NDLI: Age-enhanced endoplasmic reticulum stress contributes to increased Atg9A inhibition of STING-mediated IFN-ß production during Streptococcus pneumoniae infection.

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Age-enhanced endoplasmic reticulum stress contributes to increased Atg9A inhibition of STING-mediated IFN-ß production during Streptococcus pneumoniae infection.

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Age-enhanced endoplasmic reticulum stress contributes to increased Atg9A inhibition of STING-mediated IFN-ß production during Streptococcus pneumoniae infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Stout-Delgado, Heather W. Lowry, Virginia Shirali, Anushree C. Mitzel, Dana N. Liu, Yushi
Description	Author Affiliation: Mitzel DN ( Animal Biosafety Level 3 Management Support, Lovelace Respiratory Research Institute, Albuquerque, NM 87108)
Abstract	Pneumococcal infections remain a leading cause of death in persons ≥ 65 y of age. Recent reports have illustrated detrimental changes in the endoplasmic reticulum stress response or unfolded protein response in aging and age-related diseases; however, the relationship between aging, the unfolded protein response, and innate immune responses to Streptococcus pneumoniae has not been fully elucidated. Our results illustrate that stimulator of IFN genes-mediated production of IFN-ß during S. pneumoniae infection is decreased in aged hosts. Enhanced endoplasmic reticulum stress in response to S. pneumoniae augmented inositol-requiring protein 1/X-box binding protein 1-mediated production of autophagy-related gene 9 (Atg9a). Knockdown of Atg9a or treatment with gemcitabine HCl resulted in enhanced stimulator of IFN genes-mediated production of IFN-ß by aged macrophages. Consecutive treatments with gemcitabine during in vivo S. pneumoniae infection decreased morbidity and mortality in aged hosts, which was associated with decreased Atg9a expression, increased IFN-ß production, and improved bacterial clearance from lung tissue. Taken together, data presented in this study provide new evidence as to why older persons are more susceptible to S. pneumoniae, and provide a possible mechanism to enhance these responses, thereby decreasing morbidity and mortality in this population.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1303090
Journal	The Journal of Immunology
Issue Number	9
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Aging Immunology Endoplasmic Reticulum Stress Interferon-beta Biosynthesis Membrane Proteins Pneumococcal Infections Animals Blotting, Western Cells, Cultured Enzyme-linked Immunosorbent Assay Flow Cytometry Immunoprecipitation Metabolism Mice Mice, Inbred Balb C Rna, Small Interfering Real-time Polymerase Chain Reaction Transfection Vesicular Transport Proteins Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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