Interleukin 1 beta down-regulates collagen and augments collagenase expression in human intestinal smooth muscle cells

Graham, Martin F.; Willey, Amy; Adams, John W.; Yager, Dorne R.; Diegelmann, Robert F.

doi:10.1053/gast.1996.v110.pm8566579

Cited by 56 publications

(34 citation statements)

References 2 publications

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“…We also observed an increase in the number of PCNA positive ileal smooth muscle cells at 2 days after trinitrobenzene sulfonic acid (TNBS)-induced ileitis (our unpublished data). IL-1␤ is a recognized proinflammatory cytokine that induces proliferation in numerous cell types (8), including intestinal smooth muscle cells (11,12,26). We confirmed the proliferative effect of IL-1␤ using primary rat ileal smooth muscle cells (our unpublished data).…”

Section: Discussionsupporting

confidence: 70%

“…These reports suggest that IL-1␤ possesses both direct proliferative and indirect (through COX-2/iNOS expression) anti-proliferative roles in vascular and airway smooth muscle cells. In contrast to results in vascular and airway smooth muscles, IL-1␤ directly stimulates proliferation of cultured human ileal smooth muscle cells (26) and human and mouse primary smooth muscle cells (11,12). The difference in the response to IL-1␤ may be due to cell-specific difference in the ability to express COX-2 and iNOS.…”

Section: Discussionmentioning

confidence: 74%

“…As for the intestine, previous reports have reported that IL-1␤ directly induces the proliferation of cultured intestinal smooth muscle cells (11,12,26). These finding strongly suggest a role of IL-1␤ in inflammation-induced thickening of the intestinal smooth muscle layer; however, limited data are available regarding the effects of IL-1␤ on proliferation of smooth muscle under more physiological conditions.…”

Section: Interleukin-1␤; Intestinementioning

confidence: 98%

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IL-1β inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages

Hori¹,

Momotani²,

Elorza³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ohama T, Hori M, Momotani E, Elorza M, Gerthoffer WT, Ozaki H. IL-1␤ inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages. Am J Physiol Gastrointest Liver Physiol 292: G1315-G1322, 2007. First published January 18, 2007 doi:10.1152/ajpgi.00487.2006.-Intestinal inflammation causes hyperplasia of smooth muscle that leads to thickening of the smooth muscle layer, resulting in dysmotility. IL-1␤ is a proinflammatory cytokine that plays a central role in intestinal inflammation. In this study, to evaluate the effect of IL-1␤ on proliferation of ileal smooth muscle cells in vivo, we utilized an organ culture system. When rat ileal smooth muscle tissue was cultured under serum-free conditions for 3 days, most smooth muscle cells maintained their arrangement and kept their contractile phenotype. When 10% FBS was added, an increased number of smooth muscle cells per unit area was observed. Moreover, immunohistochemical staining for PCNA demonstrated that FBS induced proliferation of smooth muscle cells. IL-1␤ inhibited the proliferative effect of FBS. Furthermore, IL-1␤ upregulated inducible nitric oxide (NO) synthase and cyclooxygenase-2 mRNA and protein and thus stimulated NO and PGE 2 productions. Moreover, exogenously applied NO and PGE 2 inhibited the increase of bromodeoxyuridine-positive cells stimulated with FBS. Immunostaining revealed that the majority of cyclooxygenase-2 and inducible NO synthase was located in the dense network of macrophages resident in the muscularis, which were immunoreactive to ED2. Based on these findings, IL-1␤ acts as an anti-proliferative mediator, which acts indirectly through the production of PGE 2 and NO from resident macrophage within ileal smooth muscle tissue.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 74%

Section: Interleukin-1␤; Intestinementioning

confidence: 98%

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IL-1β inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages

Hori¹,

Momotani²,

Elorza³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Intestinal smooth muscle cells receive neural input from axons that originate within the intestine, and disruption of the intrinsic nerve has been shown to lead to proliferation of smooth muscle cells (Lourenssen et al, 2005). As an alternative mechanism, in studies using cultured intestinal smooth muscle cells, IL-1β has been shown to directly affect smooth muscle cells and promote their proliferative activity (Owens and Grisham, 1993;Graham et al, 1996;Hogaboam et al, 1997). Thus, it appears that IL-1β is involved in hyperplasia of the smooth muscle layer.…”

Section: Other Mechanismsmentioning

confidence: 99%

Mechanism of abnormal intestinal motility in inflammatory bowel disease: how smooth muscle contraction is reduced?

