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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: Alcohol Clin Exp Res. 2019 Jun 3;43(7):1427–1438. doi: 10.1111/acer.14110

Figure 10. Hypothesis schematic showing the effects of IL-17 on myofibroblast development in chronic alcohol ingestion.

Figure 10.

In the current study, we showed that in the otherwise healthy animals, chronic alcohol ingestion increased systemic Th17 immune response. Acute injury caused a persistent increase in IL-17 in the lung. Alcohol, IL-17, and TGFβ1 independently inhibited Thy-1 expression by lung fibroblasts and IL-17 and TGFβ1 additively decreased Thy-1 expression leading to myofibroblast differentiation. We believe this sequence of events is one of the mechanisms by which alcohol induces fibroproliferative disrepair following acute lung injury.