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Lipopolysaccharide O-antigen promotes persistent murine bacteremia.

Publication ,  Journal Article
Lugo, JZ; Price, S; Miller, JE; Ben-David, I; Merrill, VA; Mancuso, P; Weinberg, JB; Younger, JG
Published in: Shock
February 2007

Bacteremia is a common complication of pneumonia with Klebsiella pneumoniae. In the previous work, we have shown that the lipopolysaccharide (LPS) O-antigen in K. pneumoniae O1:K2 contributes to lethality during pneumonia in part by promoting bacteremia. In the current work, we studied an O-antigen-deficient K. pneumoniae strain to further evaluate this polysaccharide's role in bloodstream infection. Cultured macrophage and murine bacteremia models were studied. In vitro, O-antigen-deficient bacteria, compared with wild-type organisms, were stronger activators of the murine alveolar macrophage cell line MH-S as assessed by nuclear localization of RelA/p65 and by secretion of cytokines and chemokines. O-antigen-deficient Klebsiellae were also more susceptible to killing by murine neutrophils. In vivo, the absence of O-antigen allowed more rapid and complete clearance of bacteria from the bloodstream, liver, and spleen after intravenous injection in mice. Survival was also greater among animals infected with bacteria missing the O-antigen. Gene expression profiling (via reverse transcriptase-polymerase chain reaction of 84 inflammatory mediator complementary DNA) revealed that by 24 h postinfection, the livers and spleens of animals infected with O-antigen-deficient organisms had significantly downregulated cytokine and chemokine expression compared with wild-type infected animals. The O-antigen surface carbohydrate of O1:K2 serotype K. pneumoniae appears to contribute to bacterial virulence by lessening the activation of macrophages, conveying resistance to killing by neutrophils, and by promoting persistent infection in the blood, liver, and spleen after the onset of bacteremia.

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Published In

Shock

DOI

ISSN

1073-2322

Publication Date

February 2007

Volume

27

Issue

2

Start / End Page

186 / 191

Location

United States

Related Subject Headings

  • Time Factors
  • Pneumonia, Bacterial
  • O Antigens
  • Mice
  • Macrophages, Alveolar
  • Klebsiella pneumoniae
  • Klebsiella Infections
  • Gene Expression Regulation
  • Emergency & Critical Care Medicine
  • Disease Models, Animal
 

Citation

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Lugo, J. Z., Price, S., Miller, J. E., Ben-David, I., Merrill, V. A., Mancuso, P., … Younger, J. G. (2007). Lipopolysaccharide O-antigen promotes persistent murine bacteremia. Shock, 27(2), 186–191. https://doi.org/10.1097/01.shk.0000238058.23837.21
Lugo, Joanelle Z., Sarah Price, Julia E. Miller, Itzhak Ben-David, Vija A. Merrill, Peter Mancuso, Jason B. Weinberg, and John G. Younger. “Lipopolysaccharide O-antigen promotes persistent murine bacteremia.Shock 27, no. 2 (February 2007): 186–91. https://doi.org/10.1097/01.shk.0000238058.23837.21.
Lugo JZ, Price S, Miller JE, Ben-David I, Merrill VA, Mancuso P, et al. Lipopolysaccharide O-antigen promotes persistent murine bacteremia. Shock. 2007 Feb;27(2):186–91.
Lugo, Joanelle Z., et al. “Lipopolysaccharide O-antigen promotes persistent murine bacteremia.Shock, vol. 27, no. 2, Feb. 2007, pp. 186–91. Pubmed, doi:10.1097/01.shk.0000238058.23837.21.
Lugo JZ, Price S, Miller JE, Ben-David I, Merrill VA, Mancuso P, Weinberg JB, Younger JG. Lipopolysaccharide O-antigen promotes persistent murine bacteremia. Shock. 2007 Feb;27(2):186–191.

Published In

Shock

DOI

ISSN

1073-2322

Publication Date

February 2007

Volume

27

Issue

2

Start / End Page

186 / 191

Location

United States

Related Subject Headings

  • Time Factors
  • Pneumonia, Bacterial
  • O Antigens
  • Mice
  • Macrophages, Alveolar
  • Klebsiella pneumoniae
  • Klebsiella Infections
  • Gene Expression Regulation
  • Emergency & Critical Care Medicine
  • Disease Models, Animal