Pivotal advance: glycyrrhizin restores the impaired production of beta-defensins in tissues surrounding the burn area and improves the resistance of burn mice to Pseudomonas aeruginosa wound infection.
The decreased production of antimicrobial peptides in tissues surrounding the burn sites has been described in patients with severe burn injury. Small numbers of Pseudomonas aeruginosa spread easily to the whole body of burn mice when infected at burn site tissues. Gr-1(+)CD11b(+) cells, demonstrated in tissues surrounding the burn site, are inhibitory on the production of antimicrobial peptides by EK. In this paper, the decreased production of antimicrobial peptides by EK influenced by Gr-1(+)CD11b(+) cells was shown to be restored by glycyrrhizin. CCL2 and IL-10 were determined to be effector soluble factors for the suppressor activities of Gr-1(+)CD11b(+) cells on antimicrobial peptide production by EK. However, Gr-1(+)CD11b(+) cells, which were treated previously with glycyrrhizin, did not produce these soluble factors. Also, sepsis stemming from P. aeruginosa burn-site infection was not demonstrated in burn mice treated with glycyrrhizin. These results suggest that through the improved production of antimicrobial peptides in tissues surrounding the burn area, sepsis stemming from P. aeruginosa wound infection is controllable by glycyrrhizin in severely burned mice.
Yoshida
Tsuyoshi
T
Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, USA.
Yoshida
Shohei
S
Kobayashi
Makiko
M
Herndon
David N
DN
Suzuki
Fujio
F
D000818:Animals; D002056:Burns / Q000150:complications* / Q000382:microbiology; D018932:Chemokine CCL2 / Q000502:physiology; D004353:Drug Evaluation, Preclinical; D024901:Drug Resistance, Multiple, Bacterial; D019695:Glycyrrhizic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D016753:Interleukin-10 / Q000502:physiology; D007378:Interleukins / Q000032:analysis; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011552:Pseudomonas Infections / Q000188:drug therapy / Q000209:etiology / Q000276:immunology / Q000517:prevention & control*; D011550:Pseudomonas aeruginosa / Q000187:drug effects; D016176:T-Lymphocyte Subsets / Q000276:immunology; D014946:Wound Infection / Q000188:drug therapy / Q000209:etiology / Q000382:microbiology / Q000517:prevention & control*; D023083:beta-Defensins / Q000096:biosynthesis* / Q000235:genetics
C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; C120555:Defb1 protein, mouse; D007378:Interleukins; D023083:beta-Defensins; C540070:beta-defensin 3, mouse; D016753:Interleukin-10; D019695:Glycyrrhizic Acid