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Biology subjects

Banks, D. A.

Publications and source records attributed to Banks, D. A..

2 recordsLinked to original sources

Legionella pneumophila inhibits type I interferon signaling to avoid cell-intrinsic host cell defense.

The host type I interferon (IFN) response protects against Legionella pneumophila infections. Other bacterial pathogens inhibit type I IFN-mediated cell signaling; however, the interaction between this signaling pathway and L. pneumophila has not been well described. Here, we demonstrate that L. pneumophila inhibits the IFN-{beta} signaling pathway but does not inhibit IFN-{psi}-mediated cell signaling. The addition of IFN-{beta} to L. pneumophila-infected macrophages limited bacterial growth independently of NOS2 and reactive nitrogen species. The type IV secretion system of L. pneumophila is required to inhibit IFN-{beta}-mediated cell signaling. Finally, we show that the inhibition of the IFN-{beta} signaling pathway occurs downstream of STAT1 and STAT2 phosphorylation. In conclusion, our findings describe a novel host cell signaling pathway inhibited by L. pneumophila via its type IV secretion system.

microbiology↗

Mycobacterium tuberculosis inhibits autocrine type I interferon signaling to increase intracellular survival.

The type I interferons (IFN- and -{beta}) are important for host defense against viral infections. In contrast, their role in defense against non-viral pathogens is more ambiguous. Here we report that IFN-{beta}-signaling in macrophages has protective capacity against Mycobacterium tuberculosis (Mtb) via the increased production of nitric oxide. Furthermore, Mtb is able to inhibit IFN-/{beta}-receptor-mediated cell signaling and the transcription of 309 IFN-{beta} stimulated genes which includes genes associated with innate host cell defense. The molecular mechanism of inhibition by Mtb involves reduced phosphorylation of the IFNAR-associated protein kinases JAK1 and TYK2 leading to reduced phosphorylation of the downstream targets STAT1 and STAT2. Overall, our study supports the novel concept that Mtb evolved to inhibit autocrine type I IFN signaling in order to evade host defense mechanisms.

microbiology↗