Dopamine modulates hemocyte phagocytosis via a D1-like receptor in the rice stem borer, Chilo suppressalis

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作者
Shun-Fan Wu
Gang Xu
David Stanley
Jia Huang
Gong-Yin Ye
机构
[1] State Key Laboratory of Rice Biology & Key Laboratory of Agricultural Entomology of Ministry of Agriculture,
[2] Institute of Insect Sciences,undefined
[3] Zhejiang University,undefined
[4] College of Plant Protection,undefined
[5] Nanjing Agricultural University,undefined
[6] State & Local Joint Engineering Research Center of Green Pesticide Invention and Application,undefined
[7] USDA – Agricultural Research Service,undefined
[8] BCIRL,undefined
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Dopamine (DA) is a signal moiety bridging the nervous and immune systems. DA dysregulation is linked to serious human diseases, including addiction, schizophrenia and Parkinson’s disease. However, DA actions in the immune system remain incompletely understood. In this study, we found that DA modulates insect hemocyte phagocytosis using hemocytes prepared from the rice stem borer (RSB), Chilo suppressalis. We investigated whether insect hemocytes are capable of de novo DA production. Here we show that exposing hemocytes to lipopolysaccharide (LPS) led to induction of DA-generating enzymes. Exogenous DA induced rapid phosphorylation of extracellular signal-regulated kinase (ERK) in naïve hemocytes. Activation of ERK was inhibited by preincubating with a DOP1 receptor antagonist. Thus, DA signaling via the DOP1 receptor may contribute to early hemocyte activation. DA synthesized and released from hemocytes may act in an autocrine mechanism to stimulate or maintain phagocytic activity. Consistent with this hypothesis, we found that inhibition of DA synthesis with α-methyl-DL-tyrosine methyl ester hydrochloride or blockage of DOP1 receptor with antagonist SCH23390 impaired hemocyte phagocytosis. Topical DA application also significantly decreased RSB mortality following challenge with the insect pathogenic fungus, Beauveria bassiana. We infer that a DA-dependent signaling system operates in hemocytes to mediate phagocytotic functions.
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