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. 2020 Dec 1;52(12):1871–1878. doi: 10.1038/s12276-020-00531-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — The damaged epithelium in diseased alveoli upregulates IL-11 and other factors, which in turn cause epithelial dysfunction by inducing epithelial–mesenchymal transition and senescence. Injury signals from the injured epithelium, including IL-11 itself, trigger IL-11 secretion from fibroblasts. IL-11 then acts in an autocrine/paracrine manner to drive/amplify profibrotic fibroblast effector functions, including proliferation, migration, invasion, and myofibroblast differentiation, via an ERK-dependent mechanism. IL-11-stimulated fibroblasts and myofibroblasts also acquire resistance to apoptosis and secrete extracellular matrix components, along with proinflammatory cytokines/chemokines (e.g., IL-6, CCL2, CXCL1), leading to the recruitment and activation of immune cells to the injury site. Inflammation perpetuates a vicious profibrotic loop that further activates fibroblasts. IL-11 expressed by fibroblasts may also contribute to paracrine activation of epithelial cells, causing chronic epithelial dysfunction and impaired regeneration.