Cytokine mRNA Expression in Intestine from Normal and Inflammatory Bowel Disease Patients

McCabe, Robert P.; Secrist, Heather; Botney, Mitchell D.; Egan, Maureen; Peters, Marion G.

doi:10.1006/clin.1993.1007

Cited by 76 publications

(34 citation statements)

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“…This finding is consistent with data from McCabe ct al. [6]. who suggested that IL-4 is produced in the intestinal mucosa in extremely minute amounts.…”

Section: Discussionmentioning

confidence: 99%

“…[n addition to these proinflammatory cytokines a compensatory anti-inflariimatory response has been suggested in the inflamed mucosa. mainly due to observations showing an increased expression of IL-I receptor antagonist and transforming growth factor-beta (TGf-ii) [5,6]. So far, little is known about the concentration of the more immunoregulatory and/or anti-inflammatory effective cytokines.…”

Section: Introductionmentioning

confidence: 99%

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Altered Th1/Th2 cytokine profiles in the intestinal mucosa of patients with inflammatory bowel disease as assessed by quantitative reversed transcribed polymerase chain reaction (RT-PCR)

Niessner

Volk

1995

Clinical and Experimental Immunology

358

109

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SUMMARYCytokines serve a central function as key factors in the regulatioti of the intestinal immune response and mediation of tissue damage in inflammatory bowel disease (IBD). Abnormalities in the expression of immunoregulatory cytokines such as IL-2. IL-4. IL-IO and interferon-gamma (IFN-7) may indicate a dysregulation of intestinal immunity probably associated with pathogenic events. Therefore, cytokine niRNA concentrations were determined in the mucosa of patients with IBD at sites of active (n = 13) and inactive {« = 12) ulcerative colitis (UC), active {n -II) and inactive [n = II) Crohn's disease (CD) and in control patients in = 14) using quantitative RT-PCR. IL-IO tnRNA concentrations were significantly increased in patients with both active UC {P < 0001) and active CDiP < 0-005) compared with control patients. IFN--, mRNA concentrations were also significantly increased both in patients with active UC {P < 0'02) and active CD (/'<0 05) compared with control patients, whereas IL-2 mRNA levels were significantly {P < 002) increased only in active CD. IL-4 mRNA expression in the intestinal mucosa was frequently below the detection limit. Our results detiionstrale that chronic intestinal intlymmation in patients with CD is characteri:^ed by an increase of Thl-Iike cytokines. Furthermore, the increased IL-IO mRNA expression at sites of active IBD suggests that lL-10 is an important regulatory cotnponent involved in the control of the inflamtiiatory response in inflammatory bowel disease.

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“…This finding is consistent with data from McCabe ct al. [6]. who suggested that IL-4 is produced in the intestinal mucosa in extremely minute amounts.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Altered Th1/Th2 cytokine profiles in the intestinal mucosa of patients with inflammatory bowel disease as assessed by quantitative reversed transcribed polymerase chain reaction (RT-PCR)

Niessner

Volk

1995

Clinical and Experimental Immunology

358

109

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“…Another study showed that TGF-b1 expression in uninvolved mucosa of UC patients was lower than that in normal mucosa [17]. In contrast, TGF-b expression was reported to be elevated in active IBD patients, especially in lamina propria lymphocytes [13,18]. Del Zotto et al reported that lamina propria lymphocytes isolated from inflamed mucosa of UC patients showed increased TGF-b1 production compared to controls when stimulated with CD2 and CD28 [19].…”

Section: Tgf-b In Ibd Tgf-b Productionmentioning

confidence: 99%

TGF-β in inflammatory bowel disease: a key regulator of immune cells, epithelium, and the intestinal microbiota

2017

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Inflammatory bowel disease (IBD) is defined as chronic intestinal inflammation, and includes ulcerative colitis and Crohn's disease. Multiple factors are involved in the pathogenesis of IBD, and the condition is characterized by aberrant mucosal immune reactions to intestinal microbes in genetically susceptible hosts. Transforming growth factor-b (TGF-b) is an immune-suppressive cytokine produced by many cell types and activated by integrins. Active TGF-b binds to its receptor and regulates mucosal immune reactions through the TGF-b signaling pathway. Dysregulated TGF-b signaling is observed in the intestines of IBD patients. TGF-b signal impairment in specific cell types, such as T-cells and dendritic cells, results in spontaneous colitis in mouse models. In addition, specific intestinal microbes contribute to immune homeostasis by modulating TGF-b production. In this review, we describe the role of TGF-b in intestinal immunity, focusing on immune cells, epithelium, and intestinal microbes. In addition, we present potential therapeutic strategies for IBD that target TGF-b.

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“…Low rates of proliferation of LP T cells could be due to several causes. The LP contains large amounts of transforming growth factor-beta (TGF-) and IL-10 [17], which are anti-proliferative. There is also the possibility that there is insufficient antigen in the LP to induce them to proliferate, although the fact that ex vivo, in excess of gluten, LP T cells in coeliac biopsies fail to proliferate [18] would argue against this.…”

Section: Cd3 Cells In CD Intestinementioning

confidence: 99%

The distribution of dividing T cells throughout the intestinal wall in inflammatory bowel disease (IBD)

Fell

Walker-Smith

Spencer

et al. 1996

Clinical and Experimental Immunology

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T cell hypersensitivity has been implicated in the tissue damage in Crohn's disease (CD). All studies to date have examined mucosal T cells, although much of the tissue damage occurs in the submucosa and muscle layers. The aim of this work was to study T cell proliferation throughout the intestinal wall in children with IBD. Surgical resection material from 19 children with CD (10 ileal, 10 colonic), seven with ulcerative colitis (UC), and 12 normal controls was studied. The distribution of dividing T cells was investigated by double‐immunohistochemistry using Ki67 to identify proliferating cells, and CD3 to identify T cells. In ileal and colonic lamina propria virtually no Ki67+, CD3+ cells were seen in control, UC or CD tissue. In contrast, there were significantly more Ki67+, CD3+ cells within the lymphoid follicles of ileal and colonic CD than in the follicles in UC and controls. Increased numbers of Ki67+, CD3+ cells were present in the submucosa, muscle layers (M) and serosa in Crohn's ileitis and colitis compared with the lamina propria (LP), although only in the muscle of the colon was the difference statistically significant (LP, 0.4% (0–1%); M, 1.6% (0–5.2%); P = 0.03). Pooling data from ileal and colonic CD, however, did show significantly increased Ki67+, CD3+ cells in both serosa and muscle layers compared with the LP. Dividing T cells have been identified in the deeper layers of the gut wall in CD. These may contribute to the fibrosis and muscle hyperplasia characteristic of the condition.

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Cytokine mRNA Expression in Intestine from Normal and Inflammatory Bowel Disease Patients

Cited by 76 publications

References 0 publications

Altered Th1/Th2 cytokine profiles in the intestinal mucosa of patients with inflammatory bowel disease as assessed by quantitative reversed transcribed polymerase chain reaction (RT-PCR)

Altered Th1/Th2 cytokine profiles in the intestinal mucosa of patients with inflammatory bowel disease as assessed by quantitative reversed transcribed polymerase chain reaction (RT-PCR)

TGF-β in inflammatory bowel disease: a key regulator of immune cells, epithelium, and the intestinal microbiota

The distribution of dividing T cells throughout the intestinal wall in inflammatory bowel disease (IBD)

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