ArticleJournal of inflammation research2026
From Bibliometrics to Preliminary Clinical Evidence: TRP Channel-Mediated Neuroimmune Crosstalk in Temperature-Sensitive Airway Hyperresponsiveness.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Temperature variability is a critical environmental trigger for airway hyperresponsiveness (AHR); however, the specific neuroimmune mechanisms linking thermal stress to respiratory inflammation remain underexplored. Methods: We integrated a macroscopic bibliometric analysis of the global literature (1925-2024) with an exploratory clinical validation. To corroborate emergent bibliometric trends, nasal mucosal biopsies were collected from patients with temperature-sensitive AHR (n=9) and normal controls (NC, n=9). The localized expression of transient receptor potential (TRP) channels (TRPV1, TRPM8, and TRPA1) was evaluated using reverse transcription-quantitative PCR (RT-qPCR) and semi-quantitative immunohistochemistry (IHC). Furthermore, local neuroimmune interactions were assessed by evaluating the spatial co-localization of TRP channels with substance P (SP) via immunofluorescence (IF) and semi-quantitative analysis. Results: Bibliometric mapping revealed a progressive paradigm shift from broad epidemiological associations toward specific molecular mechanisms, identifying TRP channels as central research hotspots. In the exploratory clinical cohort, both RT-qPCR and IHC analyses confirmed that TRPV1, TRPM8, and TRPA1 were significantly upregulated in the nasal mucosa of AHR patients compared to controls (all FDR-adjusted q < 0.05, supported by large effect sizes). Additionally, IF imaging demonstrated robust spatial co-localization of these overexpressed TRP channels with SP, structurally supporting the presence of local neurogenic inflammation. Conclusion: By bridging bibliometric trends with experimental corroboration, this study highlights TRP channels as pivotal "thermosensory switches" in AHR neuroimmune crosstalk. These findings provide preliminary clinical evidence that TRP-mediated pathways may drive the transition from external thermal fluctuations to mucosal inflammatory cascades. Given the exploratory nature of the current cohort size, our results offer a targeted biomolecular framework for future large-scale investigations into climate-sensitive respiratory diseases.
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