Prevention and reversal of experimental colitis by a monoclonal antibody which inhibits leukocyte adherence

Wallace, John L.; Higa, A.; McKnight, G. Webb; MacIntyre, D. Euan

doi:10.1007/bf00917626

Cited by 68 publications

(30 citation statements)

References 29 publications

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“…[41][42][43][44] Few studies have directly examined the role of these molecules during experimental colitis with these reports documenting modification of trinitrobenzene sulfonic acid (TNBS) colitis with anti-CD18 or CD11b/ CD18 antibodies. 45,46 We report here that the b 2 integrin LFA-1 (CD11a/CD18) plays an important pathological role, whereas Mac-1 (CD11b/CD18) provides a critical regulatory role in DSS-induced experimental colitis. Several possible explanations could account for the difference in outcome regarding CD11b.…”

Section: Discussionmentioning

confidence: 99%

Regulation of dextran sodium sulfate induced colitis by leukocyte beta 2 integrins

Abdelbaqi

Chidlow

Matthews

et al. 2006

Laboratory Investigation

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Section: Discussionmentioning

confidence: 99%

Regulation of dextran sodium sulfate induced colitis by leukocyte beta 2 integrins

Abdelbaqi

Chidlow

Matthews

et al. 2006

Laboratory Investigation

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“…The double adhesion molecule deficiency (Pselectin/ICAM-1) followed the same trend. It is intriguing that acute administration of anti-adhesion therapy reduced mucosal dysfunction in TNBS-induced colitis in rabbits, but this was examined over 24 h, not longer [34]. The difference may be related to acute treatment with antibody versus more long-term therapy in these adhesion molecule-deficient animals.…”

Section: Discussionmentioning

confidence: 99%

Intestinal inflammation in adhesion molecule-deficient mice: an assessment of P-selectin alone and in combination with ICAM-1 or E-selectin

McCafferty

Smith

Granger

et al. 1999

Journal of Leukocyte Biology

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Biopsy specimens from patients with inflammatory bowel disease have demonstrated an up-regulation of P-selectin, suggesting a role for P-selectin in intestinal inflammation. We examined the role of P-selectin in experimental intestinal inflammation using mice deficient in P-selectin alone or in combination with either ICAM-1 or E-selectin. Colitis was induced using acetic acid or trinitrobenzene sulfonic acid (TNBS). Damage scores and neutrophil infiltration 24 h post acetic acid were not different between wild-type and P-selectin-or P-selectin/ICAM-1-deficient mice, whereas P/E-selectin-deficient mice had enhanced leukocyte recruitment and damage. At 72 h an attenuation in damage scores and a slight decrease in neutrophil infiltration was observed in the P-and P/ICAM-deficient animals. The P/E-selectin-deficient mice maintained enhanced leukocyte recruitment and damage. In wild-type mice P-selectin expression was elevated 48 and 72 h post acetic acid-induced inflammation. Surprisingly, P-selectin or P-selectin/ICAM-1 deficiency did not improve the inflammation induced by TNBS over 7 days. In fact, increased mortality was observed. Antiadhesion therapy may play only a limited, beneficial role and often a detrimental role in intestinal inflammation. J. Leukoc. Biol. 66: 67-74; 1999.

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“…Conversely, it implies that disruption of these processes could attenuate the inflammatory infiltrate. Indeed, one report has indicated that monoclonal antibodies targeted to CDl 1 / 18 ameliorated inflammation in a rodent model of colonic inflammation induced by an exogenous agent (26).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of colitis in the cotton-top tamarin by anti-alpha 4 integrin monoclonal antibody.

Podolsky¹,

Lobb²,

King³

et al. 1993

J. Clin. Invest.

320

147

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Recent studies have demonstrated the induced expression of endothelial adhesion molecules including E-selectin (also called endothelial leukocyte adhesion molecule-i), vascular cell adhesion molecule and intercellular adhesion molecule in actively involved mucosa of patients with ulcerative colitis and Crohn's disease. Similar induction has been demonstrated in the colon of the Cotton-top tamarin (CTU), a New World primate that experiences a spontaneous acute and chronic colitis resembling ulcerative colitis.To assess the potential importance of leukocyte adhesion as a necessary step in acute colitis, the effect of parenteral mAb directed against adhesion molecules on CIT colitis was evaluated in placebo-controlled blinded trials. Serial administration ofeither of two anti-E-selectin mAb designated BB1 1 and EH8 effectively coated endothelial surfaces expressing this vascular adhesion molecule. Although colitis activity was slightly diminished after the 10-d treatment period in CIT receiving either BB1 1 or EH8, this reduction was not significantly different than that seen in animals given a placebo control when assessed by a previously validated standardized scale of inflammatory activity: mean histologic activity grade 2.2±0.2 pretreatment vs 1.5±0.5 posttreatment in group receiving mAb and 2.1±0.1 pretreatment vs 1.3±0.5 posttreatment in the placebo group (P > 0.2). In contrast, administration of an anti-a4 integrin mAb designated HP1 /2 that binds VLA4 (a4f31) and presumably a4187 integrins resulted in significant attenuation of acute colitis when compared to both pretreatment activity index (P = 0.005) and the placebo control group (P < 0.01 ): mean histologic activity grade 1.6±0.3 pretreatment vs 0.2±0.1 posttreatment in the group receiving HP1 /2 and 1.8±0.5 pretreatment and 1.2±0.2 posttreatment in the placebo control group.These studies using a model of spontaneous colitis in the CMT demonstrate the feasibility of modulation of leukocytevascular adhesion and/or other integrin-mediated events possibly including T cell aggregation and T cell-stromal interactions, as well as lymphocyte homing. These results suggest both that these processes are important and possibly essential elements in sustaining acute colitis and that their disruption may result in therapeutic benefit. (J. Clin. Invest. 1993. 92: Address correspondence to Daniel K. Podolsky, M.D., GI Unit, Jackson 7,

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Prevention and reversal of experimental colitis by a monoclonal antibody which inhibits leukocyte adherence

Cited by 68 publications

References 29 publications

Regulation of dextran sodium sulfate induced colitis by leukocyte beta 2 integrins

Regulation of dextran sodium sulfate induced colitis by leukocyte beta 2 integrins

Intestinal inflammation in adhesion molecule-deficient mice: an assessment of P-selectin alone and in combination with ICAM-1 or E-selectin

Attenuation of colitis in the cotton-top tamarin by anti-alpha 4 integrin monoclonal antibody.

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