title: Ultrafine particles in the airway aggravated experimental lung injury through impairment in Treg function.
abstract: Acute lung injury (ALI) is a life-threatening condition characterized by rapid-onset alveolar-capillary damage mediated by pathogenic proinflammatory immune responses. Since exposure to airway particulate matter (PM) could significantly change the inflammatory status of the individual, we investigated whether PM instillation in the airway could alter the course of ALI, using a murine model with experimental lung injury induced by intratracheal LPS challenge. We found that PM-treated mice presented significantly aggravated lung injury, which was characterized by further reductions in body weight, increased protein concentration in the bronchoalveolar lavage (BAL), and higher mortality rate, compared to control saline-treated mice. The PM-treated mice also presented elevated lung and systemic type 1 T helper cell (Th1) frequency as well as reduced lung regulatory T cell (Treg) frequency, which was associated with severity of lung injury. Further examinations revealed that the Treg function was impaired in PM-treated mice, characterized by significantly repressed transforming growth factor beta production. Adoptive transfer of functional Tregs from control mice to PM-treated mice significantly improved their prognosis after intratracheal LPS challenge. Together, these results demonstrated that first, PM in the airway aggravated lung injury; second, severity of lung injury was associated with T cell subset imbalance in PM-treated mice; and third, PM treatment induced quantitative as well as qualitative changes in the Tregs.
authors.affiliation: Affiliated Bayi Brain Hospital, PLA Army General Hospital, Beijing, 100700, China.
authors.forename: Guanggang
authors.initials: G
authors.lastname: Li
authors.affiliation: Affiliated Bayi Brain Hospital, PLA Army General Hospital, Beijing, 100700, China.
authors.forename: Yinghua
authors.initials: Y
authors.lastname: Cao
authors.affiliation: Affiliated Bayi Brain Hospital, PLA Army General Hospital, Beijing, 100700, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Affiliated Bayi Brain Hospital, PLA Army General Hospital, Beijing, 100700, China.
authors.forename: Ruxiang
authors.initials: R
authors.lastname: Xu
authors.affiliation: Department of Oncology, General Hospital of Shenyang Military Area Command, Shenyang, 110016, China. Electronic address: drzhendongzheng@126.com.
authors.forename: Zhendong
authors.initials: Z
authors.lastname: Zheng
authors.affiliation: Emergency Center, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China. Electronic address: haihansong@126.com.
authors.forename: Haihan
authors.initials: H
authors.lastname: Song
mesh_terms: D000818:Animals; D004781:Environmental Exposure / Q000009:adverse effects*; D055370:Lung Injury / Q000139:chemically induced* / Q000276:immunology* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D052638:Particulate Matter / Q000009:adverse effects* / Q000276:immunology*; D015996:Survival Rate; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000502:physiology
chemical_list: D052638:Particulate Matter
keywords: Acute lung injury; Particulate matter; Treg