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Epithelial cells secrete chloride to regulate water release at mucosal barriers.
Epithelial tuft cells in the small intestine:
* Sense helminths.
Tuft cell activation rapidly induced epithelial chloride secretion in the small intestine.
This response required: Tuft cell-derived acetylcholine (ACh). ACh acted directly on neighboring epithelial cells to stimulate chloride secretion. Independently of neurons.
Tuft cells can also synthesize cysteinyl leukotrienes to boost immunity against helminth infections
During helminth infection, Interleukin-25 (IL-25) produced by tuft cells also activates Group 2 ILCs (ILC2) to secrete Interleukin-13 (IL-13), which triggers an immune response against parasites. The tuft cell-ILC2 circuit promotes intestinal remodeling and mediates type 2 immunity to parasite clearance.
Infections with Helminths Increased Tuft Cell Abundance, Indicating that Expansion of Tuft Cells Is a Broadly Conserved Feature of Parasite Colonization
When helminths or protozoa are present in the gut, they stimulate tuft cells to secrete the alarmin cytokine interleukin-25 (IL-25), which then triggers a Type 2 immune response.
The response is mainly driven by Group 2 ILCs (ILC2), which secrete type 2 cytokines like Interleukin-4 (IL-4), Interleukin-5 (IL-5), and Interleukin-13 (IL-13). A significant role of IL-4 and IL-13 is the extensive remodeling they induce in the intestinal epithelium. This remodeling involves an increase in mucus-producing goblet cells and tuft cell lineages, along with the unusual expression of resistin-like beta (Retnlb) by small intestinal goblet cells, where it is typically not present.
see also:
Goblet cells & Mucus
Group 2 ILCs (ILC2) & Helminth Infections / Helminthiasis
Group 2 ILCs (ILC2) & Interleukin-4 (IL-4)
Group 2 ILCs (ILC2) & Interleukin-17E (IL-17E) / Interleukin-25 (IL-25)
Interleukin-13 (IL-13) & Intestinal Mucosal Barrier / Mucus Layer
Interleukin-13 (IL-13) & Tuft Cells
Interleukin-17E (IL-17E) / Interleukin-25 (IL-25) & Tuft Cells