title: Increased resistin may suppress reactive oxygen species production and inflammasome activation in type 2 diabetic patients with pulmonary tuberculosis infection.
abstract: Although it has been known for decades that patients with type 2 diabetes mellitus (DM) are more susceptible to severe tuberculosis (TB) infection, the underlying immunological mechanisms remain unclear. Resistin, a protein produced by immune cells in humans, causes insulin resistance and has been implicated in inhibiting reactive oxygen species (ROS) production in leukocytes. Recent studies suggested that IL-1β production in patients with Mycobacteria tuberculosis infection correlates with inflammasome activation which may be regulated by ROS production in the immune cells. By investigating the level of resistin in different patient groups, we found that serum resistin levels were significantly higher in severe TB and DM-only groups when compared with mild TB cases and healthy controls. Moreover, elevation of serum resistin correlated with impairment of ROS production of neutrophils in patients with both DM and TB. In human macrophages, exogenous resistin inhibits the production of ROS which are important in the mycobacterium-induced inflammasome activation. Moreover, macrophages with defective ROS production had poor IL-1β production and ineffective control of mycobacteria growth. Our results suggest that increased resistin in severe TB and DM patients may suppress the mycobacterium-induced inflammasome activation through inhibiting ROS production by leukocytes.
authors.affiliation: Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan; Department of Internal Medicine, Taichung Veteran General Hospital, Chiayi Branch, Chiayi, Taiwan.
authors.forename: Wen-Cheng
authors.initials: WC
authors.lastname: Chao
authors.affiliation: Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan.
authors.forename: Chia-Liang
authors.initials: CL
authors.lastname: Yen
authors.affiliation: Chest Hospital, Department of Health, Tainan, Taiwan.
authors.forename: Ying-Hsun
authors.initials: YH
authors.lastname: Wu
authors.affiliation: Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan.
authors.forename: Shin-Yi
authors.initials: SY
authors.lastname: Chen
authors.affiliation: Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan.
authors.forename: Cheng-Yuan
authors.initials: CY
authors.lastname: Hsieh
authors.affiliation: Department of Medical Laboratory Science and Biotechnology, National Cheng Kung University Medical College, Tainan, Taiwan.
authors.forename: Tsung-Chain
authors.initials: TC
authors.lastname: Chang
authors.affiliation: Department of Internal Medicine, National Cheng-Kung University Hospital, College of Medicine, National Cheng-Kung University, Tainan, Taiwan.
authors.forename: Horng-Yih
authors.initials: HY
authors.lastname: Ou
authors.affiliation: Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan; Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan. Electronic address: cshieh@mail.ncku.edu.tw.
authors.forename: Chi-Chang
authors.initials: CC
authors.lastname: Shieh
mesh_terms: D000328:Adult; D000368:Aged; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000201:enzymology* / Q000276:immunology / Q000517:prevention & control; D005260:Female; D006801:Humans; D058847:Inflammasomes / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism*; D052243:Resistin / Q000097:blood* / Q000276:immunology; D014397:Tuberculosis, Pulmonary / Q000150:complications / Q000276:immunology / Q000378:metabolism*
chemical_list: D058847:Inflammasomes; D017382:Reactive Oxygen Species; D052243:Resistin
keywords: Diabetes mellitus; Inflammasome; ROS; Resistin; Tuberculosis