Abstract
The mevalonic acid synthesis pathway, cholesterol, and lipoproteins play fundamental roles in lung physiology and the innate immune response.
Recent literature investigating roles for cholesterol synthesis and trafficking in host defense against respiratory infection was critically reviewed.
The innate immune response and the cholesterol biosynthesis/trafficking network regulate one another, with important implications for pathogen invasion and host defense in the lung. The activation of pathogen recognition receptors and downstream cellular host defense functions are critically sensitive to cellular cholesterol. Conversely, microorganisms can co-opt the sterol/lipoprotein network in order to facilitate replication and evade immunity. Emerging literature suggests the potential for harnessing these insights towards therapeutic development.
Given that >50% of adults in the U.S. have serum cholesterol abnormalities and pneumonia remains a leading cause of death, the potential impact of cholesterol on pulmonary host defense is of tremendous public health significance and warrants further mechanistic and translational investigation.
Keywords: Cholesterol, innate immunity, lipoprotein, lung, pneumonia, statins.
Current Molecular Pharmacology
Title:Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense
Volume: 10
Author(s): Kristin A. Gabor and Michael B. Fessler
Affiliation:
Keywords: Cholesterol, innate immunity, lipoprotein, lung, pneumonia, statins.
Abstract: The mevalonic acid synthesis pathway, cholesterol, and lipoproteins play fundamental roles in lung physiology and the innate immune response.
Recent literature investigating roles for cholesterol synthesis and trafficking in host defense against respiratory infection was critically reviewed.
The innate immune response and the cholesterol biosynthesis/trafficking network regulate one another, with important implications for pathogen invasion and host defense in the lung. The activation of pathogen recognition receptors and downstream cellular host defense functions are critically sensitive to cellular cholesterol. Conversely, microorganisms can co-opt the sterol/lipoprotein network in order to facilitate replication and evade immunity. Emerging literature suggests the potential for harnessing these insights towards therapeutic development.
Given that >50% of adults in the U.S. have serum cholesterol abnormalities and pneumonia remains a leading cause of death, the potential impact of cholesterol on pulmonary host defense is of tremendous public health significance and warrants further mechanistic and translational investigation.
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Cite this article as:
Gabor A. Kristin and Fessler B. Michael, Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense, Current Molecular Pharmacology 2017; 10 (1) . https://dx.doi.org/10.2174/1874467209666160112123603
DOI https://dx.doi.org/10.2174/1874467209666160112123603 |
Print ISSN 1874-4672 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-4702 |
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