Murine complement interactions with Pseudomonas aeruginosa and their consequences during pneumonia

Am J Respir Cell Mol Biol. 2003 Oct;29(4):432-8. doi: 10.1165/rcmb.2002-0145OC.


Complement is necessary for defense against lung infection with Pseudomonas aeruginosa in mice. We studied in vitro interactions between complement and P. aeruginosa and in vivo effects of complement depletion to better understand this relationship. In vitro, P. aeruginosa strain UI-18 was resistant to killing by mouse serum. However, C3 opsonized the organism (via the alternative and mannose binding lectin [MBL] pathways), and C5 convertase activity on the bacterial surface was demonstrated. In vivo, compared with normal mice, complement-deficient mice experienced higher mortality and failed to sterilize their bronchoalveolar space within 24 h of inoculation. These changes did not seem to be a result of decreased inflammation because complement-deficient mice had normal neutrophil recruitment, greater lung myeloperoxidase content, and, by 24 h, a 35-fold higher level of the CXC chemokine KC. Lung static pressure-volume curves were abnormal in infected animals but were significantly more so in complement deficient mice. These data indicate that although P. aeruginosa is resistant to serum killing, C3 opsonization and C5 convertase assembly occur on its surface. This interaction in vivo plays a central role in host survival beyond just recruitment and activation of phagocytes and may serve to limit the inflammatory response to and tissue injury resulting from bacterial infection.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Chemokine CXCL1
  • Chemokines / immunology
  • Chemokines, CXC*
  • Chemotactic Factors / immunology
  • Chemotaxis, Leukocyte / immunology
  • Complement C3 / immunology
  • Complement C3 / metabolism
  • Complement C3-C5 Convertases / immunology
  • Complement C3-C5 Convertases / metabolism
  • Complement System Proteins / deficiency*
  • Disease Models, Animal
  • Female
  • Host-Parasite Interactions / immunology
  • Intercellular Signaling Peptides and Proteins / immunology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mortality
  • Peroxidase / immunology
  • Pneumonia / immunology
  • Pneumonia / metabolism
  • Pneumonia, Bacterial / immunology*
  • Pneumonia, Bacterial / physiopathology
  • Pseudomonas Infections / immunology*
  • Pseudomonas Infections / physiopathology
  • Pseudomonas aeruginosa / immunology*
  • Pulmonary Alveoli / immunology
  • Pulmonary Alveoli / microbiology
  • Respiratory Physiological Phenomena


  • Chemokine CXCL1
  • Chemokines
  • Chemokines, CXC
  • Chemotactic Factors
  • Complement C3
  • Cxcl1 protein, mouse
  • Intercellular Signaling Peptides and Proteins
  • Complement System Proteins
  • Peroxidase
  • Complement C3-C5 Convertases