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      Opsonization but not pretreatment of equine macrophages with hyperimmune plasma nonspecifically enhances phagocytosis and intracellular killing of Rhodococcus equi

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          Abstract

          Background

          Evidence regarding the efficacy of equine hyperimmune plasma to prevent pneumonia in foals caused by Rhodococcus equi is limited and conflicting.

          Hypothesis

          Opsonization with R. equi‐specific hyperimmune plasma (HIP) will significantly increase phagocytosis and decrease intracellular replication of R. equi by alveolar macrophages (AMs) compared to normal plasma (NP).

          Animals

          Fifteen adult Quarter Horses were used to collect bronchoalveolar lavage cells.

          Methods

          In the first experiment, AMs from 9 horses were pretreated (incubated) with either HIP, NP, or media only (control) and then infected with nonopsonized R. equi. In a second experiment, AMs from 6 horses were infected with R. equi either opsonized with HIP or opsonized with NP. For both experiments, AMs were lysed at 0 and 48 hours and the number of viable R. equi quantified by culture were compared among groups using linear mixed‐effects modeling with significance set at P < .05.

          Results

          Opsonization with either HIP or NP increased phagocytosis by AMs ( P < .0001) and decreased intracellular survival of organisms in AMs ( P < .0001). Pretreating AMs with either HIP or NP without opsonizing R. equi had no effects on phagocytosis or intracellular replication.

          Conclusions and Clinical Importance

          Opsonizing R. equi with either NP or HIP decreases intracellular survival of organisms in AMs, but the effect does not appear to be enhanced by using HIP. Mechanisms other than effects on AMs must explain any clinical benefits of using HIP over NP to decrease the incidence of R. equi pneumonia in foals.

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          Most cited references 34

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          Rectangular Confidence Regions for the Means of Multivariate Normal Distributions

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            Role of the 85-kilobase plasmid and plasmid-encoded virulence-associated protein A in intracellular survival and virulence of Rhodococcus equi.

            Rhodococcus equi is a facultative intracellular pathogen of macrophages and a cause of pneumonia in young horses (foals) and immunocompromised people. Isolates of R. equi from pneumonic foals typically contain large, 85- or 90-kb plasmids encoding a highly immunogenic virulence-associated protein (VapA). The objective of this study was to determine the role of the 85-kb plasmid and VapA in the intracellular survival and virulence of R. equi. Clinical isolates containing the plasmid and expressing VapA efficiently replicated within mouse macrophages in vitro, while plasmid-cured derivatives of these organisms did not multiply intracellularly. An isolate harboring the large plasmid also replicated in the tissues of experimentally infected mice, whereas its plasmid-cured derivative was rapidly cleared. All foals experimentally infected with a plasmid-containing clinical isolate developed severe bronchopneumonia, whereas the foals infected with its plasmid-cured derivative remained asymptomatic and free of visible lung lesions. By day 14 postinfection, lung bacterial burdens had increased considerably in foals challenged with the plasmid-containing clinical isolate. In contrast, bacteria could no longer be cultured from the lungs of foals challenged with the isogenic plasmid-cured derivative. A recombinant, plasmid-cured derivative expressing wild-type levels of VapA failed to replicate in macrophages and remained avirulent for both mice and foals. These results show that the 85-kb plasmid of R. equi is essential for intracellular replication within macrophages and for development of disease in the native host, the foal. However, expression of VapA alone is not sufficient to restore the virulence phenotype.
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              Antibodies protect against intracellular bacteria by Fc receptor-mediated lysosomal targeting.

              The protective effect of antibodies (Abs) is generally attributed to neutralization or complement activation. Using Legionella pneumophila and Mycobacterium bovis bacillus Calmette-Guérin as a model, we discovered an additional mechanism of Ab-mediated protection effective against intracellular pathogens that normally evade lysosomal fusion. We show that Fc receptor (FcR) engagement by Abs, which can be temporally and spatially separated from bacterial infection, renders the host cell nonpermissive for bacterial replication and targets the pathogens to lysosomes. This process is strictly dependent on kinases involved in FcR signaling but not on host cell protein synthesis or protease activation. Based on these findings, we propose a mechanism whereby Abs and FcR engagement subverts the strategies by which intracellular bacterial pathogens evade lysosomal degradation.
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                Author and article information

                Contributors
                ncohen@tamu.edu
                Journal
                J Vet Intern Med
                J Vet Intern Med
                10.1111/(ISSN)1939-1676
                JVIM
                Journal of Veterinary Internal Medicine
                John Wiley & Sons, Inc. (Hoboken, USA )
                0891-6640
                1939-1676
                16 December 2020
                Jan-Feb 2021
                : 35
                : 1 ( doiID: 10.1111/jvim.v35.1 )
                : 590-596
                Affiliations
                [ 1 ] Department of Large Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station Texas USA
                Author notes
                [* ] Correspondence

                Noah D. Cohen, Department of Large Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 660 Raymond Stotzer Parkway, College Station, TX 77843‐4475.

                Email: ncohen@ 123456tamu.edu

                Article
                JVIM16002
                10.1111/jvim.16002
                7848299
                33326149
                © 2020 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC. on behalf of the American College of Veterinary Internal Medicine.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                Page count
                Figures: 4, Tables: 2, Pages: 7, Words: 4886
                Product
                Funding
                Funded by: Link Equine Research Endowment of Texas A&M University College of Veterinary Medicine Infectious Disease Epidemiology Program
                Categories
                Standard Article
                EQUINE
                Standard Articles
                Immunology
                Custom metadata
                2.0
                January/February 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.7 mode:remove_FC converted:01.02.2021

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