Putting on the brakes: Bacterial impediment of wound healing

被引:43
作者
Brothers, Kimberly M. [1 ]
Stella, Nicholas A. [1 ]
Hunt, Kristin M. [1 ]
Romanowski, Eric G. [1 ]
Liu, Xinyu [2 ]
Klarlund, Jes K. [1 ]
Shanks, Robert M. Q. [1 ]
机构
[1] Univ Pittsburgh, Sch Med, Charles T Campbell Ophthalm Microbiol Lab, UPMC Eye Ctr,Ophthalmol & Visual Sci Res Ctr,Dept, Pittsburgh, PA 15260 USA
[2] Univ Pittsburgh, Dept Chem, Pittsburgh, PA 15260 USA
关键词
ORGAN-CULTURE MODEL; PSEUDOMONAS-AERUGINOSA; SERRATIA-MARCESCENS; LIPOPOLYSACCHARIDE; ENDOTOXIN; SURFACE; ACTIVATION; EXPRESSION; EPITHELIUM; VIRULENCE;
D O I
10.1038/srep14003
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
The epithelium provides a crucial barrier to infection, and its integrity requires efficient wound healing. Bacterial cells and secretomes from a subset of tested species of bacteria inhibited human and porcine corneal epithelial cell migration in vitro and ex vivo. Secretomes from 95% of Serratia marcescens, 71% of Pseudomonas aeruginosa, 29% of Staphylococcus aureus strains, and other bacterial species inhibited epithelial cell migration. Migration of human foreskin fibroblasts was also inhibited by S. marcescens secretomes indicating that the effect is not cornea specific. Transposon mutagenesis implicated lipopolysaccharide (LPS) core biosynthetic genes as being required to inhibit corneal epithelial cell migration. LPS depletion of S. marcescens secretomes with polymyxin B agarose rendered secretomes unable to inhibit epithelial cell migration. Purified LPS from S. marcescens, but not from Escherichia coli or S. marcescens strains with mutations in the waaG and waaC genes, inhibited epithelial cell migration in vitro and wound healing ex vivo. Together these data suggest that S. marcescens LPS is sufficient for inhibition of epithelial wound healing. This study presents a novel host-pathogen interaction with implications for infections where bacteria impact wound healing and provides evidence that secreted LPS is a key factor in the inhibitory mechanism.
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页数:14
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