Pathogenic mechanisms of P. aeruginosa keratitis: a review of the role of T cells, Langerhans cells, PMN, and cytokines.

Abstract:

:The aim of this article is to review our current understanding of the role of cytokines, chemokines, T cells, Langerhans cells, and neutrophils (PMN) and their interactions in vivo in the host response to Pseudomonas aeruginosa ocular challenge. The cellular/cytokine network in vivo has begun to be unraveled, and the data discussed provide substantive evidence for a regulatory role of CD4(+) T cells (Th1 type) contributing directly to persistence of PMN in the cornea of susceptible C57BL/6 (cornea perforates) versus resistant BALB/c (cornea heals) mice. Additionally, in the susceptible mouse model, CD4(+) T cells interact with Langerhans cells and B7/CD28 ligation appears critical for antigen presentation and the susceptibility response. Various cytokines and chemokines (e.g., MIP-1alpha, IL-1beta, MIP-2, IL-12, and IFN-gamma) and their pattern of sustained upregulation after infection in susceptible versus resistant mice also will be discussed in light of an in vivo cytokine network. T-cell-mediated pathogenic mechanisms are of importance in development of the susceptible response to P. aeruginosa ocular infection. In the absence of T-cell infiltration into the cornea, PMN do not persist in the stroma, and cytokines and chemokines are better balanced, resulting in decreased stromal destruction and the resistance response.

journal_name

DNA Cell Biol

journal_title

DNA and cell biology

authors

Hazlett LD

doi

10.1089/10445490260099665

keywords:

subject

Has Abstract

pub_date

2002-05-01 00:00:00

pages

383-90

issue

5-6

eissn

1044-5498

issn

1557-7430

journal_volume

21

pub_type

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