Blocking both E-Selectin and P-Selectin Inhibits Endotoxin-Induced Leukocyte Infiltration into the Eye

Whitcup, Scott M.; Kozhich, Alexander; Lobanoff, Mark C.; Wolitzky, Barry A.; Chan, Chi‐Chao

doi:10.1006/clin.1996.4324

Cited by 24 publications

(26 citation statements)

References 26 publications

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“…This discrepancy is consistent with the report by Suzuma et al (1997) that anti-P-selectin antibody suppressed leukocyte in®ltration but not protein leakage in EIU eyes. Similar dissociation of leukocyte in®ltration and vascular permeability has been often observed in experiments using anti-E-selectin mAb, antiintracellular adhesion molecule-1 mAb, antileukocyte function antigen-1 mAb, and IL-10 in animal models of uveitis (Whitcup et al, , 1997Hayashi et al, 1996;Kanagawa et al, 1996). The production of PGE2 would be related to the protein leakage into the aqueous humor as Herbort et al (1988) have reported.…”

Section: Discussionsupporting

confidence: 64%

Suppressive Effects of Histamine H1 Receptor Antagonist Diphenhydramine on the Leukocyte Infiltration during Endotoxin-induced Uveitis

Yamashiro

Kiryu

Tsujikawa

et al. 2001

Experimental Eye Research

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Section: Discussionsupporting

confidence: 64%

Suppressive Effects of Histamine H1 Receptor Antagonist Diphenhydramine on the Leukocyte Infiltration during Endotoxin-induced Uveitis

Yamashiro

Kiryu

Tsujikawa

et al. 2001

Experimental Eye Research

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“…12 Monoclonal antibody blocking of several CAMs suppresses intraocular inflammation in animal models of endotoxin-induced uveitis. 13,14 In PDR fibrovascular membranes express ICAM-1 on proliferating vascular endothelial cells, on other infiltrating cells in the membrane, and sometimes within extracellular matrix. The expression of VCAM-1 in diabetic epiretinal membranes is similar to that of ICAM-1, although in some cases its expression appears to be limited to activated endothelial cells of the neovasculature.…”

Section: Introductionmentioning

confidence: 99%

Soluble cellular adhesion molecules in proliferative vitreoretinopathy and proliferative diabetic retinopathy

Barile

Chang

Park

et al. 1999

Current Eye Research

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Soluble forms of ICAM-1 and VCAM-1 are increased in the vitreous cavity of patients with RD due to PDR or PVR, reflecting the inflammatory nature of these conditions and suggesting a possible role for these mediators in the pathogenesis of proliferative retinal disease. The vitreous levels of these sCAMs at the time of surgery may serve as a marker of inflammation, but their specific levels do not predict the likelihood of recurrent proliferation or surgical anatomic success in most cases of PVR and PDR.

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“…In the endotoxin-induced model of uveitis (EIU) (17,18), adhesion molecules critically contribute to the inflammatory outcome. Pand E-selectin (19,20), ␤ 2 -integrins (21,22), ICAM-1 (23,24), VCAM-1, and VLA-4 (25) play distinct roles in the ocular inflammatory responses to endotoxin. Pselectin blockade results in only a partial reduction of leukocyte infiltration into the vitreous of EIU animals, whereas blockade of both P-and E-selectin causes additional reduction (20).…”

mentioning

confidence: 99%

“…Pand E-selectin (19,20), ␤ 2 -integrins (21,22), ICAM-1 (23,24), VCAM-1, and VLA-4 (25) play distinct roles in the ocular inflammatory responses to endotoxin. Pselectin blockade results in only a partial reduction of leukocyte infiltration into the vitreous of EIU animals, whereas blockade of both P-and E-selectin causes additional reduction (20). Similarly, blockade of all selectins with sialyl Lewis X, a tetrasaccharide expressed on cell surface molecules, reduces leukocyte infiltration into the aqueous humor of EIU animals more than P-selectin blockade alone (19).…”

mentioning

confidence: 99%

Surprising up‐regulation of P‐selectin glycoprotein ligand‐1 (PSGL‐1) in endotoxin‐induced uveitis

Almulki¹,

Noda²,

Amini³

et al. 2008

FASEB j.

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P-selectin glycoprotein ligand-1 (PSGL-1) is constitutively expressed on leukocytes and was thought to be down-regulated with cell activation. However, this work shows the surprising finding of functional PSGL-1 up-regulation during acute inflammation. PSGL-1 function was studied in our autoperfusion assay, in which blood from a mouse carotid flows through a microchamber coated with a fixed density of P-selectin. Under the inflammatory conditions--uveitis induced by systemic lipopolysaccharide injection--we recorded significantly reduced leukocyte rolling velocity, which suggests PSGL-1 up-regulation; however, flow cytometry showed reduced PSGL-1. When bound leukocytes were released from the vasculature by PSGL-1 blockade, a large peripheral blood leukocyte (PBL) population showed elevated PSGL-1, which could account for the reduced PSGL-1 in the remaining unbound population. In the eye, systemic blockade of PSGL-1 with a monoclonal antibody or recombinant soluble PSGL-1 drastically reduced the severe manifestations of uveitis. Furthermore, PSGL-1 blockade was significantly more effective in reducing retinal leukostasis than was P-selectin blockade. Our results provide surprising evidence for functional PSGL-1 up-regulation in PBLs during acute inflammation. The temporal overlap between PSGL-1 and P-selectin up-regulation reveals an as yet unrecognized collaboration between this receptor-ligand pair, increasing efficiency of the first steps of the leukocyte recruitment cascade.

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Blocking both E-Selectin and P-Selectin Inhibits Endotoxin-Induced Leukocyte Infiltration into the Eye

Cited by 24 publications

References 26 publications

Suppressive Effects of Histamine H1 Receptor Antagonist Diphenhydramine on the Leukocyte Infiltration during Endotoxin-induced Uveitis

Suppressive Effects of Histamine H1 Receptor Antagonist Diphenhydramine on the Leukocyte Infiltration during Endotoxin-induced Uveitis

Soluble cellular adhesion molecules in proliferative vitreoretinopathy and proliferative diabetic retinopathy

Surprising up‐regulation of P‐selectin glycoprotein ligand‐1 (PSGL‐1) in endotoxin‐induced uveitis

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