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To investigate interactions between common\n PD<\/jats:styled-content>\n mutations and immune responses to environmental pathogens, we studied responses to\n Pseudomonas aeruginosa<\/jats:italic>\n (\n P. aeruginosa<\/jats:italic>\n ) in peripheral blood mononuclear cells (\n PBMCs<\/jats:styled-content>\n ) from\n PD<\/jats:styled-content>\n patients with\n leucine\u2010rich repeat kinase 2<\/jats:italic>\n (\n \n LRRK2<\/jats:italic>\n )\n <\/jats:styled-content>\n mutations,\n \n GBA1<\/jats:italic>\n <\/jats:styled-content>\n mutations, and idiopathic disease (\n iPD<\/jats:styled-content>\n ) relative to neurologically healthy controls (\n NHC<\/jats:styled-content>\n ).\n <\/jats:p>\n <\/jats:sec>\n \n Objectives<\/jats:title>\n \n The goal was to test the hypothesis that\n \n LRRK2<\/jats:italic>\n <\/jats:styled-content>\n and\n \n GBA<\/jats:italic>\n <\/jats:styled-content>\n modify the human peripheral immune response to bacteria, specifically\n P. aeruginosa<\/jats:italic>\n , based on prior animal studies involving\n Lrrk2<\/jats:italic>\n mutations and microbial pathogens.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n PBMCs<\/jats:styled-content>\n from\n \n LRRK2<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD<\/jats:styled-content>\n ,\n \n GBA<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD<\/jats:styled-content>\n , and\n iPD<\/jats:styled-content>\n patients plus age\u2010 and sex\u2010matched controls were treated ex vivo with live\n P. aeruginosa<\/jats:italic>\n and pharmacological agents that block\n LRRK2<\/jats:styled-content>\n kinase activity (\n MLi<\/jats:styled-content>\n \u20102) or enhance glucocerebrosidase (\n GCase<\/jats:styled-content>\n ) activation (\n NCGC00188758<\/jats:styled-content>\n ) to measure enzymatic activities and cytokine release.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n \n GBA<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD PBMCs<\/jats:styled-content>\n exhibited increased\n P. aeruginosa<\/jats:italic>\n \u2010dependent secretion of specific inflammatory cytokines including\n interleukin<\/jats:styled-content>\n \u20101\u03b2. Antigen presentation was increased in\n \n LRRK2<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD<\/jats:styled-content>\n nonclassical monocytes treated with the\n GCase<\/jats:styled-content>\n activator. Levels of\n pRab10<\/jats:styled-content>\n , a proxy for\n LRRK2<\/jats:styled-content>\n kinase activity, were increased in\n \n GBA<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD<\/jats:styled-content>\n classical monocytes relative to\n NHC<\/jats:styled-content>\n and\n iPD<\/jats:styled-content>\n .\n GCase<\/jats:styled-content>\n activator treatment increased\n pRab10<\/jats:styled-content>\n expression in\n \n LRRK2<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD<\/jats:styled-content>\n intermediate monocytes.\n \n GBA<\/jats:italic>\n <\/jats:styled-content>\n \u2010\n PD<\/jats:styled-content>\n and individual treatments with\n MLi<\/jats:styled-content>\n \u20102 or\n GCase<\/jats:styled-content>\n activator were associated with reduced\n P. aeruginosa<\/jats:italic>\n \u2010dependent\n LRRK2<\/jats:styled-content>\n protein levels in\n PBMC<\/jats:styled-content>\n subsets.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n This work demonstrates that\n PD<\/jats:styled-content>\n \u2010linked mutations in\n \n LRRK2<\/jats:italic>\n <\/jats:styled-content>\n and\n \n GBA1<\/jats:italic>\n <\/jats:styled-content>\n converge on peripheral blood immune cell dysregulation, as evinced by the ability of\n LRRK2<\/jats:styled-content>\n inhibitors and\n GCase<\/jats:styled-content>\n activators to modulate the ex vivo immune response to bacterial exposure. \u00a9 2025 The Author(s).\n Movement Disorders<\/jats:italic>\n published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/mds.70123","type":"journal-article","created":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T10:56:18Z","timestamp":1763549778000},"page":"651-666","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Parkinson's\u2010Linked\n LRRK2<\/i>\n and\n GBA1<\/i>\n Mutations Modulate the 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