Protocols for Pei and Oliveira et al. "LRRK2 G2019S mutation incites increased cell-intrinsic neutrophil effector functions and intestinal inflammation in a model of infectious colitis." V.2
Collection Citation: Jessica Pei, Nathalia L. Oliveira, Sherilyn Junelle Recinto, Alexandra Kazanova, Ziyi Li, Katalina Couto, Susan Westfall, Ahmed Fahmy, Celso M. Queiroz-Junior, Ajitha Thanabalasuriar 2025. Protocols for Pei and Oliveira et al. "LRRK2 G2019S mutation incites increased cell-intrinsic neutrophil effector functions and intestinal inflammation in a model of infectious colitis.". protocols.io https://dx.doi.org/10.17504/protocols.io.bp2l6y5ervqe/v2Version created by Jessica Pei
License: This is an open access collection distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Parkinson’s Disease (PD) is a neurodegenerative disorder often preceded by gastrointestinal dysfunction. Mutations in leucine-rich repeat kinase 2 (LRRK2) are known risk factors for both PD and inflammatory bowel disease (IBD), suggesting a link between PD and the gastrointestinal tract. Using single cell RNA-sequencing and spectral flow cytometry, we demonstrated that the LRRK2 Gly2019Ser (G2019S) mutation is associated with an increased neutrophil presence in the colonic lamina propria during Citrobacter rodentium infection. This concurred with a Th17 skewing, upregulated Il17-a,and greater colonic pathology during infection. In vitro experiments showed enhanced kinase-dependent neutrophil chemotaxis and neutrophil extracellular trap (NET) formation in LRRK2 G2019S mice compared to wild-type counterparts. Our results add to the understanding of LRRK2-driven immune cell dysregulation and its contribution to PD, offering insights into potential biomarkers for early diagnosis and intervention in PD.
