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The pro-apoptotic Bcl-2 family protein, Bim, is an important regulator of apoptosis. In this study we investigated the effect of Bim expression on post-stroke functional outcomes, brain injury and inflammatory mechanisms. Wild type (WT) and Bim-deficient mice underwent 1-h middle cerebral artery occlusion (MCAO) followed by 23\u00a0h of reperfusion. At 24-h post-stroke, we assessed functional deficit, infarct volume, immune cell death, as well as the number of infiltrating immune cells in the brain and circulating immune cells. Bim deficiency did not affect infarct volume (P\u2009&gt;\u20090.05), but resulted in less motor impairment (~\u2009threefold greater latency to fall in hanging grip strength test, P\u2009&lt;\u20090.05) and a lower median clinical score than WT mice (P\u2009&lt;\u20090.05). Additionally following MCAO, Bim-deficient mice exhibited fewer myeloid cells (particularly neutrophils) in the ischemic brain hemisphere and less apoptosis of CD3<jats:sup>+<\/jats:sup> T cells in the spleen and thymus compared with WT (all P\u2009&lt;\u20090.05). After MCAO, Bim-deficient mice also tended to have more M2-polarised macrophages in the brain than WT mice. In sham-operated mice, we found that Bim deficiency resulted in greater numbers of circulating total CD45<jats:sup>+<\/jats:sup> leukocytes, Ly6C<jats:sup>lo+<\/jats:sup> monocytes and CD3<jats:sup>+<\/jats:sup> T cells, although MCAO did not affect the number of circulating cells at 24\u00a0h in either genotype. Our findings suggest that Bim deficiency modulates post-stroke outcomes, including reductions in motor impairment, brain inflammation and systemic post-stroke leukocyte apoptosis. Bim could therefore serve as a potential therapeutic target for stroke.<\/jats:p>","DOI":"10.1007\/s12017-022-08703-4","type":"journal-article","created":{"date-parts":[[2022,2,11]],"date-time":"2022-02-11T18:02:41Z","timestamp":1644602561000},"page":"405-414","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Bim Deletion Reduces Functional Deficits Following Ischemic Stroke in Association with Modulation of Apoptosis and Inflammation"],"prefix":"10.1007","volume":"24","author":[{"given":"Jason A.","family":"Glab","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamsa","family":"Puthalakath","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenpeng R.","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antony","family":"Vinh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grant R.","family":"Drummond","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6525-9097","authenticated-orcid":false,"given":"Christopher G.","family":"Sobey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. Michael","family":"De Silva","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyun Ah","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,2,11]]},"reference":[{"issue":"5","key":"8703_CR1","doi-asserted-by":"publisher","first-page":"516","DOI":"10.1038\/nm.4068","volume":"22","author":"C Benakis","year":"2016","unstructured":"Benakis, C., Brea, D., Caballero, S., Faraco, G., Moore, J., Murphy, M., Sita, G., Racchumi, G., Ling, L., Pamer, E. G., Iadecola, C., & Anrather, J. (2016). Commensal microbiota affects ischemic stroke outcome by regulating intestinal gammadelta T cells. 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