title: Intercellular adhesion molecule-2 (ICAM-2) and Pseudomonas aeruginosa ocular infection.
abstract: In a previous study, ICAM-1-deficient knockout (KO) mice were able to recruit inflammatory cells into Pseudomonas aeruginosa-infected eyes and resolve the infection as well as wild-type (WT) mice. Based on this observation, it was hypothesized that ICAM-2 could serve as a surrogate receptor for leukocyte recruitment in lieu of ICAM-1. To test this hypothesis, ICAM-2 expression was first examined in both uninfected and P. aeruginosa-infected eyes (6 h postinfection) by immunohistochemistry and RT-PCR. Similar to ICAM-1, ICAM-2 was constitutively expressed on the vascular endothelium of the iris, ciliary body, and conjunctiva of uninfected eyes. Unlike ICAM-1, ICAM-2 was not expressed in the cornea nor upregulated following P. aeruginosa infection. The role of ICAM-2 in P. aeruginosa ocular infection was then addressed through a monoclonal antibody (MAb) blockade of ICAM-2 in infected ICAM-1 KO and WT mice. MAb blockade of ICAM-2 resulted in fewer infiltrating inflammatory cells (as ascertained by histopathology) in the anterior chamber of eyes of ICAM-1-KO and WT mice 24 h postinfection. However, a myeloperoxidase assay of infected corneas showed no statistical difference (P > 0.11) between the two groups in infiltrating PMN. Collectively, these data suggest that constitutively expressed ICAM-2 does play a role in recruiting inflammatory cells into the anterior chamber of the eye during P. aeruginosa infection. Furthermore, inflammatory cell recruitment into the P. aeruginosa-infected cornea appears to be mediated by an ICAM-independent pathway.
authors: Department of Immunology/Microbiology, Wayne State University, School of Medicine, Detroit, Michigan 48201, USA. jhobden@med.wayne.edu
authors: Jeffrey A
authors: JA
authors: Hobden
mesh_terms: D000818:Animals; D019138:Antibodies, Blocking; D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D003315:Cornea / Q000382:microbiology; D003320:Corneal Ulcer / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D015818:Eye Infections, Bacterial / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D005260:Female; D007124:Immunoenzyme Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D011552:Pseudomonas Infections / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D019138:Antibodies, Blocking; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015815:Cell Adhesion Molecules; C065289:ICAM2 protein, human; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1