Interleukin 4 in inflammatory bowel disease and mucosal immune reactivity

West, Gail; Matsuura, Toshihiro; Levine, Alan D.; Klein, John S.; Fiocchi, Claudio

doi:10.1053/gast.1996.v110.pm8964392

Cited by 130 publications

(68 citation statements)

References 3 publications

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“…In other studies of older patients with previously established CD or UC and taking various medications, decreased production of IL-4 from isolated lamina propria CD4 ϩ T cells or mononuclear cells compared with control subjects was determined (6,7). The opposing results from these studies may be on the basis that total mRNA detection techniques will detect IL-4 mRNA from cellular sources other than mononuclear cells and mRNA expression does not necessarily correlate with protein expression.…”

Section: Discussionmentioning

confidence: 99%

Peripheral Blood Intracellular Cytokine Analysis in Children Newly Diagnosed with Inflammatory Bowel Disease

et al. 2002

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Section: Discussionmentioning

confidence: 99%

Peripheral Blood Intracellular Cytokine Analysis in Children Newly Diagnosed with Inflammatory Bowel Disease

et al. 2002

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“…, stimulation of IgE production (3,4), inhibition of superoxide anion generation by monocytes, down-regulation of the activity of proinflammatory cytokines IL-1 and TNF (5,6), and promotion of T cell differentiation into the type 2 cytokine-secreting cells that characterize nematode infection and atopic disorders (7). Although IL-4 and the related cytokine IL-13 have critical roles in host protection against gastrointestinal nematode parasites (7,8), there is little information on the in vivo effects of IL-4 on intestinal function that are related to host protection.…”

Section: Nterleukin-4 Is An Immunoregulatory Cytokine Produced Primmentioning

confidence: 99%

The Role of IL-4 in Heligmosomoides polygyrus-Induced Alterations in Murine Intestinal Epithelial Cell Function

Shea‐Donohue

Sullivan

Finkelman

et al. 2001

The Journal of Immunology

132

140

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IL-4 and IL-13 promote gastrointestinal worm expulsion, at least in part, through effects on nonlymphoid cells, such as intestinal epithelial cells. The role of IL-4/IL-13 in the regulation of intestinal epithelial function during Heligmosomoides polygyrus (Hp) infection was investigated in BALB/c mice infected with Hp or treated with a long-lasting formulation of recombinant mouse IL-4/αIL-4 complexes (IL-4C) for 7 days. Separate groups of BALB/c mice were drug-cured of initial infection and later reinfected and treated with anti-IL-4R mAb, an antagonist of IL-4 and IL-13 receptor binding, or with a control mAb. Segments of jejunum were mounted in Ussing chambers, and short circuit current responses to acetylcholine, histamine, serotonin, PGE2, and glucose were determined. Although only modest changes in epithelial cell function were observed during primary Hp infection, IL-4C or a secondary Hp infection each induced more dramatic changes, including increased mucosal permeability, reduced sodium-linked glucose absorption, and increased Cl− secretory response to PGE2. Some, but not all, effects of IL-4C and Hp infection were dependent on enteric nerves. Hp-induced changes in epithelial function were attenuated or prevented by anti-IL-4R mAb. Thus, IL-4/IL-13 mediate many of the effects of Hp infection on intestinal epithelial cell function and do so both through direct effects on epithelial cells and through indirect, enteric nerve-mediated prosecretory effects. These immune system-independent effector functions of IL-4/IL-13 may be important for host protection against gastrointestinal nematodes.

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“…However IL-4 was not increased and overall, the CD4 cells from UC patients produced IFN-␥ in an order of magnitude greater than that they made IL-5. Others have also shown that IL-4 is decreased in UC [26,27]. Where the Th2 paradigm might have some merit is in the sense of helping antibody responses.…”

Section: The Nature Of the T-cell Response In Uc Is Still Unclearmentioning

confidence: 99%

Recent Developments in the Immunology of Inflammatory Bowel Disease

2000

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Crohn's disease and ulcerative colitis are caused by excessive immune reactivity in the gut wall. Analysis of the type of immune responses ongoing in diseased gut has revealed important features which suggest that these conditions are different. In Crohn's disease tissue there is considerable evidence for an ongoing T helper cell type 1 response, with excess interleukin‐12, interferon‐γ and TNF‐α. There is circumstantial evidence in patients that this response is directed against the normal bacterial flora and definitive evidence in mouse models that T cell responses to the flora cause gut disease. In ulcerative colitis, the role of tissue damaging T cell responses in the gut mucosa is much less clear and there is more evidence that the lesion is owing to antibody‐mediated hypersensitivity. Although different types of immune reactions initiate tissue injury in both Crohn's disease and ulcerative colitis, the downstream events which actually damage the tissue are the same in each condition. Elevated cytokine concentrations in the mucosa lead to the production of excess matrix degrading enzymes by gut fibroblasts, loss of mucosal integrity and ulceration. The same process also leads to an increased production of epithelial growth factors such as KGF Keratinocyte Growth Factor by gut fibroblasts and produces the crypt cell hyperplasia characteristic of all gut inflammatory conditions.

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Interleukin 4 in inflammatory bowel disease and mucosal immune reactivity

Cited by 130 publications

References 3 publications

Peripheral Blood Intracellular Cytokine Analysis in Children Newly Diagnosed with Inflammatory Bowel Disease

Peripheral Blood Intracellular Cytokine Analysis in Children Newly Diagnosed with Inflammatory Bowel Disease

The Role of IL-4 in Heligmosomoides polygyrus-Induced Alterations in Murine Intestinal Epithelial Cell Function

Recent Developments in the Immunology of Inflammatory Bowel Disease

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