Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis

Bendjelloul, Farid; Malý, Petr; Mandys, Václav; Jirkovská, Marie; Prokešová, L.; Tučková, Ludmila; Tlaskalová‐Hogenová, Helena

doi:10.1046/j.1365-2249.2000.01090.x

Cited by 77 publications

(58 citation statements)

References 34 publications

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“…We have also reported that loss of all ␤ 2 -integrins in DSS colitis results in severely decreased leukocyte recruitment and disease pathology with a concomitant reduction in vascular density accenting the role of increased leukocyte recruitment in pathological angiogenesis during experimental colitis (1,31). Moreover, Bendjelloul et al (14) found that ICAM-1 Ϫ/Ϫ mice are protected in DSS-induced colitis, providing further evidence for the importance of this molecule in IBD. VCAM-1, which binds ␣ 4 ␤ 1 and members of the ␤ 2 integrin family, is present on endothelium typically upon activation (expression induced by inflammatory cytokines) and is involved in the slow rolling of monocytes and lymphocytes during inflammatory cell recruitment.…”

Section: Angiogenic Mediators In Ibd and Experimental Colitissupporting

confidence: 54%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

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Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

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Section: Angiogenic Mediators In Ibd and Experimental Colitissupporting

confidence: 54%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

View full text Add to dashboard Cite

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“…ICAM-1 is a cell-surface protein that is induced first on the endothelium of the submucosal blood vessels and whose expression precedes surface ulceration (46). It is thought to play a role in recruiting effector immune cells to the mucosa and in establishing the inflammatory process (47,48). To determine whether the IRE1β mutation acts early in the sequence of events that lead to chronic colitis, we compared the ICAM-1 staining in DSS treated IRE1β -/-and IRE1β +/-mice.…”

Section: Resultsmentioning

confidence: 99%

Increased sensitivity to dextran sodium sulfate colitis in IRE1β-deficient mice

Bertolotti¹,

Wang²,

Novoa³

et al. 2001

J. Clin. Invest.

377

352

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The epithelial cells of the gastrointestinal tract are exposed to toxins and infectious agents that can adversely affect protein folding in the endoplasmic reticulum (ER) and cause ER stress. The IRE1 genes are implicated in sensing and responding to ER stress signals. We found that epithelial cells of the gastrointestinal tract express IRE1β, a specific isoform of IRE1. BiP protein, a marker of ER stress, was elevated in the colonic mucosa of IRE1β -/-mice, and, when exposed to dextran sodium sulfate (DSS) to induce inflammatory bowel disease, mutant mice developed colitis 3-5 days earlier than did wild-type or IRE1β +/-mice. The inflammation marker ICAM-1 was also expressed earlier in the colonic mucosa of DSS-treated IRE1β -/-mice, indicating that the mutation had its impact early in the inflammatory process, before the onset of mucosal ulceration. These findings are consistent with a model whereby perturbations in ER function, which are normally mitigated by the activity of IRE1β, participate in the development of colitis.

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“…Our results also showed that ICAM-1 expression was increased from 6h to 6 days after a dose of 22.5 Gy irradiation to the colon. Enhancement of ICAM-1 expression has been reported in Crohn's disease 11) , ulcerative colitis 12) , DSS-induced colitis 13) , and trinitrobenzene sulfonic acid (TNBS)-induced colitis 14) . However, some other studies have shown unchanged expression in human IBD and TNBS-induced colitis 31) .…”

Section: Discussionmentioning

confidence: 99%

“…ICAM-1 expression on endothelium plays an important role in migration of activated leukocytes into the sites of inflammation 10) . Increased expression of ICAM-1 in the colon of patients with inflammatory bowel disease (IBD) has been reported [11][12][13][14] . Recent studies have shown that ICAM-1 expression can be induced by ionizing radiation 15,16) .…”

Section: Introductionmentioning

confidence: 99%

Expression of ICAM-1 and Acute Inflammatory Cell Infiltration in the Early Phase of Radiation Colitis in Rats

Ikeda¹,

Ito²,

Matsuu³

et al. 2000

JRR

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Radiation colitis/ICAM-1/Leukocyte/Myeloperoxidase/RatInflammatory cell infiltration of the colon is observed at an early stage of radiation-induced colitis. The emigration of inflammatory cells from the circulation requires interactions between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. To elucidate this process, the present work analyzes the kinetics of the expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of inflammatory myeloperoxidase (MPO)-positive cells in relation to the appearance of acute radiation colitis prior to an overt radiation-induced ulcer. Colon tissues were obtained from Wistar Kyoto rats at various times after 22.5 Gy irradiation to the rectum. Histologically, crypt depletion and numerous inflammatory cells were observed 4 days after irradiation, and mucosal ulcer 6 days after irradiation. ICAM-1 immunopositivity was present in the endothelial cells of small vessels in the mucosa of both control and irradiated rats. ICAM-1 mRNA expression was detected in normal colon and irradiated colon by reverse transcription-PCR. In Northern blotting, ICAM-1 mRNA levels were found to increase markedly in the irradiated colon compared to the normal colon. In Western blotting, ICAM-1 protein expression also increased with a peak one day after irradiation, and remained elevated up to 6 days thereafter. The number of MPO-positive cells in lamina propria mucosa increased in a time-dependent fashion from 6 h to 6 days after irradiation. These data suggest that up-regulation of ICAM-1 in endothelial cells and accumulation of MPO positive cells play important roles in the development of radiation-induced colonic ulcer.

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Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis

Cited by 77 publications

References 34 publications

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Increased sensitivity to dextran sodium sulfate colitis in IRE1β-deficient mice

Expression of ICAM-1 and Acute Inflammatory Cell Infiltration in the Early Phase of Radiation Colitis in Rats

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