1. Enhancing autophagy in CD11c+ antigen-presenting cells as a therapeutic strategy for acute respiratory distress syndrome
- Author
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Quach, Christine, Helou, Doumet Georges, Li, Meng, Hurrell, Benjamin Pierre, Howard, Emily, Shafiei-Jahani, Pedram, Soroosh, Pejman, Ou, Jing-hsiung James, Razani, Babak, Rehan, Virender, and Akbari, Omid
- Subjects
Biological Sciences ,Orphan Drug ,Acute Respiratory Distress Syndrome ,Rare Diseases ,Infectious Diseases ,Lung ,2.1 Biological and endogenous factors ,Respiratory ,Inflammatory and immune system ,Animals ,Mice ,Antigen-Presenting Cells ,Macrophages ,Autophagy ,Acute Lung Injury ,Poly I-C ,Respiratory Distress Syndrome ,CD11c ,CP: Immunology ,acute respiratory distress syndrome ,antigen-presenting cells ,autophagy ,lung inflammation ,lung injury ,poly(I:C) ,Biochemistry and Cell Biology ,Medical Physiology ,Biological sciences - Abstract
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.
- Published
- 2023