Abstract
Antimicrobial peptides are major host defense effectors against Pseudomonas aeruginosa skin infections. Due to the lack of such peptide production, severely burned hosts are greatly susceptible to P. aeruginosa burn wound infection. β-Defensin (HBD) production by normal human epidermal keratinocytes (NHEK) was inhibited by lineage−CD34+ cells isolated from peripheral blood of severely burned patients. Lineage−CD34+ cells obtained from severely burned patients were characterized as CD31+, while healthy donor lineage−CD34+ cells were shown to be CD31− cells. Lineage−CD34+CD31− cells did not show any inhibitory activities on HBD-1 production by NHEK. CCL2 and IL-10 released from lineage−CD34+CD31+ cells were shown to be inhibitory on the peptide production by NHEK, while these soluble factors were not produced by lineage−CD34+CD31− cells. After treatment with a mixture of mAbs for CCL2 and IL-10, the culture fluids of lineage−CD34+CD31+ cells did not show any inhibitory activities on HBD-1 production by NHEK. 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.
Highlights
Burn patients are susceptible to various infections [1,2,3]
These results indicate that the lack of antimicrobial peptide production in tissues surrounding the burn sites is a key factor for the development of sepsis caused by P. aeruginosa burn wound infections
1.6 to 1.9 ng/ml of Human b-defensin-1 (HBD-1) were produced by normal human epidermal keratinocytes (NHEK) transwell-cultured with healthy donor lineage2CD34+
Summary
Burn patients are susceptible to various infections [1,2,3]. In these patients, burn wound infections can escalate into sepsis [4]. Topical antimicrobials are effective for controlling the colonization and multiplication of the pathogen on the surface of burn wounds [4]; due to the burn-associated defects of a host’s antimicrobial innate immunity, the small numbers of P. aeruginosa that elude treatment are sufficient to spread systemically [6]. Normal mice treated with anti-murine skin antimicrobial peptide IgG did not resist skin infection with 100 CFU/mouse of P. aeruginosa [17]. These results indicate that the lack of antimicrobial peptide production in tissues surrounding the burn sites is a key factor for the development of sepsis caused by P. aeruginosa burn wound infections
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