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      Influenza A virus infection impacts systemic microbiota dynamics and causes quantitative enteric dysbiosis.

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          Abstract

          Microbiota integrity is essential for a growing number of physiological processes. Consequently, disruption of microbiota homeostasis correlates with a variety of pathological states. Importantly, commensal microbiota provide a shield against invading bacterial pathogens, probably by direct competition. The impact of viral infections on host microbiota composition and dynamics is poorly understood. Influenza A viruses (IAV) are common respiratory pathogens causing acute infections. Here, we show dynamic changes in respiratory and intestinal microbiota over the course of a sublethal IAV infection in a mouse model.

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          Microbiota regulates immune defense against respiratory tract influenza A virus infection.

          Takeshi Ichinohe, Iris K Pang, Yosuke Kumamoto … (2011)
          Although commensal bacteria are crucial in maintaining immune homeostasis of the intestine, the role of commensal bacteria in immune responses at other mucosal surfaces remains less clear. Here, we show that commensal microbiota composition critically regulates the generation of virus-specific CD4 and CD8 T cells and antibody responses following respiratory influenza virus infection. By using various antibiotic treatments, we found that neomycin-sensitive bacteria are associated with the induction of productive immune responses in the lung. Local or distal injection of Toll-like receptor (TLR) ligands could rescue the immune impairment in the antibiotic-treated mice. Intact microbiota provided signals leading to the expression of mRNA for pro-IL-1β and pro-IL-18 at steady state. Following influenza virus infection, inflammasome activation led to migration of dendritic cells (DCs) from the lung to the draining lymph node and T-cell priming. Our results reveal the importance of commensal microbiota in regulating immunity in the respiratory mucosa through the proper activation of inflammasomes.
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            Paneth cells, antimicrobial peptides and maintenance of intestinal homeostasis.

            Charles Bevins, Nita Salzman (2011)
            Building and maintaining a homeostatic relationship between a host and its colonizing microbiota entails ongoing complex interactions between the host and the microorganisms. The mucosal immune system, including epithelial cells, plays an essential part in negotiating this equilibrium. Paneth cells (specialized cells in the epithelium of the small intestine) are an important source of antimicrobial peptides in the intestine. These cells have become the focus of investigations that explore the mechanisms of host-microorganism homeostasis in the small intestine and its collapse in the processes of infection and chronic inflammation. In this Review, we provide an overview of the intestinal microbiota and describe the cell biology of Paneth cells, emphasizing the composition of their secretions and the roles of these cells in intestinal host defence and homeostasis. We also highlight the implications of Paneth cell dysfunction in susceptibility to chronic inflammatory bowel disease.
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              The co-pathogenesis of influenza viruses with bacteria in the lung.

              Jonathan A. McCullers (2014)
              Concern that a highly pathogenic virus might cause the next influenza pandemic has spurred recent research into influenza and its complications. Bacterial superinfection in the lungs of people suffering from influenza is a key element that promotes severe disease and mortality. This co-pathogenesis is characterized by complex interactions between co-infecting pathogens and the host, leading to the disruption of physical barriers, dysregulation of immune responses and delays in a return to homeostasis. The net effect of this cascade can be the outgrowth of the pathogens, immune-mediated pathology and increased morbidity. In this Review, advances in our understanding of the underlying mechanisms are discussed, and the key questions that will drive the field forwards are articulated.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Microbiome
                Title: Microbiome
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 2049-2618
                ISSN (Print): 2049-2618
                Publication date (Electronic): Jan 10 2018
                Volume: 6
                Issue: 1
                Affiliations
                [1 ] Department of Microbiology and Molecular Medicine, University Medical Center (CMU), University of Geneva, Rue Michel-Servet 1, CH-1211, Geneva, Switzerland.
                [2 ] Department of Microbiology, University of Chicago, Chicago, IL, 60637, USA.
                [3 ] Department of Microbiology and Molecular Medicine, University Medical Center (CMU), University of Geneva, Rue Michel-Servet 1, CH-1211, Geneva, Switzerland. mirco.schmolke@unige.ch.
                Article
                Publisher Item ID: 10.1186/s40168-017-0386-z
                DOI: 10.1186/s40168-017-0386-z
                PMC ID: 5763955
                PubMed ID: 29321057
                SO-VID: 4ccd22f8-fe4a-4b65-a9cd-0a50874f6b9d
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