NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection

ABSTRACT The inflammatory response to Chlamydia infection is likely to be multifactorial and involve a variety of ligand-dependent and -independent recognition pathways. We previously reported the presence of NOD1/NOD2-dependent endoplasmic reticulum (ER) stress-induced inflammation during Chlamydia...

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Autores principales:	Oanh H. Pham, Bokyung Lee, Jasmine Labuda, A. Marijke Keestra-Gounder, Mariana X. Byndloss, Renée M. Tsolis, Stephen J. McSorley
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2020
Materias:	Chlamydia innate immunity NOD ER stress inflammation Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/3acb15e5e9f04ec2a6f2b6c47dfd3fcb
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spelling	oai:doaj.org-article:3acb15e5e9f04ec2a6f2b6c47dfd3fcb2021-11-15T15:56:46ZNOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection10.1128/mBio.00979-202150-7511https://doaj.org/article/3acb15e5e9f04ec2a6f2b6c47dfd3fcb2020-06-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00979-20https://doaj.org/toc/2150-7511ABSTRACT The inflammatory response to Chlamydia infection is likely to be multifactorial and involve a variety of ligand-dependent and -independent recognition pathways. We previously reported the presence of NOD1/NOD2-dependent endoplasmic reticulum (ER) stress-induced inflammation during Chlamydia muridarum infection in vitro, but the relevance of this finding to an in vivo context is unclear. Here, we examined the ER stress response to in vivo Chlamydia infection. The induction of interleukin 6 (IL-6) production after systemic Chlamydia infection correlated with expression of ER stress response genes. Furthermore, when tauroursodeoxycholate (TUDCA) was used to inhibit the ER stress response, an increased bacterial burden was detected, suggesting that ER stress-driven inflammation can contribute to systemic bacterial clearance. Mice lacking both NOD1 and NOD2 or RIP2 exhibited slightly higher systemic bacterial burdens after infection with Chlamydia. Overall, these data suggest a model where RIP2 and NOD1/NOD2 proteins link ER stress responses with the induction of Chlamydia-specific inflammatory responses. IMPORTANCE Understanding the initiation of the inflammatory response during Chlamydia infection is of public health importance given the impact of this disease on young women in the United States. Many young women are chronically infected with Chlamydia but are asymptomatic and therefore do not seek treatment, leaving them at risk of long-term reproductive harm due to inflammation in response to infection. Our manuscript explores the role of the endoplasmic reticulum stress response pathway initiated by an innate receptor in the development of this inflammation.Oanh H. PhamBokyung LeeJasmine LabudaA. Marijke Keestra-GounderMariana X. ByndlossRenée M. TsolisStephen J. McSorleyAmerican Society for MicrobiologyarticleChlamydiainnate immunityNODER stressinflammationMicrobiologyQR1-502ENmBio, Vol 11, Iss 3 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Chlamydia innate immunity NOD ER stress inflammation Microbiology QR1-502
spellingShingle	Chlamydia innate immunity NOD ER stress inflammation Microbiology QR1-502 Oanh H. Pham Bokyung Lee Jasmine Labuda A. Marijke Keestra-Gounder Mariana X. Byndloss Renée M. Tsolis Stephen J. McSorley NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection
description	ABSTRACT The inflammatory response to Chlamydia infection is likely to be multifactorial and involve a variety of ligand-dependent and -independent recognition pathways. We previously reported the presence of NOD1/NOD2-dependent endoplasmic reticulum (ER) stress-induced inflammation during Chlamydia muridarum infection in vitro, but the relevance of this finding to an in vivo context is unclear. Here, we examined the ER stress response to in vivo Chlamydia infection. The induction of interleukin 6 (IL-6) production after systemic Chlamydia infection correlated with expression of ER stress response genes. Furthermore, when tauroursodeoxycholate (TUDCA) was used to inhibit the ER stress response, an increased bacterial burden was detected, suggesting that ER stress-driven inflammation can contribute to systemic bacterial clearance. Mice lacking both NOD1 and NOD2 or RIP2 exhibited slightly higher systemic bacterial burdens after infection with Chlamydia. Overall, these data suggest a model where RIP2 and NOD1/NOD2 proteins link ER stress responses with the induction of Chlamydia-specific inflammatory responses. IMPORTANCE Understanding the initiation of the inflammatory response during Chlamydia infection is of public health importance given the impact of this disease on young women in the United States. Many young women are chronically infected with Chlamydia but are asymptomatic and therefore do not seek treatment, leaving them at risk of long-term reproductive harm due to inflammation in response to infection. Our manuscript explores the role of the endoplasmic reticulum stress response pathway initiated by an innate receptor in the development of this inflammation.
format	article
author	Oanh H. Pham Bokyung Lee Jasmine Labuda A. Marijke Keestra-Gounder Mariana X. Byndloss Renée M. Tsolis Stephen J. McSorley
author_facet	Oanh H. Pham Bokyung Lee Jasmine Labuda A. Marijke Keestra-Gounder Mariana X. Byndloss Renée M. Tsolis Stephen J. McSorley
author_sort	Oanh H. Pham
title	NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection
title_short	NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection
title_full	NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection
title_fullStr	NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection
title_full_unstemmed	NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection
title_sort	nod1/nod2 and rip2 regulate endoplasmic reticulum stress-induced inflammation during <italic toggle="yes">chlamydia</italic> infection
publisher	American Society for Microbiology
publishDate	2020
url	https://doaj.org/article/3acb15e5e9f04ec2a6f2b6c47dfd3fcb
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NOD1/NOD2 and RIP2 Regulate Endoplasmic Reticulum Stress-Induced Inflammation during <italic toggle="yes">Chlamydia</italic> Infection

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