Impaired interferon-γ signaling promotes the development of silicosis.

Molecular biology Molecular physiology Physiology

Journal

iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038

Informations de publication

Date de publication:
15 Jul 2022
Historique:
received: 22 02 2022
revised: 18 05 2022
accepted: 15 06 2022
entrez: 8 7 2022
pubmed: 9 7 2022
medline: 9 7 2022
Statut: epublish

Résumé

Silicosis is caused by inhalation of crystalline silica dust particles and known as one of the most serious occupational diseases worldwide. However, little is known about intrinsic factors leading to disease susceptibility. Single-cell sequencing of bronchoalveolar lavage fluid cells of mine workers with silicosis and their co-workers who did not develop silicosis revealed that the impaired interferon (IFN)-γ signaling in myeloid cells was strongly associated with the occurrence of silicosis. Global or myeloid cell-specific deletion of interferon γ receptor (IFN-γR) markedly enhanced the crystalline silica-induced pulmonary injury in wild-type but not in NLRP3 deficient mice.

Identifiants

pubmed: 35800765
doi: 10.1016/j.isci.2022.104647
pii: S2589-0042(22)00919-1
pmc: PMC9254453
doi:

Types de publication

Journal Article

Langues

eng

Pagination

104647

Informations de copyright

© 2022.

Déclaration de conflit d'intérêts

The authors declare no competing interests.

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Auteurs

Zhouyangfan Peng (Z)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Mingwu Duan (M)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Yiting Tang (Y)

Department of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province 410000, P.R. China.

Jianfeng Wu (J)

State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, China.

Kai Zhao (K)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Yanjun Zhong (Y)

ICU Center, The Second Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Zhihui He (Z)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Jie Meng (J)

Department of Respiratory Diseases and Critical Care Illness, The 3Road Xiangya Hospital, Central South University, Changsha 410000, P.R. China.
Hunan Key Laboratory of Organ Fibrosis, Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Fangping Chen (F)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Xianzhong Xiao (X)

Key Laboratory of Sepsis Translational Medicine of Hunan, Central South University, Changsha, Hunan Province 410000, P.R. China.
Department of Pathophysiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province 410000, P.R. China.

Haichao Wang (H)

The Feinstein Institute for Medical Research, Northwell Health, 350 Community Drive, Manhasset, NY 11030, USA.

Timothy R Billiar (TR)

Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.

Ben Lu (B)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.
Key Laboratory of Sepsis Translational Medicine of Hunan, Central South University, Changsha, Hunan Province 410000, P.R. China.
Department of Pathophysiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province 410000, P.R. China.

Fang Liang (F)

Department of Hematology and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410000, P.R. China.

Classifications MeSH