Pasteurella pneumotropica evades the human complement system by acquisition of the complement regulators factor H and C4BP

PLoS One. 2014 Oct 27;9(10):e111194. doi: 10.1371/journal.pone.0111194. eCollection 2014.

Abstract

Pasteurella pneumotropica is an opportunist Gram negative bacterium responsible for rodent pasteurellosis that affects upper respiratory, reproductive and digestive tracts of mammals. In animal care facilities the presence of P. pneumotropica causes severe to lethal infection in immunodeficient mice, being also a potential source for human contamination. Indeed, occupational exposure is one of the main causes of human infection by P. pneumotropica. The clinical presentation of the disease includes subcutaneous abscesses, respiratory tract colonization and systemic infections. Given the ability of P. pneumotropica to fully disseminate in the organism, it is quite relevant to study the role of the complement system to control the infection as well as the possible evasion mechanisms involved in bacterial survival. Here, we show for the first time that P. pneumotropica is able to survive the bactericidal activity of the human complement system. We observed that host regulatory complement C4BP and Factor H bind to the surface of P. pneumotropica, controlling the activation pathways regulating the formation and maintenance of C3-convertases. These results show that P. pneumotropica has evolved mechanisms to evade the human complement system that may increase the efficiency by which this pathogen is able to gain access to and colonize inner tissues where it may cause severe infections.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Complement C3-C5 Convertases / metabolism
  • Complement C4b-Binding Protein / immunology*
  • Complement Factor H / immunology*
  • Humans
  • Pasteurella pneumotropica / immunology*

Substances

  • Complement C4b-Binding Protein
  • Complement Factor H
  • Complement C3-C5 Convertases

Grants and funding

Funding provided by Grant #2010/50043-0, Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP). A.S.R. was supported by a fellowship from the Programa de Apoyos para la Superación del Personal Académico (PASPA-DGAPA) from Universidad Nacional Autónoma de México (UNAM). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.