{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T01:12:21Z","timestamp":1792026741489,"version":"4.4.0"},"reference-count":295,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T00:00:00Z","timestamp":1773187200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neurol."],"abstract":"<jats:p>Bacterial infections of the central nervous system (CNS) are characterized by rapid and devastating neuroinflammation. While inflammation plays an important physiological role in defense against bacteria, such responses within the confines of the cranium can be lethal. Glial cells, including microglia and astrocytes, can perceive bacteria or their products and then respond in a manner that can promote inflammation, changes to blood\u2013brain barrier integrity, and recruit leukocytes into the CNS. In this review, we have summarized their ability to produce chemotactic factors in response to bacterial components and clinically relevant bacterial pathogens of the CNS. Importantly, we have highlighted the fact that the chemotactic factors produced by bacterially challenged glia tend to preferentially recruit neutrophils, and we have described how such cells could then respond to the presence of bacteria to further promote glial activation and their own recruitment. This then, could form a vicious cycle that precipitates the rapid inflammatory CNS damage associated with bacterial infection. However, it is also becoming apparent that glia, and perhaps neutrophils, can adjust their responses to bacteria temporally in such a way as to break this positive feedback loop, and we have described the available evidence for the delayed production for anti-inflammatory mediators by these cells following challenge. Finally, we have discussed the present limitations in our understanding of these cell\u2013cell interactions and their study that must be overcome before we can manipulate such a glia-neutrophil axis for therapeutic purposes.<\/jats:p>","DOI":"10.3389\/fneur.2026.1765892","type":"journal-article","created":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T05:37:18Z","timestamp":1773207438000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["The glia-neutrophil axis: an understudied crosstalk in bacteria-induced neuroinflammation"],"prefix":"10.3389","volume":"17","author":[{"given":"Andrew M.","family":"Dunphy","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, University of North Carolina at Charlotte","place":["Charlotte, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian","family":"Marriott","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of North Carolina at Charlotte","place":["Charlotte, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,11]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"830","DOI":"10.1002\/glia.23726","article-title":"Pathology of inflammatory diseases of the nervous system: human disease versus animal models","volume":"68","author":"Lassmann","year":"2020","journal-title":"Glia"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"e1010234","DOI":"10.1371\/journal.ppat.1010234","article-title":"Pathogens infecting the central nervous system","volume":"18","author":"Le Govic","year":"2022","journal-title":"PLoS Pathog"},{"key":"ref3","doi-asserted-by":"publisher","first-page":"e2424802","DOI":"10.1001\/jamanetworkopen.2024.24802","article-title":"Global case fatality of bacterial meningitis during an 80-year period: a systematic review and Meta-analysis","volume":"7","author":"van Ettekoven","year":"2024","journal-title":"JAMA Netw Open"},{"key":"ref4","doi-asserted-by":"publisher","first-page":"21","DOI":"10.1002\/ana.25389","article-title":"Lyme Neuroborreliosis: clinical outcomes, controversy, pathogenesis, and Polymicrobial infections","volume":"85","author":"Garcia-Monco","year":"2019","journal-title":"Ann Neurol"},{"key":"ref5","doi-asserted-by":"publisher","first-page":"947","DOI":"10.1097\/INF.0000000000001603","article-title":"Staphylococcus aureus central nervous system infections in children","volume":"36","author":"Vallejo","year":"2017","journal-title":"Pediatr Infect Dis J"},{"key":"ref6","doi-asserted-by":"publisher","first-page":"127","DOI":"10.1186\/s12974-023-02817-7","article-title":"Lung infection by Pseudomonas aeruginosa induces neuroinflammation and blood-brain barrier dysfunction in mice","volume":"20","author":"Villalba","year":"2023","journal-title":"J Neuroinflammation"},{"key":"ref7","doi-asserted-by":"crossref","first-page":"1343503","DOI":"10.3389\/fimmu.2023.1343503","article-title":"Bystander activation of microglia by Brucella abortus-infected astrocytes induces neuronal death via IL-6 trans-signaling","volume":"14","author":"Rodriguez","year":"2023","journal-title":"Front Immunol"},{"key":"ref8","doi-asserted-by":"crossref","first-page":"163","DOI":"10.1186\/s12974-014-0163-x","article-title":"Neisseria meningitidis elicits a pro-inflammatory response involving IkappaBzeta in a human blood-cerebrospinal fluid barrier model","volume":"11","author":"Borkowski","year":"2014","journal-title":"J Neuroinflammation"},{"key":"ref9","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1007\/978-1-61779-346-2_1","article-title":"Neisseria meningitidis: biology, microbiology, and epidemiology","volume":"799","author":"Rouphael","year":"2012","journal-title":"Methods Mol Biol"},{"key":"ref10","doi-asserted-by":"crossref","first-page":"347","DOI":"10.1172\/JCI2406","article-title":"Pneumococcal trafficking across the blood-brain barrier. 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