ArticleScientific reports2023
Myeloid deletion of talin-1 reduces mucosal macrophages and protects mice from colonic inflammation.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Integrative Proteomics and Phosphoproteomics Profiling of Chronic Enteropathy Associated withBiomedicines · 2026Article
- Targeting Talin1 to reprogram dendritic cell activation landscapes: A mechanistically grounded cell therapy for multiple sclerosis model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Advanced N-glycoproteomics and proteomics approach revealed sexually dimorphic molecular signatures in primary mouse hepatocyte.Analytical and bioanalytical chemistry · 2025Article
- Aconitate Decarboxylase 1 Downregulates Colitis and Maintains Homeostasis of the Gut Metabolome and Microbiome.Gastro hep advances · 2025Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
The intestinal immune response is crucial in maintaining a healthy gut, but the enhanced migration of macrophages in response to pathogens is a major contributor to disease pathogenesis. Integrins are ubiquitously expressed cellular receptors that are highly involved in immune cell adhesion to endothelial cells while in the circulation and help facilitate extravasation into tissues. Here we show that specific deletion of the Tln1 gene encoding the protein talin-1, an integrin-activating scaffold protein, from cells of the myeloid lineage using the Lyz2-cre driver mouse reduces epithelial damage, attenuates colitis, downregulates the expression of macrophage markers, decreases the number of differentiated colonic mucosal macrophages, and diminishes the presence of CD68-positive cells in the colonic mucosa of mice infected with the enteric pathogen Citrobacter rodentium. Bone marrow-derived macrophages lacking expression of Tln1 did not exhibit a cell-autonomous phenotype; there was no impaired proinflammatory gene expression, nitric oxide production, phagocytic ability, or surface expression of CD11b, CD86, or major histocompatibility complex II in response to C. rodentium. Thus, we demonstrate that talin-1 plays a role in the manifestation of infectious colitis by increasing mucosal macrophages, with an effect that is independent of macrophage activation.
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Registered trials
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