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      Respiratory Barrier as a Safeguard and Regulator of Defense Against Influenza A Virus and Streptococcus pneumoniae


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          The primary function of the respiratory system of gas exchange renders it vulnerable to environmental pathogens that circulate in the air. Physical and cellular barriers of the respiratory tract mucosal surface utilize a variety of strategies to obstruct microbe entry. Physical barrier defenses including the surface fluid replete with antimicrobials, neutralizing immunoglobulins, mucus, and the epithelial cell layer with rapidly beating cilia form a near impenetrable wall that separates the external environment from the internal soft tissue of the host. Resident leukocytes, primarily of the innate immune branch, also maintain airway integrity by constant surveillance and the maintenance of homeostasis through the release of cytokines and growth factors. Unfortunately, pathogens such as influenza virus and Streptococcus pneumoniae require hosts for their replication and dissemination, and prey on the respiratory tract as an ideal environment causing severe damage to the host during their invasion. In this review, we outline the host-pathogen interactions during influenza and post-influenza bacterial pneumonia with a focus on inter- and intra-cellular crosstalk important in pulmonary immune responses.

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          Airway mucus function and dysfunction.

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            Recognition of single-stranded RNA viruses by Toll-like receptor 7.

            Viral infection of mammalian host results in the activation of innate immune responses. Toll-like receptors (TLRs) have been shown to mediate the recognition of many types of pathogens, including viruses. The genomes of viruses possess unique characteristics that are not found in mammalian genomes, such as high CpG content and double-stranded RNA. These genomic nucleic acids serve as molecular signatures associated with viral infections. Here we show that TLR7 recognizes the single-stranded RNA viruses, vesicular stomatitis virus and influenza virus. The recognition of these viruses by plasmacytoid dendritic cells and B cells through TLR7 results in their activation of costimulatory molecules and production of cytokines. Moreover, this recognition required intact endocytic pathways. Mice deficient in either the TLR7 or the TLR adaptor protein MyD88 demonstrated reduced responses to in vivo infection with vesicular stomatitis virus. These results demonstrate microbial ligand recognition by TLR7 and provide insights into the pathways used by the innate immune cells in the recognition of viral pathogens.
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              Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus


                Author and article information

                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                04 February 2020
                : 11
                [1] 1Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center , Memphis, TN, United States
                [2] 2Division of Pulmonology, Allergy-Immunology, and Sleep, College of Medicine, University of Tennessee Health Science Center , Memphis, TN, United States
                [3] 3Le Bonheur Children's Hospital, Children's Foundation Research Institute , Memphis, TN, United States
                [4] 4Division of Critical Care Medicine, College of Medicine, University of Tennessee Health Science Center , Memphis, TN, United States
                Author notes

                Edited by: Nadeem Khan, University of North Dakota, United States

                Reviewed by: Rahul D. Pawar, Stanford University, United States; John F. Alcorn, University of Pittsburgh, United States

                *Correspondence: Amali E. Samarasinghe amali.samarasinghe@ 123456uthsc.edu

                This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Copyright © 2020 LeMessurier, Tiwary, Morin and Samarasinghe.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 14 November 2019
                : 03 January 2020
                Page count
                Figures: 3, Tables: 0, Equations: 0, References: 219, Pages: 15, Words: 13390
                Funded by: National Institutes of Health 10.13039/100000002
                Award ID: NIH R01-AI125481

                co-infection,lung mucosa,epithelial cells,barrier defense,respiratory tract
                co-infection, lung mucosa, epithelial cells, barrier defense, respiratory tract


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