4.5 Article

The effect of loss of O-antigen ligase on phagocytic susceptibility of motile and non-motile Pseudomonas aeruginosa

期刊

MOLECULAR IMMUNOLOGY
卷 92, 期 -, 页码 106-115

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2017.10.015

关键词

Pseudomonas aeruginosa; Phagocytosis; WaaL; O-antigen; O-antigen ligase

资金

  1. National Institutes of Health (NIH) [P30 RRO 32136-01, P30 GM106394, R21 AI121820]
  2. Cystic Fibrosis Foundation Research Development Program [STANT019R0, STANT011R0]
  3. NIH [R01 A1103003]
  4. Canadian Institutes of Health Research [MOP-14687]
  5. Canadian Foundation of Innovation

向作者/读者索取更多资源

The bacterial pathogen Pseudomonas aeruginosa undergoes adaptation and selection over the course of chronic respiratory tract infections which results in repeatedly-observed phenotypic changes that are proposed to enable its persistence. Two of the clinically significant P. aeruginosa phenotypic changes are loss of flagellar motility and modifications to LPS structure, including loss of O-antigen expression. The effect of loss of O-antigen, frequently described as conversion from smooth to rough LPS, and the combined effect of loss of motility and O-antigen on phagocytic susceptibility by immune cells remain unknown. To address this, we generated genetic deletion mutants of waaL, which encodes the O-antigen ligase responsible for linking O-antigen to lipid A-core oligosaccharide, in both motile and non-motile P. aeruginosa strains. With the use of these bacterial strains we provide the first demonstration that, despite a progressive selection for P. aeruginosa with rough LPS during chronic pulmonary infections, loss of the LPS O-antigen does not confer phagocytic resistance in vitro. However, use of the waaLmotABmotCD mutant revealed that loss of motility confers resistance to phagocytosis regardless of the smooth or rough LPS phenotype. These findings reveal how the O-antigen of P. aeruginosa can influence bacterial clearance during infection and expand our current knowledge about the impact of bacterial phenotypic changes during chronic infection.

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