Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome

Summary: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe clinical disorders that mainly develop from viral respiratory infections, sepsis, and chest injury. Antigen-presenting cells play a pivotal role in propagating uncontrolled inflammation and injury through the...

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Main Authors: Christine Quach, Doumet Georges Helou, Meng Li, Benjamin Pierre Hurrell, Emily Howard, Pedram Shafiei-Jahani, Pejman Soroosh, Jing-hsiung James Ou, Babak Razani, Virender Rehan, Omid Akbari
Format: Article
Language:English
Published: Elsevier 2023-08-01
Series:Cell Reports
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Online Access:http://www.sciencedirect.com/science/article/pii/S221112472301001X
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author Christine Quach
Doumet Georges Helou
Meng Li
Benjamin Pierre Hurrell
Emily Howard
Pedram Shafiei-Jahani
Pejman Soroosh
Jing-hsiung James Ou
Babak Razani
Virender Rehan
Omid Akbari
author_facet Christine Quach
Doumet Georges Helou
Meng Li
Benjamin Pierre Hurrell
Emily Howard
Pedram Shafiei-Jahani
Pejman Soroosh
Jing-hsiung James Ou
Babak Razani
Virender Rehan
Omid Akbari
author_sort Christine Quach
collection DOAJ
description Summary: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe clinical disorders that mainly develop from viral respiratory infections, sepsis, and chest injury. Antigen-presenting cells play a pivotal role in propagating uncontrolled inflammation and injury through the excess secretion of pro-inflammatory cytokines and recruitment of immune cells. Autophagy, a homeostatic process that involves the degradation of cellular components, is involved in many processes including lung inflammation. Here, we use a polyinosinic-polycytidylic acid (poly(I:C))-induced lung injury mouse model to mimic viral-induced ALI/ARDS and show that disruption of autophagy in macrophages exacerbates lung inflammation and injury, whereas autophagy induction attenuates this process. Therefore, induction of autophagy in macrophages can be a promising therapeutic strategy in ALI/ARDS.
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spelling doaj.art-bbea48a4c930453db7dcc96d68fc6f7d2023-08-31T05:02:27ZengElsevierCell Reports2211-12472023-08-01428112990Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndromeChristine Quach0Doumet Georges Helou1Meng Li2Benjamin Pierre Hurrell3Emily Howard4Pedram Shafiei-Jahani5Pejman Soroosh6Jing-hsiung James Ou7Babak Razani8Virender Rehan9Omid Akbari10Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USADepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USAUSC Libraries Bioinformatics Service, University of Southern California, Los Angeles, CA 90089, USADepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USADepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USADepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USAJanssen Research and Development, San Diego, CA 92121, USADepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USAUniversity of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA 15261, USA; Pittsburgh VA Medical Center, Pittsburgh, PA 15240, USADivision of Neonatology, Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA 90502, USADepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Corresponding authorSummary: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe clinical disorders that mainly develop from viral respiratory infections, sepsis, and chest injury. Antigen-presenting cells play a pivotal role in propagating uncontrolled inflammation and injury through the excess secretion of pro-inflammatory cytokines and recruitment of immune cells. Autophagy, a homeostatic process that involves the degradation of cellular components, is involved in many processes including lung inflammation. Here, we use a polyinosinic-polycytidylic acid (poly(I:C))-induced lung injury mouse model to mimic viral-induced ALI/ARDS and show that disruption of autophagy in macrophages exacerbates lung inflammation and injury, whereas autophagy induction attenuates this process. Therefore, induction of autophagy in macrophages can be a promising therapeutic strategy in ALI/ARDS.http://www.sciencedirect.com/science/article/pii/S221112472301001XCP: Immunology
spellingShingle Christine Quach
Doumet Georges Helou
Meng Li
Benjamin Pierre Hurrell
Emily Howard
Pedram Shafiei-Jahani
Pejman Soroosh
Jing-hsiung James Ou
Babak Razani
Virender Rehan
Omid Akbari
Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
Cell Reports
CP: Immunology
title Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
title_full Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
title_fullStr Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
title_full_unstemmed Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
title_short Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
title_sort enhancing autophagy in cd11c antigen presenting cells as a therapeutic strategy for acute respiratory distress syndrome
topic CP: Immunology
url http://www.sciencedirect.com/science/article/pii/S221112472301001X
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