Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28529959
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Getting "Inside" Type I IFNs: Type I IFNs in Intracellular Bacterial Infections
#MMPMID28529959
Snyder DT
; Hedges JF
; Jutila MA
J Immunol Res
2017[]; 2017
(?): 9361802
PMID28529959
show ga
Type I interferons represent a unique and complex group of cytokines, serving
many purposes during innate and adaptive immunity. Discovered in the context of
viral infections, type I IFNs are now known to have myriad effects in infectious
and autoimmune disease settings. Type I IFN signaling during bacterial infections
is dependent on many factors including whether the infecting bacterium is
intracellular or extracellular, as different signaling pathways are activated. As
such, the repercussions of type I IFN induction can positively or negatively
impact the disease outcome. This review focuses on type I IFN induction and
downstream consequences during infection with the following intracellular
bacteria: Chlamydia trachomatis, Listeria monocytogenes, Mycobacterium
tuberculosis, Salmonella enterica serovar Typhimurium, Francisella tularensis,
Brucella abortus, Legionella pneumophila, and Coxiella burnetii. Intracellular
bacterial infections are unique because the bacteria must avoid, circumvent, and
even co-opt microbial "sensing" mechanisms in order to reside and replicate
within a host cell. Furthermore, life inside a host cell makes intracellular
bacteria more difficult to target with antibiotics. Because type I IFNs are
important immune effectors, modulating this pathway may improve disease outcomes.
But first, it is critical to understand the context-dependent effects of the type
I IFN pathway in intracellular bacterial infections.
free
free
free
