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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911902/ https://www.ncbi.nlm.nih.gov/pubmed/24498256 http://dx.doi.org/10.1371/journal.pone.0082926 |
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author | Yoshida, Shohei Lee, Jong O. Nakamura, Kiwamu Suzuki, Sumihiro Hendon, David N. Kobayashi, Makiko Suzuki, Fujio |
author_facet | Yoshida, Shohei Lee, Jong O. Nakamura, Kiwamu Suzuki, Sumihiro Hendon, David N. Kobayashi, Makiko Suzuki, Fujio |
author_sort | Yoshida, Shohei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3911902 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-39119022014-02-04 Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes Yoshida, Shohei Lee, Jong O. Nakamura, Kiwamu Suzuki, Sumihiro Hendon, David N. Kobayashi, Makiko Suzuki, Fujio PLoS One Research Article 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. Public Library of Science 2014-02-03 /pmc/articles/PMC3911902/ /pubmed/24498256 http://dx.doi.org/10.1371/journal.pone.0082926 Text en © 2014 Yoshida et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Yoshida, Shohei Lee, Jong O. Nakamura, Kiwamu Suzuki, Sumihiro Hendon, David N. Kobayashi, Makiko Suzuki, Fujio Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes |
title | Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes |
title_full | Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes |
title_fullStr | Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes |
title_full_unstemmed | Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes |
title_short | Lineage(−)CD34(+)CD31(+) Cells That Appear in Association with Severe Burn Injury Are Inhibitory on the Production of Antimicrobial Peptides by Epidermal Keratinocytes |
title_sort | lineage(−)cd34(+)cd31(+) cells that appear in association with severe burn injury are inhibitory on the production of antimicrobial peptides by epidermal keratinocytes |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911902/ https://www.ncbi.nlm.nih.gov/pubmed/24498256 http://dx.doi.org/10.1371/journal.pone.0082926 |
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