Myeloid differentiation factor-88 (MyD88) is essential for control of primary in vivo Francisella tularensis LVS infection, but not for control of intra-macrophage bacterial replication

Microbes and Infection
Carmen M CollazoKaren L Elkins

Abstract

The means by which Francisella tularensis, the causative agent of tularemia, are recognized by mammalian immune systems are poorly understood. Here we wished to explore the contribution of the MyD88/Toll-like receptor signaling pathway in initiating murine responses to F. tularensis Live Vaccine Strain (LVS). MyD88 knockout (KO) mice, but not TLR2-, TLR4- or TLR9-deficient mice, rapidly succumbed following in vivo bacterial infection via the intradermal route even with a very low dose of LVS (5 x 10(1)) that was 100,000-fold less than the LD(50) of normal wild-type (WT) mice. By day 5 after LVS infection, bacterial organ burdens were 5-6 logs higher in MyD88 knockout mice; further, unlike infected WT mice, levels of interferon-gamma in the sera of LVS-infected MyD88 KO were undetectable. An in vitro culture system was used to assess the ability of bone marrow macrophages derived from either KO or WT mice to support bacterial growth, or to control intracellular bacterial replication when co-cultured with immune lymphocytes. In this assay, bacterial replication was similar in macrophages derived from either WT or any of the TLR KO mice. Bacterial growth was controlled in co-cultures containing macrophages from MyD88 KO mice or TL...Continue Reading

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Citations

Jul 2, 2008·Proceedings of the National Academy of Sciences of the United States of America·Jyothi M KetavarapuBernard P Arulanandam
Mar 27, 2013·Infection and Immunity·Lydia M BarriganJeffrey A Frelinger
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Feb 13, 2008·PLoS Pathogens·Duangjit KanistanonRobert K Ernst
Sep 25, 2008·Future Microbiology·Thomas J Cremer, Susheela Tridandapani
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Sep 25, 2014·Frontiers in Immunology·Lydia M RobertsJeffrey A Frelinger
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Jul 25, 2019·Frontiers in Cellular and Infection Microbiology·Klara Kubelkova, Ales Macela

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