The arthritis severity quantitative trait locus Cia7 regulates neutrophil migration into inflammatory sites

T. Laragione, M. Brenner, N. C. Yarlett, A. Mello, E. J. Miller, C. N. Metz, B. Sherry, P. S. Gulko

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Neutrophils are required for the development of arthritis in rodents, and are the predominant cell in the synovial fluid of active rheumatoid arthritis. We hypothesized that neutrophil migration into the inflammed joint is genetically regulated. In addition, this genetic regulation would be accounted for by one of the arthritis loci that we have previously identified in an intercross between arthritis-susceptible DA and arthritis-resistant ACI rats studied for collagen-induced arthritis. We used the synovial-like air pouch model injected with carrageenan, and tested DA, ACI, and four congenic strains. ACI exudates had a significantly lower number of neutrophils compared with DA. Transfer of DA alleles at Cia7 into the ACI background, as in ACI.DA(Cia7) congenics, was enough to increase exudate neutrophil numbers to levels identical to DA, and this locus accounted for the difference between parental strains. None of the other congenic intervals explained the differences in exudate neutrophil counts. In conclusion, we have identified a novel function for Cia7, and determined that it regulates neutrophil migration into a synovial-like inflammatory site. Our data revealed no intrinsic defect in neutrophil responses to chemotactic agents, and suggest that Cia7 regulates an as yet unidentified factor central to neutrophil recruitment into inflammed tissues.

Original languageEnglish
Pages (from-to)147-153
Number of pages7
JournalGenes and Immunity
Volume8
Issue number2
DOIs
StatePublished - Mar 2007
Externally publishedYes

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