Commensal microflora induce host defense and decrease bacterial translocation in burn mice through toll-like receptor 4Reportar como inadecuado




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Journal of Biomedical Science

, 17:48

First Online: 12 June 2010Received: 15 February 2010Accepted: 12 June 2010DOI: 10.1186-1423-0127-17-48

Cite this article as: Chen, LW., Chang, WJ., Chen, PH. et al. J Biomed Sci 2010 17: 48. doi:10.1186-1423-0127-17-48

Abstract

BackgroundMajor burn is associated with decreased gut barrier function and increased bacterial translocation BT. This study is to investigate whether commensal microflora induce host defense and decrease BT in burn mice.

MethodsFirst, we treated Wild type WT mice with antibiotics in drinking water for 4 weeks to deplete gut commensal microflora. At week 3, drinking water was supplemented with lipopolysaccharide LPS; a ligand for TLR4, to trigger TLRs in gut. The intestinal permeability, glutathione level, NF-κB DNA-binding activity, TLR4 expression of intestinal mucosa, BT to mesenteric lymph nodes MLNs, and bacterial killing activity of peritoneal cells were measured after thermal injury. Second, lung of animals were harvested for MPO activity and TNFα mRNA expression assay. Third, WT animals were treated with oral antibiotics with or without LPS supplement after burn. At 48 hr after burn, TLR4 expression of intestinal mucosa and bacterial killing activity of cells were examined. Finally, bacterial killing activity and BT to MLNs after thermal injury in C3H-HeJ TLR4 mutant mice were measured.

ResultsBurn induced BT to MLNs in WT mice. Commensal depletion decreased TLR4 expression as well as NF-κB activation of intestine, myeloperoxidase MPO activity as well as TNFα expression of lung, and bacterial killing activity of peritoneal cells. Oral LPS supplement markedly reduced 81% of burn-induced BT and increased TLR4 expression, MPO activity of lung, as well as bacterial killing activity of peritoneal cells. LPS supplement did not change BT or bacterial killing activity in C3H-HeJ mice.

ConclusionsCollectively, commensal microflora induce TLR4 expression of intestine and bacterial killing activity of inflammatory cells in burn. TLR4 ligand increases bacterial killing activity and decreases burn-induced BT. Taken together with the abolition of LPS effect in TLR4 mutant mice, we conclude that commensal microflora induce host defense and decrease bacterial translocation in burn mice through toll-like receptor 4.

AbbreviationsTLRstoll-like receptors

MLNsmesenteric lymph nodes

LPSlipopolysaccharide

BTbacterial translocation

LTAlipoteichoic acid

TBSAtotal body surface area

FITCfluorescein isothiocyanate

MPOmyeloperoxidase

WTWild type

GSHglutathione

Electronic supplementary materialThe online version of this article doi:10.1186-1423-0127-17-48 contains supplementary material, which is available to authorized users.

Lee-Wei Chen and Ching-Mei Hsu contributed equally to this work.

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Autor: Lee-Wei Chen - Wei-Jung Chang - Pei-Hsuan Chen - Ching-Mei Hsu

Fuente: https://link.springer.com/







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