{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T10:53:27Z","timestamp":1790333607397,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2003,11,1]],"date-time":"2003-11-01T00:00:00Z","timestamp":1067644800000},"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":[[2003,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Neonatal mice have a delayed CD4-mediated inflammatory response to Pneumocystis carinii (PC) infection in the lungs that corresponds to a delayed TNF-\u03b1 response and a delayed clearance of the organisms compared with adult mice. Since TNF-\u03b1 is known to drive the up-regulation of adhesion molecules, we examined the expression and function of adhesion molecules in the lungs of neonatal mice. The expression of both ICAM-1 and VCAM-1 was significantly lower in the lungs of PC-infected neonatal mice compared with adults. Additionally, migration of neonatal T cells across endothelial cells expressing VCAM-1 and monocyte chemotactic protein-1 was aberrant compared with that in adult T cells, although \u03b14\u03b21 integrin-mediated adhesion of neonatal lymphocytes was comparable to that of adult lymphocytes. Treatment of neonatal mice with exogenous TNF-\u03b1 resulted in increased expression of ICAM-1 and VCAM-1 as well as increased expression of chemokines, resulting in infiltration of CD4+ cells into the lungs. Treatment with exogenous TNF-\u03b1 resulted in a trend (although not statistically significant) toward a reduction of PC organisms from the lungs. These data indicate that neonatal lung endothelial cells do not up-regulate ICAM-1 and VCAM-1 in response to PC infection, probably due to depressed TNF-\u03b1 production. Additionally, neonatal T cells are defective in the ability to migrate across endothelial cells.<\/jats:p>","DOI":"10.4049\/jimmunol.171.9.4700","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:52:48Z","timestamp":1398027168000},"page":"4700-4707","source":"Crossref","is-referenced-by-count":44,"title":["TNF-\u03b1-Dependent ICAM-1- and VCAM-1-Mediated Inflammatory Responses Are Delayed in Neonatal Mice Infected with\n                    <i>Pneumocystis carinii<\/i>"],"prefix":"10.1093","volume":"171","author":[{"given":"Mahboob H","family":"Qureshi","sequence":"first","affiliation":[{"name":"Departments of Microbiology, Immunology, and Molecular Genetics, University of Kentucky , Lexington, KY 40536"},{"name":"Veterans Administration Medical Center , Lexington, KY 40536"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joan","family":"Cook-Mills","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Cincinnati , Cincinnati, OH 45267"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis E","family":"Doherty","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine, University of Kentucky , Lexington, KY 40536"},{"name":"Veterans Administration Medical Center , Lexington, KY 40536"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beth A","family":"Garvy","sequence":"additional","affiliation":[{"name":"Departments of Microbiology, Immunology, and Molecular Genetics, University of Kentucky , Lexington, KY 40536"},{"name":"Departments of Internal Medicine, University of Kentucky , Lexington, KY 40536"},{"name":"Veterans Administration Medical Center , Lexington, KY 40536"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,11,1]]},"reference":[{"key":"2026020210205077000_R1","first-page":"35","volume-title":"Immunol. 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