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Innate immune response to Burkholderia mallei

PURPOSE OF REVIEW: Burkholderia mallei is a facultative intracellular pathogen that causes the highly contagious and often the fatal disease, glanders. With its high rate of infectivity via aerosol and recalcitrance toward antibiotics, this pathogen is considered a potential biological threat agent....

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Autores principales: Saikh, Kamal U., Mott, Tiffany M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407631/
https://www.ncbi.nlm.nih.gov/pubmed/28177960
http://dx.doi.org/10.1097/QCO.0000000000000362
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author Saikh, Kamal U.
Mott, Tiffany M.
author_facet Saikh, Kamal U.
Mott, Tiffany M.
author_sort Saikh, Kamal U.
collection PubMed
description PURPOSE OF REVIEW: Burkholderia mallei is a facultative intracellular pathogen that causes the highly contagious and often the fatal disease, glanders. With its high rate of infectivity via aerosol and recalcitrance toward antibiotics, this pathogen is considered a potential biological threat agent. This review focuses on the most recent literature highlighting host innate immune response to B. mallei. RECENT FINDINGS: Recent studies focused on elucidating host innate immune responses to the novel mechanisms and virulence factors employed by B. mallei for survival. Studies suggest that pathogen proteins manipulate various cellular processes, including host ubiquitination pathways, phagosomal escape, and actin–cytoskeleton rearrangement. Immune-signaling molecules such as Toll-like receptors, nucleotode-binding oligomerization domain, myeloid differentiation primary response protein 88, and proinflammatory cytokines such as interferon-gamma and tumor necrosis factor-α, play key roles in the induction of innate immune responses. Modifications in B. mallei lipopolysaccharide, in particular, the lipid A acyl groups, stimulate immune responses via Toll-like receptor4 activation that may contribute to persistent infection. SUMMARY: Mortality is high because of septicemia and immune pathogenesis with B. mallei exposure. An effective innate immune response is critical to controlling the acute phase of the infection. Both vaccination and therapeutic approaches are necessary for complete protection against B. mallei.
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spelling pubmed-54076312017-05-10 Innate immune response to Burkholderia mallei Saikh, Kamal U. Mott, Tiffany M. Curr Opin Infect Dis PATHOGENESIS AND IMMUNE RESPONSE: Edited by Dennis L. Stevens PURPOSE OF REVIEW: Burkholderia mallei is a facultative intracellular pathogen that causes the highly contagious and often the fatal disease, glanders. With its high rate of infectivity via aerosol and recalcitrance toward antibiotics, this pathogen is considered a potential biological threat agent. This review focuses on the most recent literature highlighting host innate immune response to B. mallei. RECENT FINDINGS: Recent studies focused on elucidating host innate immune responses to the novel mechanisms and virulence factors employed by B. mallei for survival. Studies suggest that pathogen proteins manipulate various cellular processes, including host ubiquitination pathways, phagosomal escape, and actin–cytoskeleton rearrangement. Immune-signaling molecules such as Toll-like receptors, nucleotode-binding oligomerization domain, myeloid differentiation primary response protein 88, and proinflammatory cytokines such as interferon-gamma and tumor necrosis factor-α, play key roles in the induction of innate immune responses. Modifications in B. mallei lipopolysaccharide, in particular, the lipid A acyl groups, stimulate immune responses via Toll-like receptor4 activation that may contribute to persistent infection. SUMMARY: Mortality is high because of septicemia and immune pathogenesis with B. mallei exposure. An effective innate immune response is critical to controlling the acute phase of the infection. Both vaccination and therapeutic approaches are necessary for complete protection against B. mallei. Lippincott Williams & Wilkins 2017-06 2017-04-26 /pmc/articles/PMC5407631/ /pubmed/28177960 http://dx.doi.org/10.1097/QCO.0000000000000362 Text en Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. http://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0
spellingShingle PATHOGENESIS AND IMMUNE RESPONSE: Edited by Dennis L. Stevens
Saikh, Kamal U.
Mott, Tiffany M.
Innate immune response to Burkholderia mallei
title Innate immune response to Burkholderia mallei
title_full Innate immune response to Burkholderia mallei
title_fullStr Innate immune response to Burkholderia mallei
title_full_unstemmed Innate immune response to Burkholderia mallei
title_short Innate immune response to Burkholderia mallei
title_sort innate immune response to burkholderia mallei
topic PATHOGENESIS AND IMMUNE RESPONSE: Edited by Dennis L. Stevens
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407631/
https://www.ncbi.nlm.nih.gov/pubmed/28177960
http://dx.doi.org/10.1097/QCO.0000000000000362
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