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Increased IL-6 and Potential IL-6 trans-signalling in the airways after an allergen challenge. | LitMetric

AI Article Synopsis

  • IL-6 is implicated in asthma by driving inflammation and airway dysfunction, regulated by its receptor components IL-6R and GP130, which exist in both membrane and soluble forms.
  • The study analyzed changes in IL-6 signalling proteins in the airways of allergy sufferers before and after exposure to an allergen, using various laboratory methods for protein and gene expression analysis.
  • Results showed increases in IL-6, sIL-6R, and sGP130 in the airways post-allergen challenge, indicating enhanced IL-6 trans-signalling activity, which may lead to increased production of inflammatory markers like MCP-1 by bronchial fibroblasts.

Article Abstract

Background: In asthma, IL-6 is a potential cause of enhanced inflammation, tissue damage and airway dysfunction. IL-6 signalling is regulated by its receptor, which is composed of two proteins, IL-6R and GP130. In addition to their membrane form, these two proteins may be found as extracellular soluble forms. The interaction of IL-6 with soluble IL-6R (sIL-6R) can trigger IL-6 trans-signalling in cells lacking IL-6R. Conversely, the soluble form of GP130 (sGP130) competes with its membrane form to inhibit IL-6 trans-signalling.

Objectives: We aimed to analyse IL-6 trans-signalling proteins in the airways of subjects after an allergen challenge.

Methods: We used a model of segmental bronchoprovocation with an allergen (SBP-Ag) in human subjects with allergy. Before and 48 h after SBP-Ag, bronchoalveolar lavages (BALs) allowed for the analysis of proteins in BAL fluids (BALFs) by ELISA, and membrane proteins on the surface of BAL cells by flow cytometry. In addition, we performed RNA sequencing (RNA-seq) and used proteomic data to further inform on the expression of the IL-6R subunits by eosinophils, bronchial epithelial cells and lung fibroblasts. Finally, we measured the effect of IL-6 trans-signalling on bronchial fibroblasts, in vitro.

Results: IL-6, sIL-6R, sGP130 and the molar ratio of sIL-6R/sGP130 increased in the airways after SBP-Ag, suggesting the potential for enhanced IL-6 trans-signalling activity. BAL lymphocytes, monocytes and eosinophils displayed IL-6R on their surface and were all possible providers of sIL-6R, whereas GP130 was highly expressed in bronchial epithelial cells and lung fibroblasts. Finally, bronchial fibroblasts activated by IL-6 trans-signalling produced enhanced amounts of the chemokine, MCP-1 (CCL2).

Conclusion And Clinical Relevance: After a bronchial allergen challenge, we found augmentation of the elements of IL-6 trans-signalling. Allergen-induced IL-6 trans-signalling activity can activate fibroblasts to produce chemokines that can further enhance inflammation and lung dysfunction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8020336PMC
http://dx.doi.org/10.1111/cea.13832DOI Listing

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