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Contribution of Interferon Signaling to Host Defense Against Pseudomonas aeruginosa

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Bacterial Activation of Type I Interferons

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Summary

The opportunistic pathogen Pseudomonas aeruginosa is a common cause of infection in immunocompromised individuals, and often associated with hospital acquired pneumonias. P. aeruginosa activates type I interferon (IFN) signaling through the release of lipopolysaccharide (LPS) from the bacterial surface. Interaction between LPS and the host receptor TLR4 initiates type I IFN through the adaptor proteins TRIF and IRF3. The role of type I IFN signaling during infection is unclear at best; however, defective type I IFN signaling has been linked to the chronic respiratory infections observed in cystic fibrosis patients. This chapter will discuss how type I IFN in activated by P. aeruginosa, the current data describing its contribution to host defense, and the potential contributions of other IFN pathways in the response to this pathogen.

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Authors and Affiliations

  1. Department of Pediatrics, Columbia University, 650 W 168th Street, New York, NY, 10032, USA

    Taylor S. Cohen & Alice Prince

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  1. Taylor S. Cohen
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  2. Alice Prince
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Correspondence to Alice Prince .

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Editors and Affiliations

  1. Columbia University, New York, New York, USA

    Dane Parker

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© 2014 Springer International Publishing Switzerland

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Cohen, T.S., Prince, A. (2014). Contribution of Interferon Signaling to Host Defense Against Pseudomonas aeruginosa . In: Parker, D. (eds) Bacterial Activation of Type I Interferons. Springer, Cham. https://doi.org/10.1007/978-3-319-09498-4_6

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