Human colonic microvascular endothelial cells is a model of inflammatory bowel disease

Welton, Mark L.

doi:10.1016/s0002-9610(97)00141-4

Cited by 2 publications

(2 citation statements)

References 26 publications

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“…In the middle 1980s it was recognised that the colonic and ileal endothelial cells in inflammatory bowel disease have altered cellular expression. Culture of these microvascular endothelial cells has resulted in the discovery of several unique properties of these cells in Crohn's disease [68,69].…”

Section: Vessel Wall Changesmentioning

confidence: 99%

Crohn's disease: in defense of a microvascular aetiology

Thornton

Solomon

2002

Int J Colorectal Dis

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Proving cause and effect will always be a difficult task given the self-perpetuating nature of the inflammatory and coagulation cascades and our inability at present to identify persons who subsequently develop Crohn's disease at a point prior to mucosal inflammation. Results to date however, are supportive of each of these factors, alone or in combination playing an integral part in the development of microvascular ischaemia, a pathological process which appears to precede the classic changes which characterize Crohn's disease.

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Section: Vessel Wall Changesmentioning

confidence: 99%

Crohn's disease: in defense of a microvascular aetiology

Thornton

Solomon

2002

Int J Colorectal Dis

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“…IBD is associated with increased vascular permeability, clinically apparent as mucosal oedema and loss of the submucosal vascular pattern. The disease is also characterized by marked angiogenesis, seen in the pronounced mucosal friability and antimesenteric corkscrew vessels (Welton, 1997). Griga, Tromm, Spranger & May (1998) and Griga, Voigt, Gretzer, Brasch & May (1999) documented increased serum levels of vascular endothelial growth factor (VEGF) in both active ulcerative colitis and active Crohn's disease patients but not in patients with inactive disease.…”

Section: Introductionmentioning

confidence: 99%

Effects of in vivo treatment with interleukins 1β and 6 on rat mesenteric vascular bed reactivity

Salvatore

Salvia

Piepoli

et al. 2003

Auton Autocoid Pharmacol

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1. Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1beta and 6 (ILs). In this disease, it has been shown that an abnormal microcirculatory system is implicated. 2. Therefore, the effects of in vivo treatment for three days with interleukins 1beta and 6 were investigated on rat isolated mesenteric vascular bed (MVB). 3. A significant concentration-dependent increase in vascular response to noradrenaline (NA) was found, with a significant difference in Emax between control (93.01 +/- 16.78 mmHg) and treated preparations (137.91 +/- 5.20 mmHg). Endothelin-1(ET-1) induced a significantly greater increase of perfusion pressure in treated rats in comparison with control rats at the highest concentration used (0.1 microm). 4. The concentration-dependent decrease of perfusion pressure induced by acetylcholine (ACh) in MVB precontracted with NA was significantly reduced in specimens from treated rats in comparison with control rats, with a significant difference in Emax between control and treated preparations. 5. Perivascular nerve stimulation (PNS) evoked contractions with no difference between treatments. Similarly, no difference in relaxant effect was found after PNS in specimens precontracted with NA, in the presence of guanethidine. 6. These findings indicate that the precocious inflammation acts only at postsynaptic level, facilitating vascular contraction. These data seem to support the hypothesis that vascular dysfunction caused by overproduction of ILs may contribute, among other immunological factors, to vasculitis in IBD that leads to intestinal ischaemia through vasoconstriction.

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Human colonic microvascular endothelial cells is a model of inflammatory bowel disease

Cited by 2 publications

References 26 publications

Crohn's disease: in defense of a microvascular aetiology

Crohn's disease: in defense of a microvascular aetiology

Effects of in vivo treatment with interleukins 1β and 6 on rat mesenteric vascular bed reactivity

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