{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T08:41:02Z","timestamp":1776328862963,"version":"3.50.1"},"reference-count":45,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2012,5,8]],"date-time":"2012-05-08T00:00:00Z","timestamp":1336435200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/2.0"},{"start":{"date-parts":[[2012,5,8]],"date-time":"2012-05-08T00:00:00Z","timestamp":1336435200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/2.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Neuroinflammation"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>\nAbstract\n<\/jats:title>\n          <jats:sec>\n            <jats:title>\nBackground<\/jats:title>\n            <jats:p>Histamine is commonly acknowledged as an inflammatory mediator in peripheral tissues, leaving its role in brain immune responses scarcely studied. Therefore, our aim was to uncover the cellular and molecular mechanisms elicited by this molecule and its receptors in microglia-induced inflammation by evaluating cell migration and inflammatory mediator release.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\nMethods<\/jats:title>\n            <jats:p>Firstly, we detected the expression of all known histamine receptor subtypes (H<jats:sub>1<\/jats:sub>R, H<jats:sub>2<\/jats:sub>R, H<jats:sub>3<\/jats:sub>R and H<jats:sub>4<\/jats:sub>R), using a murine microglial cell line and primary microglia cell cultures from rat cortex, by real-time PCR analysis, immunocytochemistry and Western blotting. Then, we evaluated the role of histamine in microglial cell motility by performing scratch wound assays. Results were further confirmed using murine cortex explants. Finally, interleukin-1beta (IL-1\u03b2) and tumor necrosis factor-alpha (TNF-\u03b1) levels were evaluated by ELISA measurements to determine the role of histamine on the release of these inflammatory mediators.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\nResults<\/jats:title>\n            <jats:p>After 12 h of treatment, 100 \u03bcM histamine and 10 \u03bcg\/ml histamine-loaded poly (lactic-<jats:italic>co<\/jats:italic>-glycolic acid) microparticles significantly stimulated microglia motility via H<jats:sub>4<\/jats:sub>R activation. In addition, migration involves \u03b15\u03b21 integrins, and p38 and Akt signaling pathways. Migration of microglial cells was also enhanced in the presence of lipopolysaccharide (LPS, 100 ng\/ml), used as a positive control. Importantly, histamine inhibited LPS-stimulated migration <jats:italic>via<\/jats:italic> H<jats:sub>4<\/jats:sub>R activation. Histamine or H<jats:sub>4<\/jats:sub>R agonist also inhibited LPS-induced IL-1\u03b2 release in both N9 microglia cell line and hippocampal organotypic slice cultures.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\nConclusions<\/jats:title>\n            <jats:p>To our knowledge, we are the first to show a dual role of histamine in the modulation of microglial inflammatory responses. Altogether, our data suggest that histamine per se triggers microglia motility, whereas histamine impedes LPS-induced microglia migration and IL-1\u03b2 release. This last datum assigns a new putative anti-inflammatory role for histamine, acting via H<jats:sub>4<\/jats:sub>R to restrain exacerbated microglial responses under inflammatory challenge, which could have strong repercussions in the treatment of CNS disorders accompanied by microglia-derived inflammation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1742-2094-9-90","type":"journal-article","created":{"date-parts":[[2012,5,8]],"date-time":"2012-05-08T16:27:35Z","timestamp":1336494455000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":107,"title":["Histamine modulates microglia function"],"prefix":"10.1186","volume":"9","author":[{"given":"Raquel","family":"Ferreira","sequence":"first","affiliation":[]},{"given":"Tiago","family":"Santos","sequence":"additional","affiliation":[]},{"given":"Joana","family":"Gon\u00e7alves","sequence":"additional","affiliation":[]},{"given":"Gra\u00e7a","family":"Baltazar","sequence":"additional","affiliation":[]},{"given":"Lino","family":"Ferreira","sequence":"additional","affiliation":[]},{"given":"Fabienne","family":"Agasse","sequence":"additional","affiliation":[]},{"given":"Liliana","family":"Bernardino","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2012,5,8]]},"reference":[{"key":"585_CR1_585","doi-asserted-by":"publisher","first-page":"127","DOI":"10.1007\/s11481-006-9015-5","volume":"1","author":"G Garden","year":"2006","unstructured":"Garden G, M\u00f6ller T: Microglia biology in health and disease. \n                           J Neuroimmune Pharmacol 2006, 1:127\u2013137.","journal-title":"J Neuroimmune Pharmacol"},{"key":"585_CR2_585","doi-asserted-by":"publisher","first-page":"57","DOI":"10.1038\/nrn2038","volume":"8","author":"ML Block","year":"2007","unstructured":"Block ML, Zecca L, Hong J-S: Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. \n                           Nat Rev Neurol 2007, 8:57\u201369.","journal-title":"Nat Rev Neurol"},{"key":"585_CR3_585","doi-asserted-by":"publisher","first-page":"13","DOI":"10.1016\/S0889-1591(02)00055-7","volume":"17","author":"S Rivest","year":"2003","unstructured":"Rivest S: Molecular insights on the cerebral innate immune system. \n                           Brain Behav Immun 2003, 17:13\u201319.","journal-title":"Brain Behav Immun"},{"key":"585_CR4_585","first-page":"885","volume":"420","author":"J Cohen","year":"2002","unstructured":"Cohen J: The immunopathogenesis of sepsis. 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