Intercellular adhesion molecule-2 (ICAM-2) and Pseudomonas aeruginosa ocular infection.
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.[1]References
- Intercellular adhesion molecule-2 (ICAM-2) and Pseudomonas aeruginosa ocular infection. Hobden, J.A. DNA Cell Biol. (2003) [Pubmed]
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