The type I interferons (IFNs) have been studied extensively in the context of viral infections, and have now been recognized as influencing the outcome of bacterial infections. The innate immune system possesses numerous receptors, including TLRs, RIG-like and cytosolic receptors to recognize specific molecular patterns of invading pathogens, be they viral or bacterial. Several of these receptors result in the activation of the type I signaling pathway via intracellular recognition of products such as: DNA, RNA, LPS, and peptidoglycan. Type I IFN signaling leads to the activation of inteferons alpha and beta that via the IFNAR receptor and JAK/STAT signaling influence the transcription of hundreds of genes. The receptors that lead to type I IFN signaling can be found on numerous cell types in the airways: epithelial cells, macrophages, and dendritic cells, which all respond to pathogens in unique ways to produce type I IFNs. The effect of type I IFNs on the infection outcome is variable. Type I IFNs can lead to protective as well as sensitizing effects depending upon the bacterial pathogen and the site of infection. Type I IFNs are able to exert their effects through both direct activation of antimicrobial gene products as well as immunomodulation of cell activation and chemotaxis. Bacterial pathogens, both intracellular and extracellular are able to activate the type I IFN response in the airway. Their ability to activate this pathway and the host outcome will be discussed.
All Science Journal Classification (ASJC) codes
- Immunology and Microbiology(all)