{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T20:28:48Z","timestamp":1791404928468,"version":"4.3.3"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2001,3,1]],"date-time":"2001-03-01T00:00:00Z","timestamp":983404800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Infiltration of neutrophils and eosinophils into the mammalian cornea can result in loss of corneal clarity and severe visual impairment. To identify mediators of granulocyte recruitment to the corneal stroma, we determined the relative contribution of chemokine receptors CXC chemokine receptor (CXCR)-2 (IL-8R homologue) and CCR1 using a murine model of ocular onchocerciasis (river blindness) in which neutrophils and eosinophils migrate from peripheral vessels to the central cornea. CXCR2\u2212\/\u2212 and CCR1\u2212\/\u2212 mice were immunized s.c. and injected into the corneal stroma with Ags from the parasitic helminth Onchocerca volvulus. We found that production of macrophage-inflammatory protein (MIP)-2, KC, and MIP-1\u03b1 was localized to the corneal stroma, rather than to the epithelium, which was consistent with the location of neutrophils in the cornea. CCR1 deficiency did not inhibit neutrophil or eosinophil infiltration to the cornea or development of corneal opacification. In marked contrast, neutrophil recruitment to the corneas of CXCR2\u2212\/\u2212 mice was significantly impaired (p &amp;lt; 0.0001 compared with control, BALB\/c mice) with only occasional neutrophils detected in the central cornea. Furthermore, CXCR2\u2212\/\u2212 mice developed only mild corneal opacification compared with BALB\/c mice. These differences were not due to impaired KC and MIP-2 production in the corneal stroma of CXCR2\u2212\/\u2212 mice, which was similar to BALB\/c mice. Furthermore, although MIP-1\u03b1 production was lower in CXCR2\u2212\/\u2212 mice than BALB\/c mice, eosinophil recruitment to the cornea was not impaired. These observations demonstrate the critical role for CXCR2 expression in neutrophil infiltration to the cornea and may indicate a target for immune intervention in neutrophil-mediated corneal inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.166.6.4035","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T23:32:32Z","timestamp":1398036752000},"page":"4035-4041","source":"Crossref","is-referenced-by-count":49,"title":["CXC Chemokine Receptor 2 But Not C-C Chemokine Receptor 1 Expression Is Essential for Neutrophil Recruitment to the Cornea in Helminth-Mediated Keratitis (River Blindness)"],"prefix":"10.1093","volume":"166","author":[{"given":"Laurie R","family":"Hall","sequence":"first","affiliation":[{"name":"Departments of Medicine and Ophthalmology, Case Western Reserve University and University Hospitals of Cleveland , Cleveland, OH 44106"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenia","family":"Diaconu","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Ophthalmology, Case Western Reserve University and University Hospitals of Cleveland , Cleveland, OH 44106"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roopa","family":"Patel","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Ophthalmology, Case Western Reserve University and University Hospitals of Cleveland , Cleveland, OH 44106"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Pearlman","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Ophthalmology, Case Western Reserve University and University Hospitals of Cleveland , Cleveland, OH 44106"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,3,15]]},"reference":[{"key":"2025032713593235500_R1","first-page":"903","volume-title":"J. 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