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

Major 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. Methods: First, 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. | Chen et al. Journal of Biomedical Science 2010 17 48 http content 17 1 48 a NSC The cost of publication In Journal of Blomodlcal Science Is boms by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Commensal microflora induce host defense and decrease bacterial translocation in burn mice through toll-like receptor 4 Lee-Wei Chen 21 2 Wei-Jung Chang 1 2 Pei-Hsuan Chen2 and Ching-Mei Hsu 23 Abstract Background Major 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. Methods First 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-kB 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 TNFa 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. Results Burn induced BT to MLNs in WT mice. Commensal depletion decreased TLR4 expression as well as NF-kB activation of intestine myeloperoxidase MPO activity as well as TNFa 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 .

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