title: Positive Feedback Cycle of TNFα Promotes Staphylococcal Enterotoxin B-Induced THP-1 Cell Apoptosis.
abstract: Staphylococcal enterotoxin B (SEB) has been demonstrated to be of importance inStaphylococcus aureusrelated diseases, such as atopic dermatitis (AD). Dysregulated apoptosis in AD is remarkable, and SEB can induce apoptosis of various cell types. However, the mechanisms by which SEB induces apoptosis and influences disease processes remain unclear. In this study, the recombinant SEB-induced THP-1 monocyte apoptosis was demonstrated in the absence of preliminary cell activation in a time- and dose-dependent manner. SEB could up-regulate the expression of tumor necrosis factor alpha (TNFα) in THP-1 cells and induce apoptosis via an extrinsic pathway. TNFα could in turn increase the expression of HLA-DRa, the SEB receptor on the cell surface. As a result, a positive feedback cycle of TNFα was established. TNFα expression and SEB-induced apoptosis were decreased by knocking down the expression of either HLA-DRa or TNFR1. Therefore, the feedback cycle of TNFα is crucial for SEB functions. This work provides insights into the mechanisms of SEB-induced monocyte apoptosis and emphasizes the major role of TNFα in future related studies.
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Weilong
authors.initials: W
authors.lastname: Shang
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Jizhen
authors.initials: J
authors.lastname: Yuan
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Hu
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Huagang
authors.initials: H
authors.lastname: Peng
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Junmin
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Qiwen
authors.initials: Q
authors.lastname: Hu
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Bei
authors.initials: B
authors.lastname: Jiang
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Yinan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Shu
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Hu
authors.affiliation: Department of Microbiology, College of Basic Medical Sciences, Third Military Medical University Chongqing, China.
authors.forename: Xiancai
authors.initials: X
authors.lastname: Rao
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3; D053181:Caspase 8; D018929:Cell Culture Techniques; D045744:Cell Line, Tumor / Q000187:drug effects*; D003876:Dermatitis, Atopic / Q000382:microbiology; D004768:Enterotoxins / Q000235:genetics / Q000302:isolation & purification / Q000378:metabolism / Q000494:pharmacology*; D015870:Gene Expression; D059805:HLA-DR alpha-Chains / Q000378:metabolism; D006801:Humans; D034741:RNA, Small Interfering; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000378:metabolism; D011994:Recombinant Proteins; D013211:Staphylococcus aureus / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D004768:Enterotoxins; D059805:HLA-DR alpha-Chains; D034741:RNA, Small Interfering; D047888:Receptors, Tumor Necrosis Factor, Type I; D011994:Recombinant Proteins; C506235:TNFRSF1A protein, human; D014409:Tumor Necrosis Factor-alpha; C031818:enterotoxin B, staphylococcal; D053148:Caspase 3; D053181:Caspase 8
keywords: THP-1 cells; apoptosis; atopic dermatitis; staphylococcal enterotoxin B; tumor necrosis factor alpha