MIP-1alpha regulates CD4+ T cell chemotaxis and indirectly enhances PMN persistence in Pseudomonas aeruginosa corneal infection
| Autor: | K A, Kernacki, R P, Barrett, S, McClellan, L D, Hazlett |
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| Rok vydání: | 2001 |
| Předmět: |
CD4-Positive T-Lymphocytes
Immunity Cellular Mice Inbred BALB C Neutrophils Macrophage Inflammatory Proteins Eye Infections Bacterial Recombinant Proteins Corneal Diseases Mice Inbred C57BL Chemotaxis Leukocyte Leukocyte Count Mice Pseudomonas aeruginosa Animals Pseudomonas Infections Chemokine CCL4 Chemokine CCL3 |
| Zdroj: | Journal of leukocyte biology. 70(6) |
| ISSN: | 0741-5400 |
| Popis: | The role of macrophage inflammatory protein-1alpha (MIP-1alpha) 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-1alpha exacerbated disease and was associated with an increased number of neutrophils (PMNs) in the cornea. Treatment of BALB/c mice with rMIP-1alpha 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-1alpha polyclonal antibody also significantly reduced PMN numbers and pathology. Collectively, evidence is provided that MIP-1alpha directly contributed to CD4+ T cell recruitment and indirectly to PMN persistence in the infected cornea. |
| Databáze: | OpenAIRE |
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