Microbiota regulation of viral infections through interferon signaling

Wirusanti, Nurul I; Baldridge, Megan T.; Harris, Vanessa

doi:10.1016/j.tim.2022.01.007

Cited by 62 publications

(39 citation statements)

References 118 publications

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“…While several hundred ISGs with various known functions have been identified, type I IFN has been primarily studied in its role in antiviral immunity (Schoggins et al, 2011; Schoggins, 2019). Recent work revealed that commensal microbes are involved in maintaining tonic type I IFN necessary to mount an effective antiviral immune response (Abt et al, 2012; Ganal et al, 2012; Yang et al; Bradley et al, 2019; Wirusanti et al, 2022). Apart from the induction of antiviral ISGs, type I IFN can promote dendritic cell (DC) activation and maturation to enhance antigen presentation to prime adaptive (Honda et al, 2003; Simmons et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Commensal bacteria promote type I interferon signaling to maintain immune tolerance

Ayala

Matsuo

Hsü

et al. 2021

Preprint

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Type I interferons (IFN) play essential roles in numerous physiological processes, acting as central coordinators in the host response against pathogens. Upon sensing of microbial ligands, host cells rapidly activate the type I IFN response to prime innate and adaptive immune responses. Recent studies suggest tonic IFN are maintained by commensal microbes and critical in mounting an effective immune response to viral pathogens. Further, emerging developments have extended an immunoregulatory role of type I IFN in the maintenance of immune homeostasis. Yet whether immunomodulatory bacteria from the gut microbiota operate through IFN signaling to promote immune tolerance remains largely unanswered. Here we show that commensal microbes are necessary to maintain type I IFN responses in intestinal tissues. Specifically, Bacteroides fragilis induced type I IFN response in dendritic cells (DCs) and this pathway is necessary for the induction of IL-10-producing Foxp3+ regulatory T cells (Tregs). In addition, we show upregulation of type I IFN related genes in Tregs from mesenteric lymph nodes and colonic lamina propria of mice colonized with B. fragilis. Our findings demonstrate type I interferon signaling plays an important role in microbiota-mediated immune tolerance in the gut.

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Section: Introductionmentioning

confidence: 99%

Commensal bacteria promote type I interferon signaling to maintain immune tolerance

Ayala

Matsuo

Hsü

et al. 2021

Preprint

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“…The commensal gastrointestinal microbiome competitively restricts pathogen survival and proliferation, by metabolizing and consuming nutrients on one side and by producing inhibitory molecules on the other [ 101 ]. The gastrointestinal microbiota coevolved with the host’s immune system and established a delicate balance to maintain homeostasis in the gut [ 108 ]. These microorganisms have a fundamental effect on regulating immune cell development, differentiation and defense against pathogen invasion [ 109 ].…”

Section: The Mechanism Of Sara-mediated Igl and Related Inflammatory ...mentioning

confidence: 99%

The Role of Rumen Microbiota and Its Metabolites in Subacute Ruminal Acidosis (SARA)-Induced Inflammatory Diseases of Ruminants

Xiang

et al. 2022

Microorganisms

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Subacute ruminal acidosis (SARA) is a common metabolic disease in ruminants. In the early stage of SARA, ruminants do not exhibit obvious clinical symptoms. However, SARA often leads to local inflammatory diseases such as laminitis, mastitis, endometritis and hepatitis. The mechanism by which SARA leads to inflammatory diseases is largely unknown. The gut microbiota is the totality of bacteria, viruses and fungi inhabiting the gastrointestinal tract. Studies have found that the gut microbiota is not only crucial to gastrointestinal health but also involved in a variety of disease processes, including metabolic diseases, autoimmune diseases, tumors and inflammatory diseases. Studies have shown that intestinal bacteria and their metabolites can migrate to extraintestinal distal organs, such as the lung, liver and brain, through endogenous pathways, leading to related diseases. Combined with the literature, we believe that the dysbiosis of the rumen microbiota, the destruction of the rumen barrier and the dysbiosis of liver function in the pathogenesis of SARA lead to the entry of rumen bacteria and/or metabolites into the body through blood or lymphatic circulation and place the body in the “chronic low-grade” inflammatory state. Meanwhile, rumen bacteria and/or their metabolites can also migrate to the mammary gland, uterus and other organs, leading to the occurrence of related inflammatory diseases. The aim of this review is to describe the mechanism by which SARA causes inflammatory diseases to obtain a more comprehensive and profound understanding of SARA and its related inflammatory diseases. Meanwhile, it is also of great significance for the joint prevention and control of diseases.

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“…As an effector cytokine at the core of host antiviral immunity, the expression of IFN-β is regulated by the intestinal microbiota [29][30][31]. It is hypothesized that the intestinal microbiota can modulate the IFN-I response in the IBV infection model.…”

Section: Depletion Of Spf Chickens' Intestinal Microbiota Greatly Imp...mentioning

confidence: 99%

Chicken intestinal microbiota modulation of resistance to nephropathogenic infectious bronchitis virus infection through IFN-I

et al. 2022

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Background Mammalian intestinal microbiomes are necessary for antagonizing systemic viral infections. However, very few studies have identified whether poultry commensal bacteria play a crucial role in protecting against systemic viral infections. Nephropathogenic infectious bronchitis virus (IBV) is a pathogenic coronavirus that causes high morbidity and multiorgan infection tropism in chickens. Results In this study, we used broad-spectrum oral antibiotics (ABX) to treat specific pathogen free (SPF) chickens to deplete the microbiota before infection with nephropathogenic IBV to analyze the impact of microbiota on IBV infections in vivo. Depletion of the SPF chicken microbiota increases pathogenicity and viral burden following IBV infection. The gnotobiotic chicken infection model further demonstrated that intestinal microbes are resistant to nephropathogenic IBV infection. In addition, ABX-treated chickens showed a severe reduction in macrophage activation, impaired type I IFN production, and IFN-stimulated gene expression in peripheral blood mononuclear cells and the spleen. Lactobacillus isolated from SPF chickens could restore microbiota-depleted chicken macrophage activation and the IFNAR-dependent type I IFN response to limit IBV infection. Furthermore, exopolysaccharide metabolites of Lactobacillus spp. could induce IFN-β. Conclusions This study revealed the resistance mechanism of SPF chicken intestinal microbiota to nephropathogenic IBV infection, providing new ideas for preventing and controlling nephropathogenic IBV.

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Microbiota regulation of viral infections through interferon signaling

Cited by 62 publications

References 118 publications

Commensal bacteria promote type I interferon signaling to maintain immune tolerance

Commensal bacteria promote type I interferon signaling to maintain immune tolerance

The Role of Rumen Microbiota and Its Metabolites in Subacute Ruminal Acidosis (SARA)-Induced Inflammatory Diseases of Ruminants

Chicken intestinal microbiota modulation of resistance to nephropathogenic infectious bronchitis virus infection through IFN-I

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