Authors
Qianrui Zeng, Chi Zhang, Na Xie, Shutong Chen, Chang Liu, Haodang Luo, Xiaoxing You
Published in
Journal of neuroinflammation. Jul 17, 2026. Epub Jul 17, 2026.
Abstract
Integrating physicochemical environmental cues with pathogen detection is essential for an effective and balanced host defense. While Toll-like receptors (TLRs) detect pathogen-associated molecular patterns (PAMPs), transient receptor potential (TRP) ion channels detect specific physicochemical shifts characteristic of inflamed tissues, including extracellular acidosis, hyperosmolarity, oxidative stress, and mechanical perturbations of the lipid bilayer. Emerging evidence indicates that these two sensory systems interact via a bidirectional signaling axis. This review summarizes recent advances in the molecular mechanisms of TRP-TLR crosstalk, focusing on the three principal modes: direct physical coupling, indirect functional coupling via second messengers, and spatial co-organization within membrane microdomains. We examine how TLR signaling regulates TRP channel expression and post-translational modification. Reciprocally, we detail how TRP-mediated ionic fluxes modulate TLR ligand recognition, signal amplification, and effector functions, including phagocytosis and cytokine secretion. Crucially, we illustrate how the dysregulation of this subcellular crosstalk scales up to drive tissue pathologies, including neuropathic pain sensitization, central neuroinflammation, and barrier organ dysfunction. The TRP-TLR axis represents a convergence of immune and sensory signaling. Understanding this interaction provides a basis for identifying novel therapeutic targets for infectious and inflammatory diseases.
PMID:
42469855
Bibliographic data and abstract were imported from PubMed on 18 Jul 2026.
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