Abstract
Abstract: :
Purpose: In C57BL/6 (B6) mice, interactions between CD4+ T (Th1) type T cells and Langerhans cells, including B7/CD28 costimulation, has been shown to be critical in the inflammatory response resulting in corneal perforation after infection with the opportunistic pathogen Pseudomonas aeruginosa (P. aeruginosa) (Hazlett et al., J. Immunol. 2001;166:1292-1299). However, whether draining cervical lymph nodes (CLN) provide a site of T cell sensitization to bacterial antigen(s) in this model of ocular inflammation remains unknown. The purpose of this study was to determine whether CLN are required for subsequent T cell infiltration into the cornea after ocular bacterial infection. Methods: Submaxillary and superficial cervical lymph nodes were removed bilaterally in B6 mice one day before infection with 1x106 CFU/µl P. aeruginosa topically applied to the scarified cornea. Control mice were similarly treated after sham surgery. Eyes from both groups of mice were enucleated at 3 and 5 days post infection (p.i.) and frozen sections were cut and immunostained with rat anti-mouse monoclonal antibodies against CD4 (clone H129.19) and CD25 (IL-2 receptor α chain specific, clone 7D4). Results: Positive immunostaining for CD4 T cells was detected in the cornea of B6 mice in which submaxillary and superficial CLN had been removed, as well as in sham operated B6 mice. A few positively labeled cells were first detected at 3 days p.i. and an increase in number of positively labeled cells was seen at 5 days after infection in both groups of mice. At the latter time, some of the cells were activated, as evidenced by positive immunostaining for IL-2Ra, p55 (Kwon and Hazlett, J. Immunol. 1997;159:6283-6290). Conclusion: These data provide evidence that the draining submaxillary and/or superficial CLN are not required for subsequent T cell trafficking into the cornea following infection with P. aeruginosa and suggest that T cells enter the cornea after infection from conjunctival vessels and become activated in situ.
Keywords: inflammation • Pseudomonas • bacterial disease