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Mitigation of endemic GI-tract pathogen-mediated inflammation through development of multimodal treatment regimen and its impact on SIV acquisition in rhesus macaques.
Bochart, Rachele M; Busman-Sahay, Kathleen; Bondoc, Stephen; Morrow, David W; Ortiz, Alexandra M; Fennessey, Christine M; Fischer, Miranda B; Shiel, Oriene; Swanson, Tonya; Shriver-Munsch, Christine M; Crank, Hugh B; Armantrout, Kimberly M; Barber-Axthelm, Aaron M; Langner, Charlotte; Moats, Cassandra R; Labriola, Caralyn S; MacAllister, Rhonda; Axthelm, Michael K; Brenchley, Jason M; Keele, Brandon F; Estes, Jacob D; Hansen, Scott G; Smedley, Jeremy V.
Afiliación
  • Bochart RM; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Busman-Sahay K; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Bondoc S; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Morrow DW; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Ortiz AM; Barrier Immunity Section, Lab of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United State of America.
  • Fennessey CM; AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America.
  • Fischer MB; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Shiel O; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Swanson T; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Shriver-Munsch CM; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Crank HB; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Armantrout KM; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Barber-Axthelm AM; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Langner C; Barrier Immunity Section, Lab of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United State of America.
  • Moats CR; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Labriola CS; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • MacAllister R; Division of Comparative Medicine, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Axthelm MK; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Brenchley JM; Barrier Immunity Section, Lab of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United State of America.
  • Keele BF; AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America.
  • Estes JD; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Hansen SG; Division of Pathobiology and Immunology, Oregon National Primate Research Center, and Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, United States of America.
  • Smedley JV; Infectious Disease Resource, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America.
PLoS Pathog ; 17(5): e1009565, 2021 05.
Article en En | MEDLINE | ID: mdl-33970966
Here, we assessed the efficacy of a short-course multimodal therapy (enrofloxacin, azithromycin, fenbendazole, and paromomycin) to eliminate common macaque endemic pathogens (EPs) and evaluated its impact on gastrointestinal (GI) microbiota, mucosal integrity, and local and systemic inflammation in sixteen clinically healthy macaques. Treatment combined with expanded practices resulted in successful maintenance of rhesus macaques (RM) free of common EPs, with no evidence of overt microbiota diversity loss or dysbiosis and instead resulted in a more defined luminal microbiota across study subjects. Creation of a GI pathogen free (GPF) status resulted in improved colonic mucosal barrier function (histologically, reduced colonic MPO+, and reduced pan-bacterial 16s rRNA in the MLN), reduced local and systemic innate and adaptive inflammation with reduction of colonic Mx1 and pSTAT1, decreased intermediate (CD14+CD16+) and non-classical monocytes (CD14-CD16+), reduced populations of peripheral dendritic cells, Ki-67+ and CD38+ CD4+ T cells, Ki-67+IgG+, and Ki-67+IgD+ B cells indicating lower levels of background inflammation in the distal descending colon, draining mesenteric lymph nodes, and systemically in peripheral blood, spleen, and axillary lymph nodes. A more controlled rate of viral acquisition resulted when untreated and treated macaques were challenged by low dose intrarectal SIVmac239x, with an ~100 fold increase in dose required to infect 50% (AID50) of the animals receiving treatment compared to untreated controls. Reduction in and increased consistency of number of transmitted founder variants resulting from challenge seen in the proof of concept study directly correlated with post-treatment GPF animal's improved barrier function and reduction of key target cell populations (Ki-67+ CD4+T cells) at the site of viral acquisition in the follow up study. These data demonstrate that a therapeutic and operational strategy can successfully eliminate varying background levels of EPs and their associated aberrant immunomodulatory effects within a captive macaque cohort, leading to a more consistent, better defined and reproducible research model.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Síndrome de Inmunodeficiencia Adquirida del Simio / Virus de la Inmunodeficiencia de los Simios / Microbiota / Inflamación Tipo de estudio: Observational_studies / Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: PLoS Pathog Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Síndrome de Inmunodeficiencia Adquirida del Simio / Virus de la Inmunodeficiencia de los Simios / Microbiota / Inflamación Tipo de estudio: Observational_studies / Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: PLoS Pathog Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos