the circulation. This study investigated whether plasma levels of sCD40L are higher in patients with IBD than in healthy controls. PATIENTS AND METHODS: Plasma levels of sCD40L were measured in 89 patients with Crohn's disease (CD), 56 patients with ulcerative colitis (UC), 17 patients with infectious diarrhea, and 42 healthy controls, using a specific enzyme-linked immunosorbent assay. RESULTS: In CD patients plasma levels of sCD40L were significantly higher than in healthy controls. Patients with UC and infectious diarrhea had higher sCD40L levels than healthy controls, but the differences were not significant. CD patients with fistulas and/or abscesses (n=38) had significantly higher levels of sCD40L than patients with uncomplicated CD (n=51). Only in patients with uncomplicated CD plasma levels of sCD40L correlated significantly with C-reactive protein and alpha(1)-glycoprotein. In UC patients there was a significant correlation of sCD40L with C-reactive protein. However, there was no significant correlation between plasma sCD40L levels and Crohn's disease activity index or Rachmilewitz score. CONCLUSION: Elevated plasma levels of sCD40L in CD patients supposedly reflect activation of functional CD40L in the intestine and might be a marker of intestinal inflammation.

Adolescent↗
PubMed2005

Inherent potential for production of tumor necrosis factor-alpha by human intestinal macrophages.

BACKGROUND AND AIMS: Tumor necrosis factor (TNF) production by the macrophages in intestines appears to play a critical role in the pathogenesis of Crohn's disease (CD). However, it is reported that resident intestinal macrophages (both colonic and small-bowel) do not produce TNF after lipopolysaccharide (LPS) stimulation. It has not yet been proven whether or not intestinal macrophages have an inherent potential to produce TNF. The purpose of this study is to answer this question. MATERIALS AND METHODS: Colonic macrophages were isolated from lamina propria of human large intestine and stimulated with a variety of substances: LPS, a lipid A derivative (ONO-4007), killed Streptococcus bacterial body (OK-432), phorbol 12-myristate 13-acetate, and lectins (pokeweed mitogen and Sarcophaga lectin). RESULTS: Colonic macrophages were phenotypically negative for CD14 and positive for CD68 and produced very little TNF in response to LPS, as reported previously. Of the substances tested, only Sarcophaga lectin, which is a defense protein of fleshflies (Sarcophaga peregrina), induced TNF production by the intestinal macrophages. In addition, when the colonic macrophages were cultured on immunoglobulin-A-coated dishes, their characteristic response to LPS was altered, and they produced TNF at a level 6.6 times higher than when on collagen-coated dishes. CONCLUSION: Colonic macrophages have an inherent ability to produce TNF. Activation of colonic macrophages by unknown substances may contribute to the induction of TNF production, which causes the intestinal inflammation of CD.

Antigens, CD↗