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Title: Microcystin-leucine arginine exhibits immunomodulatory roles in testicular cells resulting in orchitis
Authors: Chen, YB
Wang, J
Zhang, Q
Xiang, Z 
Li, DM
Han, XD
Keywords: Microcystin-LR
Immune responses
Testicular cells
Issue Date: 2017
Publisher: Pergamon Press
Source: Environmental pollution, 2017, v. 229, p. 964-975 How to cite?
Journal: Environmental pollution 
Abstract: Microcystin-leucine arginine (MC-LR) causes testicular inflammation and hinders spermatogenesis. However, the molecular mechanisms underlying the immune responses to MC-LR in the testis have not been elucidated in detail. In this study, we show that MC-LR induced immune responses in Sertoli cells (SC), germ cells (GC), and Leydig cells (LC) via activating phosphatidylinositol 3-kinase (PI3K)/AKT/nuclear factor kappa B (NF-kappa B), resulting in the production of pro-inflammatory cytokines and chemokines including tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and chemokine (C-X-C motif) ligand 10 (CXCL10). The observed effects were attributed to reduced activity of protein phosphatases 2A (PP2A) as a result of binding of MC-LR to the catalytic subunit of PP2A in SC and GC. By contrast, innate immune responses were triggered by Toll-like receptor 2 (TLR2) in LC because MC-LR could not enter into the LC and subsequently inhibit the PP2A activity. PI3K/AKT/NF-kappa B were also activated in SC, GC, and LC in vivo, with the enrichment of TNF-a, IL-6, MCP-1, and CXCL10 in the testis. Following chronic exposure, MC-LR-treated mice exhibited decreased sperm counts and abnormal sperm morphology. Our data demonstrate that MC-LR can activate innate immune responses in testicular cells, which provides novel insights to explore the mechanism associated with MC-LR-induced orchitis.
ISSN: 0269-7491
EISSN: 1873-6424
DOI: 10.1016/j.envpol.2017.07.081
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