Ohama

Hori

Ozaki

2007

J Smooth Muscle Res

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Intestinal inflammation alters the contractile activity of intestinal smooth muscle. Motility disorders of the gastrointestinal tract are clinically important symptoms, because they are often associated with severe interstitial inflammation. In addition, the motility disorders secondarily induce abnormal growth of the intestinal flora, and the resulting disturbance of this flora aggravates the pathogenesis of mucosal inflammation. This in turn aggravates the intestinal dysmotility; i.e., it is an inflammatory spiral. Therefore, it is important to elucidate the mechanisms involved in the changes in motor function which occur in intestinal inflammation. Recent studies have revealed several molecular mechanisms responsible for the decreased motility which occurs in an inflamed gastrointestinal tract. In the present review, we discuss the functional failure of smooth muscle cells, including changes in the activity of muscarinic receptors, ion channels and the endogenous myosin phosphatase inhibitor CPI-17.Key words: intestinal inflammation, smooth muscle, contraction, CPI-17 Motility disorders in intestinal inflammationMotility disorders of the gastrointestinal tract are extremely important clinically because they can lead to systemic disease. In humans and in animal models, intestinal inflammation results in the disturbance of motility, which may reflect changes in smooth muscle function and/or the enteric nervous system (Vermillion et al., 1993;Vrees et al., 2002). Both increased and decreased smooth muscle contractility has been observed in intestinal inflammation. In a model of nematode infection-induced gut inflammation, such as Trichinella spiralis infectioninduced gut inflammation, smooth muscle contractility is increased (Vermillion and Collins, 1988;Blennerhassett et al., 1992). On the other hand, smooth muscle contractility is decreased T. OHAMA et al. 44 in the intestinal inflammation induced by trinitrobenzene sulphonic acid (TNBS), surgical manipulation, experimental obstruction, hemorrhagic shock, or peritonitis (Kalff et al., 1998;Moreels et al., 2001; Koyluoglu et al., 2002;Hierholzer et al., 2004; Kinoshita et al., 2006; Kiyosue et al., 2006;Won et al., 2006; Kinoshita et al., 2007;Ohama et al., 2007b). These differences in contractile responses may be due to differences in cytokine profiles. Reports from the Collins group (Akiho et al., 2002;Akiho et al., 2005a;Akiho et al., 2005b) have suggested that nematode-induced hypercontractility is mediated by an increase in prostaglandin E2 (PGE2) levels after induction of the expression of Th2 cytokines such as interleukin (IL)-4 and IL-13.On the other hand, reports suggest that TNBS-induced gut inflammation is mediated mainly by Th1 cytokines such as IL-1β, tumor necrosis factor-α (TNF-α) and IL-12 (Neurath et al., 1995; Kinoshita et al., 2006; Kiyosue et al., 2006;Ohama et al., 2007b). In this review, we focused on the molecular mechanisms that are responsible for the decreased motility of the inflamed intestine. Nematode-induced hyper-co...

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“…Cell culture models are a useful tool in understanding these processes, but, until recently, in vitro studies of human colonic myofibroblasts have relied on the use of immortal cell lines (17), the growth characteristics of which are likely to be different from nontransformed cells. Studies on primary cultures of human intestinal smooth muscle cells have been performed for a limited number of mitogens (18,19), and although these cells may be important in transmural inflammation and stricture development, they are unlikely to play a role in healing and remodeling in the subepithelial layers. A novel ex vivo model has recently been established that enables pure populations of subepithelial myofibroblasts from adult human intestinal mu-cosa to be available (20).…”

Section: Introductionmentioning

confidence: 99%

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

Jobson

Billington²,

Hall³

1998

J. Clin. Invest.

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An increase in myofibroblast number may be necessary for wound healing but may also lead to postinflammatory scarring. We have, therefore, studied the role of mediators important in inflammatory bowel disease in regulating proliferation of human colonic myofibroblasts. Using primary cultures of these cells, we have shown increases in [ 3 H]thymidine incorporation in response to platelet-derived growth factor (EC 50 ϭ 14 ng/ml), basic fibroblast growth factor (EC 50 ϭ 2.2 ng/ml), and epidermal growth factor (EC 50 ϭ 1.1 ng/ml). Coulter counting of cell suspensions demonstrated increases in cell number with these growth factors along with insulin-like growth factor-I and -II. In addition the proinflammatory cytokines IL-1 ␤ and TNF-␣ produced increases in

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Interleukin 1 beta down-regulates collagen and augments collagenase expression in human intestinal smooth muscle cells

Cited by 56 publications

References 2 publications

IL-1β inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages

IL-1β inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages

Mechanism of abnormal intestinal motility in inflammatory bowel disease: how smooth muscle contraction is reduced?

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

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