Journal
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
Volume 60, Issue 1, Pages 49-56Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1574-695X.2010.00715.x
Keywords
Chlamydia; CXCL; CXC chemokine receptor-2; mice; inflammation; neutrophil
Categories
Funding
- Public Health Service [AI49354]
- Midwestern University's College Of Health Sciences
- Midwestern University's Chicago College of Osteopathic Medicine
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI049354] Funding Source: NIH RePORTER
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We tested the hypothesis that a specific chemokine receptor, CXC chemokine receptor-2 (CXCR2), mediates acute inflammatory damage during chlamydial urogenital infection, which ultimately leads to the chronic sequelae of hydrosalpinx - a surrogate marker of infertility. Homozygous CXCR2 genetic knockouts (CXCR2-/-), heterozygous littermates (CXCR2+/-) or homozygous wild-type (wt) controls (CXCR2+/+) were infected intravaginally with Chlamydia muridarum. Although no change was observed in the infection in the lower genital tract based on CXCR zygosity, a delay in the ascension of infection into the upper genital tract was seen in CXCR2-/- mice. Significantly elevated peripheral blood neutrophil counts were observed in CXCR2-/- mice when compared with controls. Reduced rates of acute inflammatory indices were observed in the affected tissue, indicating reduced neutrophil extravasation capacity in the absence of CXCR2. Of note was a reduction in the postinfection development of hydrosalpinx that correlated with CXCR2 zygosity, with both CXCR2-/- (13%) and their CXCR2+/- (35%) littermates displaying significantly lower rates of hydrosalpinx formation than the wt CXCR2-sufficient mice (93%). We conclude that CXCR2 ligands are a major chemotactic signal that induces damaging acute inflammation and the resulting chronic pathology during the repair phase of the host response, but are dispensable for the resolution of infection.
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