Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 8, Pages 5579-5586Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.8.5579
Keywords
-
Categories
Funding
- Deutsche Forschungsgemeinschaft [Ku1063/4, Ku1063/5, Ku1063/6, Ta434/2-1]
Ask authors/readers for more resources
CCR2 is thought to recruit monocytes to sites of infection. Two subpopulations of murine blood monocytes differing in Gr1 and CCR2 expression have been described. The exact role of CCR2 in migration of CCR2(low)Gr1(low) and CCR2(high)Gr1(high) monocytes into nonlymphoid tissue is controversial. In this study, we have addressed this question in a murine model of bacterial urinary tract infection. Only Gr1(high) monocytes were recruited into the infected bladder. CCR2 deficiency reduced their frequency in this organ, indicating a requirement of this chemokine receptor. Importantly, CCR2-deficient mice also showed reduced Gr1(high) monocyte numbers in the blood, but not in the bone marrow (BM), indicating that CCR2 acted at the step of monocyte release into the circulation. The same was found also in noninfected mice, indicating a further involvement of CCR2 in steady-state BM egress. An additional requirement of CCR2 in monocyte recruitment from the blood into the bladder was excluded by tracking particle-labeled endogenous monocytes and by adoptive transfer of BM-derived monocyte subsets. These findings demonstrate that CCR2 governs homeostatic and infection-triggered release of Gr1(high) monocytes from the BM into the blood but is dispensable for recruitment into a nonlymphoid tissue.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available