Suppression of LPS-induced TNF alpha production in macrophages by catecholamines is mediated through the beta2-aderenergic receptor

2022 Fiscal Year Final Research Report

• Project/Area Number: 21K20999
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0906:Surgery related to the biological and sensory functions and related fields
• Research Institution: Aichi Medical University
• Principal Investigator: FENG GUOGANG 愛知医科大学, 医学部, 助教 (70351111)
• Project Period (FY): 2021-08-30 – 2023-03-31
• Keywords: LPS / 炎症反応 / TNFα / カテコラミン / β2受容体

Outline of Final Research Achievements

Catecholamines such as adrenaline (Ad) suppressed the expression of TNFα induced by LPS in RAW264.7 cells. We had identified the mRNA expression of Ad receptor subtypes such as β2 in RAW264.7 cells. Pretreatment with propranolol and ICI118.551 (a selective β2 receptor antagonist) attenuated the inhibitory effects of these catecholamines on LPS-induced increase of TNFα expression. In contrast, isoproterenol and fenoterol, like adrenaline, suppressed LPS-induced increase of TNFα expression. Furthermore, LPS suppressed the expression of β2 receptors in RAW264.7 cells in a time-dependent manner.

Free Research Field

救急医学

Academic Significance and Societal Importance of the Research Achievements

マクロファージであるRAW264.7細胞においてカテコラミンはβ2受容体の活性化を介してLPSによる誘導された炎症反応を制御することを解明摘でき、敗血症発生機序の解明や新しい治療法の開発には新たな手掛かりが得られた。