Impact of Type I Interferons on Susceptibility to Bacterial Pathogens

Peignier, Adeline; Parker, Dane

doi:10.1016/j.tim.2021.01.007

Cited by 29 publications

(31 citation statements)

References 103 publications

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“…Five different types of PRR can sense bacterial patterns, including TLRs, RLRs, NODlike receptors (NLRs), DNA sensors, and AIM2-like receptors (ALRs). These bacterial PRRs are involved mainly in the induction of antibacterial signaling pathways, but a subset of these PRRs also induce IFN production during bacterial infection [40,41]. [18] (left panel).…”

Section: Open Accessmentioning

confidence: 99%

Microbiota regulation of viral infections through interferon signaling

Wirusanti

Baldridge

Harris

2022

Trends in Microbiology

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Section: Open Accessmentioning

confidence: 99%

Microbiota regulation of viral infections through interferon signaling

Wirusanti

Baldridge

Harris

2022

Trends in Microbiology

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“…It will be interesting in future studies to determine whether TPL-2 suppression of type I IFNs is required for efficient innate immune responses to S. Typhimurium. In addition, it will be important to evaluate the role of TPL-2 in innate immune responses to pathogenic bacteria that are dependent on type I IFN signaling, such as Helicobacter pylori and Streptococcus pneumoniae (71).…”

Section: Discussionmentioning

confidence: 99%

TPL-2 Inhibits IFN-β Expression via an ERK1/2-TCF-FOS Axis in TLR4-Stimulated Macrophages

Blair

Pattison

Chakravarty

et al. 2022

The Journal of Immunology

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TPL-2 kinase plays an important role in innate immunity, activating ERK1/2 MAPKs in myeloid cells following TLR stimulation. We investigated how TPL-2 controls transcription in TLR4-stimulated mouse macrophages. TPL-2 activation of ERK1/2 regulated expression of genes encoding transcription factors, cytokines, chemokines, and signaling regulators. Bioinformatics analysis of gene clusters most rapidly induced by TPL-2 suggested that their transcription was mediated by the ternary complex factor (TCF) and FOS transcription factor families. Consistently, TPL-2 induced ERK1/2 phosphorylation of the ELK1 TCF and the expression of TCF target genes. Furthermore, transcriptomic analysis of TCF-deficient macrophages demonstrated that TCFs mediate approximately half of the transcriptional output of TPL-2 signaling, partially via induced expression of secondary transcription factors. TPL-2 signaling and TCFs were required for maximal TLR4-induced FOS expression. Comparative analysis of the transcriptome of TLR4-stimulated Fos−/− macrophages indicated that TPL-2 regulated a significant fraction of genes by controlling FOS expression levels. A key function of this ERK1/2-TCF-FOS pathway was to mediate TPL-2 suppression of type I IFN signaling, which is essential for host resistance against intracellular bacterial infection.

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“…Type I interferons (IFN-I) such us IFNb and IFNa play a critical role during MABC infection (Ruangkiattikul et al, 2019). Activation of toll-like receptors (TLR), specifically TLR2 and TLR4 results in MyD88/TRIF/IRF3 dependent IFN-I induction (Ruangkiattikul et al, 2019;Peignier and Parker, 2021). IFN-I production in infected macrophages activates inducible nitric oxide synthase (NOS2) and nitric oxide (NO) production which can kill or induce dormancy.…”

Section: Immune Response Virulence and Genomic Featuresmentioning

confidence: 99%

Mycobacterium abscessus complex: A Review of Recent Developments in an Emerging Pathogen

Victoria

Gupta

Gómez

et al. 2021

Front. Cell. Infect. Microbiol.

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Mycobacterium abscessus complex (MABC) is one of the most clinically relevant species among nontuberculous mycobacteria. MABC’s prevalence has increased over the last two decades. Although these changes can be explained by improvements in microbiological and molecular techniques for identifying species and subspecies, a higher prevalence of chronic lung diseases may contribute to higher rates of MABC. High rates of antimicrobial resistance are seen in MABC, and patients experience multiple relapses with low cure rates. This review aims to integrate existing knowledge about MABC epidemiology, microbiological identification and familiarize readers with molecular mechanisms of resistance and therapeutic options for pulmonary infections with MABC.

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Impact of Type I Interferons on Susceptibility to Bacterial Pathogens

Cited by 29 publications

References 103 publications

Microbiota regulation of viral infections through interferon signaling

Microbiota regulation of viral infections through interferon signaling

TPL-2 Inhibits IFN-β Expression via an ERK1/2-TCF-FOS Axis in TLR4-Stimulated Macrophages

Mycobacterium abscessus complex: A Review of Recent Developments in an Emerging Pathogen

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