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      A Proteomic View of the Cross-Talk Between Early Intestinal Microbiota and Poultry Immune System

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          Abstract

          Proteomics has been used to investigate cross-talk between the intestinal microbiome and host biological processes. In this study, an in ovo technique and a proteomics approach was used to address how early bacterial colonization in the gastrointestinal tract (GIT) could modulate inflammatory and immune responses in young broilers. Embryos at 18 embryogenic days were inoculated with saline (S), 10 2 CFU of Citrobacter freundii (CF), Citrobacter species (C2), or lactic acid bacteria mixture (L) into the amnion. At 10 days posthatch, ileum samples from 12 birds per treatment were selected for tandem mass spectrometry analysis. Our further findings indicated that treatment-specific influences on early GIT microbiota resulted in different immune responses in mature broilers. Predicted functional analyses revealed activation of inflammation pathways in broilers treated in ovo with L and CF. Exposure to L enhanced functional annotation related to activation, trafficking of immune cells, and skeletal growth based-network, while CF inhibited biological functions associated with immune cell migration and inflammatory response. These results highlighted that proper immune function was dependent on specific GIT microbiota profiles, in which early-life exposure to L-based probiotic may have modulated the immune functions, whereas neonatal colonization of Enterobacteriaceae strains may have led to immune dysregulation associated with chronic inflammation.

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          Most cited references 30

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          Microbiota-mediated colonization resistance against intestinal pathogens.

          Commensal bacteria inhabit mucosal and epidermal surfaces in mice and humans, and have effects on metabolic and immune pathways in their hosts. Recent studies indicate that the commensal microbiota can be manipulated to prevent and even to cure infections that are caused by pathogenic bacteria, particularly pathogens that are broadly resistant to antibiotics, such as vancomycin-resistant Enterococcus faecium, Gram-negative Enterobacteriaceae and Clostridium difficile. In this Review, we discuss how immune- mediated colonization resistance against antibiotic-resistant intestinal pathogens is influenced by the composition of the commensal microbiota. We also review recent advances characterizing the ability of different commensal bacterial families, genera and species to restore colonization resistance to intestinal pathogens in antibiotic-treated hosts.
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            Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology

            Stress is known to suppress immune function and increase susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate asthma, and allergic, autoimmune and inflammatory diseases, although such diseases should be ameliorated by immunosuppression. Moreover, the short-term fight-or-flight stress response is one of nature’s fundamental defense mechanisms that enables the cardiovascular and musculoskeletal systems to promote survival, and it is unlikely that this response would suppress immune function at a time when it is most required for survival (e.g. in response to wounding and infection by a predator or aggressor). These observations suggest that stress may suppress immune function under some conditions while enhancing it under others. The effects of stress are likely to be beneficial or harmful depending on the type (immunoprotective, immunoregulatory/inhibitory, or immunopathological) of immune response that is affected. Studies have shown that several critical factors influence the direction (enhancing vs. suppressive) of the effects of stress or stress hormones on immune function: (1) Duration (acute vs. chronic) of stress: Acute or short-term stress experienced at the time of immune activation can enhance innate and adaptive immune responses. Chronic or long-term stress can suppress immunity by decreasing immune cell numbers and function and/or increasing active immunosuppressive mechanisms (e.g. regulatory T cells). Chronic stress can also dysregulate immune function by promoting proinflammatory and type-2 cytokine-driven responses. (2) Effects of stress on leukocyte distribution: Compartments that are enriched with immune cells during acute stress show immunoenhancement, while those that are depleted of leukocytes, show immunosuppression. (3) The differential effects of physiologic versus pharmacologic concentrations of glucocorticoids, and the differential effects of endogenous versus synthetic glucocorticoids: Endogenous hormones in physiological concentrations can have immunoenhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immunosuppressive. (4) The timing of stressor or stress hormone exposure relative to the time of activation and time course of the immune response: Immunoenhancement is observed when acute stress is experienced at early stages of immune activation, while immunosuppression may be observed at late stages of the immune response. We propose that it is important to study and, if possible, to clinically harness the immunoenhancing effects of the acute stress response, that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve. In view of the ubiquitous nature of stress and its significant effects on immunoprotection as well as immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside.
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              Targeting HMGB1 in inflammation.

              High mobility group box 1 (HMGB1), a highly conserved, ubiquitous protein present in the nuclei and cytoplasm of nearly all cell types, is a necessary and sufficient mediator of inflammation during sterile and infection-associated responses. Elevated levels of HMGB1 in serum and tissues occur during sterile tissue injury and during infection, and targeting HMGB1 with antibodies or specific antagonists is protective in established preclinical inflammatory disease models including lethal endotoxemia or sepsis, collagen-induced arthritis, and ischemia-reperfusion induced tissue injury. Future advances in this field will stem from understanding the biological basis for the success of targeting HMGB1 to therapeutic improvement in the treatment of inflammation, infection and ischemia-reperfusion induced injury. Copyright 2009. Published by Elsevier B.V.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                13 February 2020
                2020
                : 11
                Affiliations
                1Department of Animal Sciences, The Ohio State University , Columbus, OH, United States
                2Department of Poultry Science, University of Arkansas , Fayetteville, AR, United States
                Author notes

                Edited by: Krystyna Pierzchala-Koziec, University of Agriculture in Krakow, Poland

                Reviewed by: Kent M. Reed, University of Minnesota Twin Cities, United States; Paweł Tomasz Maćkowiak, Poznań University of Life Sciences, Poland; Michael Kogut, Agricultural Research Service, United States Department of Agriculture, United States

                *Correspondence: L. Bielke, bielke.1@ 123456osu.edu

                This article was submitted to Avian Physiology, a section of the journal Frontiers in Physiology

                Article
                10.3389/fphys.2020.00020
                7031415
                Copyright © 2020 Rodrigues, Wilson, Trombetta, Briggs, Duff, Chasser, Bottje and Bielke.

                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.

                Page count
                Figures: 6, Tables: 3, Equations: 0, References: 39, Pages: 13, Words: 0
                Categories
                Physiology
                Original Research

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