CCL1 released from M2b macrophages is essentially required for the maintenance of their properties.

Patients with 10-30 days postburn injury are greatly susceptible to infections. M1M (IL-10(-)IL-12(+) M) are essential cells in host antibacterial innate immunity against MRSA infections. However, these effector cells are not easily generated in hosts who are carriers of M2bM (IL-12(-)IL-10(+)CCL1(+)LIGHT(+) M). M2bM are inhibitory on M1M generation. In this study, the antibacterial resistance of mice, 10-30 days postburn injury against MRSA infection, was improved by the modulation of M2bM activities. Unburned mice inoculated with M preparations from mice, 10-30 days after burn injury, were susceptible to MRSA infection, whereas unburned mice, inoculated with M preparations from the same mice that were previously treated with CCL1 antisense ODN, were resistant to the infection. M2bM, isolated from Day 15 burn mice, lost their M2bM properties 3 days after cultivation under frequent medium changes, whereas their M2bM properties remained in the same cultures supplemented with rCCL1. In cultures, M preparations from Day 15 burn mice treated with CCL1 antisense ODN did not produce CCL1 and did convert to M1M after heat-killed MRSA stimulation. Also, Day 15 burn mice treated with the ODN became resistant against MRSA infection. These results indicate that CCL1 released from M2bM is essentially required for the maintenance of their properties. The increased susceptibility of mice, 10-30 days after burn injury to MRSA infection, may be controlled through the intervention of CCL1 production by M2bM appearing in association with severe burn injuries.