Autophagy Is Required for Neutrophil-Mediated Inflammation
| Autor: | Qin Wei, Diana L. Bonilla, Elmoataz Abdel Fattah, Abhisek Bhattacharya, Qian Xiang, N. Tony Eissa, Jin Na Shin |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Neutrophils
Inflammation Biology General Biochemistry Genetics and Molecular Biology Mice Autophagy medicine Animals lcsh:QH301-705.5 chemistry.chemical_classification Reactive oxygen species NADPH oxidase Experimental autoimmune encephalomyelitis Degranulation NADPH Oxidases medicine.disease Cell biology Mice Inbred C57BL chemistry lcsh:Biology (General) biology.protein Neutrophil degranulation Inflammation Mediators medicine.symptom Reactive Oxygen Species Intracellular |
| Zdroj: | Cell Reports, Vol 12, Iss 11, Pp 1731-1739 (2015) |
| ISSN: | 2211-1247 |
| DOI: | 10.1016/j.celrep.2015.08.019 |
| Popis: | SummaryAutophagy, an intracellular degradation and energy recycling mechanism, is emerging as an important regulator of immune responses. However, the role of autophagy in regulating neutrophil functions is not known. We investigated neutrophil biology using myeloid-specific autophagy-deficient mice and found that autophagy deficiency reduced neutrophil degranulation in vitro and in vivo. Mice with autophagy deficiency showed reduced severity of several neutrophil-mediated inflammatory and autoimmune disease models, including PMA-induced ear inflammation, LPS-induced breakdown of blood-brain barrier, and experimental autoimmune encephalomyelitis. NADPH oxidase-mediated reactive oxygen species generation was also reduced in autophagy-deficient neutrophils, and inhibition of NADPH oxidase reduced neutrophil degranulation, suggesting NADPH oxidase to be a player at the intersection of autophagy and degranulation. Overall, this study establishes autophagy as an important regulator of neutrophil functions and neutrophil-mediated inflammation in vivo. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|