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The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Open access
Rosas-Ballina, Mauricio, Ochani, Mahendar, Parrish, William R., Ochani, Kanta, Harris, Yael T., Huston, Jared M., Chavan, Sangeeta, Tracey, Kevin J.·2008·Proceedings of the National Academy of Sciences

Abstract

The autonomic nervous system maintains homeostasis through its sympathetic and parasympathetic divisions. During infection, cells of the immune system release cytokines and other mediators that cause fever, hypotension, and tissue injury. Although the effect of cytokines on the nervous system has been known for decades, only recently has it become evident that the autonomic nervous system, in turn, regulates cytokine production through neural pathways. We have previously shown that efferent vagus nerve signals regulate cytokine production through the nicotinic acetylcholine receptor subunit α7, a mechanism termed “the cholinergic antiinflammatory pathway.” Here, we show that vagus nerve stimulation during endotoxemia specifically attenuates TNF production by spleen macrophages in the red pulp and the marginal zone. Administration of nicotine, a pharmacological agonist of α7, attenuated TNF immunoreactivity in these specific macrophage subpopulations. Synaptophysin-positive nerve endings were observed in close apposition to red pulp macrophages, but they do not express choline acetyltransferase or vesicular acetylcholine transporter. Surgical ablation of the splenic nerve and catecholamine depletion by reserpine indicate that these nerves are catecholaminergic and are required for functional inhibition of TNF production by vagus nerve stimulation. Thus, the cholinergic antiinflammatory pathway regulates TNF production in discrete macrophage populations via two serially connected neurons: one preganglionic, originating in the dorsal motor nucleus of the vagus nerve, and the second postganglionic, originating in the celiac-superior mesenteric plexus, and projecting in the splenic nerve.

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Crossref · 10.1073/pnas.0803237105

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Metadata

Authors
Rosas-Ballina, M., Ochani, M., Parrish, W. R., Ochani, K., Harris, Y. T., Huston, J. M., Chavan, S., & Tracey, K. J.
Venue
Proceedings of the National Academy of Sciences
Published
2008-08-05
Volume
105
Issue
31
Pages
11008-11013
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2046775696
Cited by
753
References
10
FWCI
14.79
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia. https://app.cochat.ai/papers/10.1073/pnas.0803237105
The paper
Rosas-Ballina, M., Ochani, M., Parrish, W. R., Ochani, K., Harris, Y. T., Huston, J. M., Chavan, S., & Tracey, K. J. (2008). Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0803237105

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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