Lineage -CD34+CD31+ cells that appear in association with severe burn injury are inhibitory on the production of antimicrobial peptides by epidermal keratinocytes.
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.
Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, United States of America.
Shohei
S
Yoshida
Shriners Hospital for Children, Galveston, Texas, United States of America.
Jong O
JO
Lee
Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, United States of America.
Kiwamu
K
Nakamura
Department of Biostatistics, University of North Texas Health Science Center, Fort Worth, Texas, United States of America.
Sumihiro
S
Suzuki
Shriners Hospital for Children, Galveston, Texas, United States of America.
David N
DN
Hendon
Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, United States of America ; Shriners Hospital for Children, Galveston, Texas, United States of America.
Makiko
M
Kobayashi
Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, United States of America ; Shriners Hospital for Children, Galveston, Texas, United States of America.
Fujio
F
Suzuki
D000293:Adolescent; D000328:Adult; D018952:Antigens, CD34 / Q000276:immunology / Q000378:metabolism; D002056:Burns / Q000097:blood / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000276:immunology / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D018920:Coculture Techniques; D005260:Female; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D016753:Interleukin-10 / Q000276:immunology / Q000378:metabolism; D015603:Keratinocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000276:immunology / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D023083:beta-Defensins / Q000235:genetics / Q000276:immunology* / Q000378:metabolism
D018952:Antigens, CD34; D018932:Chemokine CCL2; C406407:DEFB1 protein, human; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D023083:beta-Defensins; D016753:Interleukin-10