Prolonged survival of scavenger receptor class A-deficient mice from pulmonary Mycobacterium tuberculosis infection

Zvjezdana Sever-Chroneos; Amy Tvinnereim; Robert L. Hunter; Zissis C. Chroneos

doi:10.1016/j.tube.2011.10.014

Prolonged survival of scavenger receptor class A-deficient mice from pulmonary Mycobacterium tuberculosis infection

Zvjezdana Sever-Chroneos, Amy Tvinnereim, Robert L. Hunter, Zissis C. Chroneos

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20 Scopus citations

Abstract

The present study tested the hypothesis that the scavenger receptor SR-A modulates granuloma formation in response to pulmonary infection with Mycobacterium tuberculosis (MTB). To test this hypothesis, we monitored survival and histopathology in WT and SR-A-deficient mice following aerosol infection with MTB Rv. SR-A-deficient (SR-A-/-) mice infected with MTB survived significantly longer than WT mice; the mean survival of SR-A-/- mice exceeded 430 days compared to 230 days for WT mice. Early granuloma formation was not impaired in SR-A-/- mice. The extended survival of SR-A-/- mice was associated with 13- and 3-fold higher number of CD4+ lymphocytes and antigen presenting cells in SR-A-/- lungs compared to WT mice 280 after infection. The histopathology of chronically infected SR-A-/- lungs, however, was marked by abundant cholesterol clefts in parenchymal lesions containing infection in multinucleated giant cells. The present study indicates SR-A as a candidate gene of the innate immune system influencing the chronic phase of M. tuberculosis infection.

Original language	English (US)
Pages (from-to)	S69-S74
Journal	Tuberculosis
Volume	91
Issue number	SUPPL. 1
DOIs	https://doi.org/10.1016/j.tube.2011.10.014
State	Published - Dec 2011

All Science Journal Classification (ASJC) codes

Microbiology
Immunology
Microbiology (medical)
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.tube.2011.10.014

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title = "Prolonged survival of scavenger receptor class A-deficient mice from pulmonary Mycobacterium tuberculosis infection",

abstract = "The present study tested the hypothesis that the scavenger receptor SR-A modulates granuloma formation in response to pulmonary infection with Mycobacterium tuberculosis (MTB). To test this hypothesis, we monitored survival and histopathology in WT and SR-A-deficient mice following aerosol infection with MTB Rv. SR-A-deficient (SR-A-/-) mice infected with MTB survived significantly longer than WT mice; the mean survival of SR-A-/- mice exceeded 430 days compared to 230 days for WT mice. Early granuloma formation was not impaired in SR-A-/- mice. The extended survival of SR-A-/- mice was associated with 13- and 3-fold higher number of CD4+ lymphocytes and antigen presenting cells in SR-A-/- lungs compared to WT mice 280 after infection. The histopathology of chronically infected SR-A-/- lungs, however, was marked by abundant cholesterol clefts in parenchymal lesions containing infection in multinucleated giant cells. The present study indicates SR-A as a candidate gene of the innate immune system influencing the chronic phase of M. tuberculosis infection.",

author = "Zvjezdana Sever-Chroneos and Amy Tvinnereim and Hunter, {Robert L.} and Chroneos, {Zissis C.}",

note = "Funding Information: Financial support for this work was provided by the Potts Memorial Foundation to ZCC, a UTHSCT Research Council Award to ZSC, and funds provided by the University of Texas Health Science Center at Tyler Office of the Director of Research . Funding Information: We thank Dr. Mark AL Atkinson, M.A. D.Phil. Director of Research for financial support, Dr. Lester Kobzik, Harvard School of Public Health for providing the SR-A-/- mice, Dr. Homayoun Shams, UTHSCT for aerosol infections, and Dr. Timothy Allen, Chair of the Department Pathology for facilitating processing and staining of tissue sections at the UTHSCT Clinical Histology Laboratory.",

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N1 - Funding Information: Financial support for this work was provided by the Potts Memorial Foundation to ZCC, a UTHSCT Research Council Award to ZSC, and funds provided by the University of Texas Health Science Center at Tyler Office of the Director of Research . Funding Information: We thank Dr. Mark AL Atkinson, M.A. D.Phil. Director of Research for financial support, Dr. Lester Kobzik, Harvard School of Public Health for providing the SR-A-/- mice, Dr. Homayoun Shams, UTHSCT for aerosol infections, and Dr. Timothy Allen, Chair of the Department Pathology for facilitating processing and staining of tissue sections at the UTHSCT Clinical Histology Laboratory.

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N2 - The present study tested the hypothesis that the scavenger receptor SR-A modulates granuloma formation in response to pulmonary infection with Mycobacterium tuberculosis (MTB). To test this hypothesis, we monitored survival and histopathology in WT and SR-A-deficient mice following aerosol infection with MTB Rv. SR-A-deficient (SR-A-/-) mice infected with MTB survived significantly longer than WT mice; the mean survival of SR-A-/- mice exceeded 430 days compared to 230 days for WT mice. Early granuloma formation was not impaired in SR-A-/- mice. The extended survival of SR-A-/- mice was associated with 13- and 3-fold higher number of CD4+ lymphocytes and antigen presenting cells in SR-A-/- lungs compared to WT mice 280 after infection. The histopathology of chronically infected SR-A-/- lungs, however, was marked by abundant cholesterol clefts in parenchymal lesions containing infection in multinucleated giant cells. The present study indicates SR-A as a candidate gene of the innate immune system influencing the chronic phase of M. tuberculosis infection.

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Prolonged survival of scavenger receptor class A-deficient mice from pulmonary Mycobacterium tuberculosis infection

Abstract

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