Acetylcholine suppresses phagocytosis via binding to muscarinic- and nicotinic-acetylcholine receptors and subsequently interfering Ca2+- and NFκB-signaling pathways in blood clam
Copyright © 2020 Elsevier Ltd. All rights reserved..
Though immunomodulation via cholinergic neurotransmitter acetylcholine (ACh), an important part of neuroendocrine-immune (NEI) regulatory network, has been well established in vertebrate species, the mechanisms remain poorly understood in invertebrates. In the present study, the immunomodulatory effect of ACh on haemocyte phagocytosis was investigated in an invertebrate bivalve species, Tegillarca granosa. Data obtained showed that in vitro ACh incubation suppressed phagocytic activity of haemocytes along with a significant elevation in intracellular Ca2+. In addition, the expressions of genes from Ca2+ signaling pathway were significantly induced whereas those from NF-κB signaling pathway were significantly down-regulated by ACh incubation. Furthermore, these adverse impacts of ACh were significantly relieved by the blocking of muscarinic acetylcholine receptors (mAChRs) or nicotinic acetylcholine receptors (nAChRs) using corresponding antagonists. Our study suggests that ACh suppresses phagocytosis via binding to both mAChRs and nAChRs, which disrupts intracellular Ca2+ homeostasis and subsequently interferes with downstream Ca2+ and NF-κB signaling pathways.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:102 |
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| Enthalten in: |
Fish & shellfish immunology - 102(2020) vom: 15. Juli, Seite 152-160 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Du, Xueying [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 15.01.2021 Date Revised 15.01.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.fsi.2020.04.030 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM309051649 |
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| 245 | 1 | 0 | |a Acetylcholine suppresses phagocytosis via binding to muscarinic- and nicotinic-acetylcholine receptors and subsequently interfering Ca2+- and NFκB-signaling pathways in blood clam |
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| 520 | |a Copyright © 2020 Elsevier Ltd. All rights reserved. | ||
| 520 | |a Though immunomodulation via cholinergic neurotransmitter acetylcholine (ACh), an important part of neuroendocrine-immune (NEI) regulatory network, has been well established in vertebrate species, the mechanisms remain poorly understood in invertebrates. In the present study, the immunomodulatory effect of ACh on haemocyte phagocytosis was investigated in an invertebrate bivalve species, Tegillarca granosa. Data obtained showed that in vitro ACh incubation suppressed phagocytic activity of haemocytes along with a significant elevation in intracellular Ca2+. In addition, the expressions of genes from Ca2+ signaling pathway were significantly induced whereas those from NF-κB signaling pathway were significantly down-regulated by ACh incubation. Furthermore, these adverse impacts of ACh were significantly relieved by the blocking of muscarinic acetylcholine receptors (mAChRs) or nicotinic acetylcholine receptors (nAChRs) using corresponding antagonists. Our study suggests that ACh suppresses phagocytosis via binding to both mAChRs and nAChRs, which disrupts intracellular Ca2+ homeostasis and subsequently interferes with downstream Ca2+ and NF-κB signaling pathways | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a AChRs | |
| 650 | 4 | |a Acetylcholine (ACh) | |
| 650 | 4 | |a Ca(2+) homeostasis | |
| 650 | 4 | |a Ca(2+) signaling pathway | |
| 650 | 4 | |a NF-κB signaling pathway | |
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| 650 | 7 | |a Receptors, Muscarinic |2 NLM | |
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| 700 | 1 | |a Han, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Ri, Sanghyok |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Tongchol |e verfasserin |4 aut | |
| 700 | 1 | |a Ju, Kwangjin |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Sun, Shuge |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Weishang |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Guangxu |e verfasserin |4 aut | |
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