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Extracellular Vesicles Derived from Gram-Negative Bacteria, such as Escherichia coli, Induce Emphysema Mainly via IL-17A-Mediated Neutrophilic Inflammation
- Extracellular Vesicles Derived from Gram-Negative Bacteria, such as Escherichia coli, Induce Emphysema Mainly via IL-17A-Mediated Neutrophilic Inflammation
- Kim, You-Sun; Lee, Won-Hee; Choi, Eun-Jeong; Choi, Jun-Pyo; Heo, Young Joo; Gho, Yong Song; Jee, Young-Koo; Oh, Yeon-Mok; Kim, Yoon-Keun
- Ewha Authors
- 김윤근; 최준표
- SCOPUS Author ID
- Issue Date
- Journal Title
- JOURNAL OF IMMUNOLOGY
- 0022-1767; 1550-6606
- vol. 194, no. 7, pp. 3361 - 3368
- AMER ASSOC IMMUNOLOGISTS
- SCI; SCIE; SCOPUS
- Recent evidence indicates that Gram-negative bacteria-derived extracellular vesicles (EVs) in indoor dust can evoke neutrophilic pulmonary inflammation, which is a key pathology of chronic obstructive pulmonary disease (COPD). Escherichia coli is a ubiquitous bacterium present in indoor dust and secretes nanometer-sized vesicles into the extracellular milieu. In the current study, we evaluated the role of E. coli-derived EVs on the development of COPD, such as emphysema. E. coli EVs were prepared by sequential ultrafiltration and ultracentrifugation. COPD phenotypes and immune responses were evaluated in C57BL/6 wild-type (WT), IFN-gamma-deficient, or IL-17A-deficient mice after airway exposure to E. coli EVs. The present study showed that indoor dust from a bed mattress harbors E. coli EVs. Airway exposure to E. coli EVs increased the production of proinflammatory cytokines, such as TNF-alpha and IL-6. In addition, the repeated inhalation of E. coli EVs for 4 wk induced neutrophilic inflammation and emphysema, which are associated with enhanced elastase activity. Emphysema and elastase activity enhanced by E. coli EVs were reversed by the absence of IFN-gamma or IL-17A genes. In addition, during the early period, lung inflammation is dependent on IL-17A and TNF-alpha, but not on IFN-gamma, and also on TLR4. Moreover, the production of IFN-gamma is eliminated by the absence of IL-17A, whereas IL-17A production is not abolished by IFN-gamma absence. Taken together, the present data suggest that E. coli-derived EVs induce IL-17A-dependent neutrophilic inflammation and thereby emphysema, possibly via upregulation of elastase activity.
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