ALX/FPR2 modulates anti-inflammatory responses in mouse submandibular gland

Ching Shuen Wang, Yinshen Wee, Chieh Hsiang Yang, James E. Melvin, Olga J. Baker

研究成果: 雜誌貢獻文章同行評審

28 引文 斯高帕斯(Scopus)


Activation of the G-protein coupled formyl peptide receptor 2 (ALX/FPR2) by the lipid mediators lipoxin A 4 and resolvin D1 (RvD1) promotes resolution of inflammation. Our previous in vitro studies indicate that RvD1 activation of ALX/FPR2 resolves cytokine-mediated inflammatory responses in mammalian cells. However, the impact of ALX/FPR2 activation on salivary gland function in vivo is unknown. The objective of this study was to determine whether submandibular glands (SMG) from ALX/FPR2 -/- mice display enhanced inflammatory responses to lipopolysaccharides (LPS) stimulation. For these studies, C57BL/6 and ALX/FPR2 -/- mice at age 8-12-week-old were treated with LPS by i.p for 24 h. Salivary gland structure and function were analyzed by histopathological assessment, saliva flow rate, quantitative PCR, Western blot analyses and immunofluorescence. Our results showed the following events in the ALX/FPR2 -/- mice treated with LPS: a) upregulated inflammatory cytokines and decreased M3R (Muscarinic Acetylcholine receptor M3) and AQP5 (Aquaporin 5) protein expression, b) decreased saliva secretion, c) increased apoptosis, d) alteration of tight junction and neuronal damage. Overall, our data suggest that the loss of ALX/FPR2 results in unresolved acute inflammation and SMG dysfunction (xerostomia) in response to LPS that is similar to human salivary gland dysfunction induced by bacterial infection.
期刊Scientific Reports
出版狀態已發佈 - 4月 11 2016

ASJC Scopus subject areas

  • 多學科


深入研究「ALX/FPR2 modulates anti-inflammatory responses in mouse submandibular gland」主題。共同形成了獨特的指紋。