regulates CD4+ T cell chemotaxis and indirectly enhances PMN persistence in Pseudomonas aeruginosa corneal infection
Department of Anatomy/Cell Biology, Wayne State University, Detroit, Michigan
Correspondence: Linda D. Hazlett, Ph.D., Wayne State University School of Medicine, Department of Anatomy/Cell Biology, 540 E. Canfield Avenue, Detroit, MI 48201. E-mail: lhazlett{at}med.wayne.edu
The role of macrophage inflammatory protein-1
(MIP-1) in cell
infiltration into Pseudomonas aeruginosa-infected cornea
and subsequent disease was examined. Greater amounts of the chemokine
(protein and mRNA) were found in the infected cornea of susceptible B6
("cornea perforates") versus resistant BALB/c ("cornea heals")
mice from 1 to 5 days postinfection. Treatment of BALB/c mice with
recombinant (r) MIP-1 exacerbated disease and was associated with an
increased number of neutrophils (PMNs) in the cornea. Treatment of
BALB/c mice with rMIP-1 also induced recruitment of activated
CD4+ T cells into the affected cornea, converting resistant
to susceptible mice. Depleting CD4+ T cells in r-treated
BALB/c mice significantly decreased PMNs in cornea tissue, suggesting
that T cells regulate persistence of PMNs at this site. In B6 mice,
administration of neutralizing MIP-1 polyclonal antibody
also significantly reduced PMN numbers and pathology. Collectively,
evidence is provided that MIP-1 directly contributed to
CD4+ T cell recruitment and indirectly to PMN persistence
in the infected cornea.
Key Words: immunity • bacterial infection • chemokines • neutrophils
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