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Karen A. Kernacki, Ronald P. Barrett, Sharon A. McClellan, Linda D. Hazlett; Aging and PMN Response to P. aeruginosa Infection. Invest. Ophthalmol. Vis. Sci. 2000;41(10):3019-3025.
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purpose. Alterations in immune system function associated with aging may
contribute to increased morbidity in this population of individuals.
The current studies were performed to determine aging-related changes
in polymorphonuclear neutrophil (PMN) function after corneal infection
with Pseudomonas aeruginosa.
methods. Total PMN number, macrophage inflammatory protein (MIP)-2 mRNA and
protein expression, and ocular bacterial load were determined in
8-week- and 12-month-old inbred BALB/c mice at various times after
infection with P. aeruginosa. In addition, 12-month-old
mice were treated systemically with the MIP-2 polyclonal antibody (pAb)
to determine the effects of MIP-2 neutralization on ocular disease and
results. Histologically, PMN infiltration into the cornea of 12-month-old mice
was delayed initially and was associated with an inability to reduce
bacterial load at later postinfection (PI) times. In addition, a
significantly greater number of PMNs were found in the cornea of
12-month-old mice at later PI times. The increase in PMN number in
12-month-old mice correlated with a persistence of MIP-2 expression in
cornea at these later times. Systemic treatment of 12-month-old mice
with neutralizing MIP-2 pAb versus normal rabbit serum (NRS) resulted
in reduced corneal PMN number and ocular disease.
conclusions. These data provide evidence that persistence of PMN in the cornea of
12-month-old mice contributes to corneal tissue destruction after P. aeruginosa challenge. Further evidence also is
provided that the chemoattractant MIP-2 contributes to the altered PMN
response in these animals.
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