ArticleFrontiers in physiology2026
Toll-like receptor 2 coordinates induction of IL-22 in lung macrophages following organic dust-induced inflammation.
Article in Frontiers in physiology, 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: Organic dust exposures, particularly in occupational settings, induce airway inflammation and contribute to the development and progression of chronic lung disease and impaired tissue regeneration. Interleukin-22 (IL-22) is a pleiotropic cytokine recognized for maintaining epithelial barrier integrity and promoting tissue repair; however, its regulation in lung myeloid cells, particularly macrophages, remains poorly understood. Toll-like receptor 2 (TLR2), a pattern recognition receptor highly expressed on lung macrophages, recognizes bacterial components abundant in organic dust and drives inflammatory signaling. We investigated the mechanistic role of TLR2 signaling in regulating IL-22 production by lung macrophages following exposure to microbial-enriched agricultural organic dust extract (DE). Methods: An immortalized lung macrophage cell line (MH-S) was stimulated with selective Toll-like receptor agonists and pharmacologic inhibitors to determine the contribution of individual TLR pathways to IL-22 production. To examine the role of TLR2 Results: TLR2 stimulation preferentially induced IL-22 production compared with other TLR pathways while simultaneously coordinating pro-inflammatory cytokine responses. Activation of the TLR2/1 heterodimer, but not TLR2/6, significantly increased IL-22 production, indicating pathway-specific regulation of reparative signaling. In vivo, repeated DE exposure resulted in significantly reduced pulmonary IL-22 expression in Discussion/Conclusion: These findings identify TLR2 as a critical regulator of IL-22-mediated reparative programming in lung macrophages following organic dust exposure. Our study reveals a previously unrecognized link between innate immune sensing and epithelial repair pathways, providing mechanistic insight into how TLR2 promotes tissue restoration after environmental lung injury. Targeting the TLR2-IL-22 axis may represent a promising therapeutic strategy for mitigating occupational dust-induced lung damage.
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