Kiwamu Nakamura

TL;DR: The increased susceptibility of mice, 10–30 days after burn injury to MRSA infection, may be controlled through the intervention of CCL1 production by M2bMΦ appearing in association with severe burn injuries.

TL;DR: Results indicate that ORM1 stimulates quiescent monocytes to polarize to M2b monocytes, which may be beneficial in controlling opportunistic infections in patients with a large amount of plasma OrM1.

TL;DR: Results indicate that M2bMϕ presented in the I-MLNMϕ populations were responsible for the impaired resistance of mice irradiated with gamma-rays to bacterial translocation and subsequent sepsis.

TL;DR: The results indicate that sepsis stemming from pseudomonal grafted site infections in a chimera model of burn injury is controllable by glycyrrhizin, and impaired antimicrobial peptide production at the infection site of severely burned patients may be restored after treatment with glycyRrhiz in.

TL;DR: Lineage−CD34+CD31+ cells that appear in association with burn injuries play a role on the inhibition of antimicrobial peptide production by skin keratinocytes through the production of CCL2 and IL-10.