<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cremin M</submitter><funding>HHS | NIH | National Institute of General Medical Sciences</funding><funding>NIAID NIH HHS</funding><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><funding>NIGMS NIH HHS</funding><pagination>L53-L63</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9829467</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>324(1)</volume><pubmed_abstract>It is becoming increasingly appreciated that the nervous and immune systems communicate bidirectionally to regulate immunological outcomes in a variety of organs including the lung. Activation of neuronal signaling can be induced by inflammation, tissue damage, or pathogens to evoke or reduce immune cell activation in what has been termed a neuroimmune reflex. In the periphery, these reflexes include the cholinergic anti-inflammatory pathway, sympathetic reflex, and sensory nociceptor-immune cell pathways. Continual advances in neuroimmunology in peripheral organ systems have fueled small-scale clinical trials that have yielded encouraging results for a range of immunopathologies such as rheumatoid arthritis. Despite these successes, several limitations should give clinical investigators p</pubmed_abstract><journal>American journal of physiology. Lung cellular and molecular physiology</journal><pubmed_title>The diversity of neuroimmune circuits controlling lung inflammation.</pubmed_title><pmcid>PMC9829467</pmcid><funding_grant_id>T32GM099608</funding_grant_id><funding_grant_id>R21 AI148188</funding_grant_id><funding_grant_id>R01 AI150647</funding_grant_id><funding_grant_id>T32 GM099608</funding_grant_id><funding_grant_id>R01AI150647</funding_grant_id><funding_grant_id>T32 GM144303</funding_grant_id><funding_grant_id>GM144303</funding_grant_id><funding_grant_id>R21AI148188</funding_grant_id><pubmed_authors>Schreiber S</pubmed_authors><pubmed_authors>Cremin M</pubmed_authors><pubmed_authors>Tay EXY</pubmed_authors><pubmed_authors>Murray K</pubmed_authors><pubmed_authors>Reardon C</pubmed_authors></additional><is_claimable>false</is_claimable><name>The diversity of neuroimmune circuits controlling lung inflammation.</name><description>It is becoming increasingly appreciated that the nervous and immune systems communicate bidirectionally to regulate immunological outcomes in a variety of organs including the lung. Activation of neuronal signaling can be induced by inflammation, tissue damage, or pathogens to evoke or reduce immune cell activation in what has been termed a neuroimmune reflex. In the periphery, these reflexes include the cholinergic anti-inflammatory pathway, sympathetic reflex, and sensory nociceptor-immune cell pathways. Continual advances in neuroimmunology in peripheral organ systems have fueled small-scale clinical trials that have yielded encouraging results for a range of immunopathologies such as rheumatoid arthritis. Despite these successes, several limitations should give clinical investigators p</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T08:34:20.552Z</modification><creation>2025-04-04T08:34:20.552Z</creation></dates><accession>S-EPMC9829467</accession><cross_references><pubmed>36410021</pubmed><doi>10.1152/ajplung.00179.2022</doi></cross_references></HashMap>