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Brain tissue-resident memory T cells (bT<jats:sub>RM<\/jats:sub>) are recruited during central nervous system infection and promote pathogen control as well as noxious inflammation. Our prior studies in young mice showed optimal recruitment of CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub> during neuroinvasive <jats:italic>Listeria monocytogenes<\/jats:italic> (<jats:italic>Lm<\/jats:italic>) infection required miR-155, and was significantly inhibited by anti-miR-155 oligonucleotides. Since <jats:italic>Lm<\/jats:italic> is an important pathogen in the elderly, we hypothesized anti-miR-155 would also inhibit accumulation of CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub> in aged mice infected with <jats:italic>Lm<\/jats:italic>.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Young (2 mo) and aged (&gt;\u200918 mo) male C57BL\/6 mice were infected intra-peritoneally with wild-type <jats:italic>Lm<\/jats:italic>, or avirulent <jats:italic>Lm<\/jats:italic> mutants lacking the genes required for intracellular motility (\u0394<jats:italic>actA<\/jats:italic>) or phagosomal escape (\u0394<jats:italic>hly<\/jats:italic>), then were given antibiotics. Brain leukocytes and their intracellular cytokine production were quantified by flow cytometry <jats:underline>&gt;<\/jats:underline>28d post-infection (p.i.). The role of miR-155 was tested by injecting mice with anti-miR-155 or control oligonucleotides along with antibiotics.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Aged mice had significantly more homeostatic CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub> than did young mice, which did not increase after infection with wild-type <jats:italic>Lm<\/jats:italic> despite 50% mortality, whereas young mice suffered no mortality after a larger inoculum. For direct comparison of post-infectious neuroinflammation after the same inoculum, young and aged mice were infected with 10<jats:sup>7<\/jats:sup>\u2009CFU \u0394<jats:italic>actA Lm<\/jats:italic>. This mutant caused no mortality and significantly increased CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub> 28d p.i. in both groups, whereas bone marrow-derived myeloid cells, particularly neutrophils, increased only in aged mice. Notably, anti-miR-155 reduced accumulation of brain myeloid cells in aged mice after infection, whereas CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub> were unaffected.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Systemic infection with <jats:italic>Lm<\/jats:italic> \u0394<jats:italic>actA<\/jats:italic> is a novel model for studying infection-induced brain inflammation in aged mice without excessive mortality. CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub> increase in both young and aged mice after infection, whereas only in aged mice bone marrow-derived myeloid cells increase long-term. In aged mice, anti-miR-155 inhibits brain accumulation of myeloid cells, but not CD8<jats:sup>+<\/jats:sup> bT<jats:sub>RM<\/jats:sub>. These results suggest young and aged mice differ in manifestations and mechanisms of infection-induced neuroinflammation and give insight for developing therapies to ameliorate brain inflammation following severe infection in the elderly.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12979-022-00281-0","type":"journal-article","created":{"date-parts":[[2022,5,25]],"date-time":"2022-05-25T05:03:58Z","timestamp":1653455038000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Systemic Listeria monocytogenes infection in aged mice induces long-term neuroinflammation: the role of miR-155"],"prefix":"10.1186","volume":"19","author":[{"given":"Benjamin R.","family":"Cassidy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William E.","family":"Sonntag","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pieter J. 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