Inflammation and fibrosis

• Published in: Matrix biology Vol. 68-69; pp. 106 - 121
• Main Author: Mack, Matthias
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.08.2018; Elsevier Science Ltd
• Subjects: Animals; Cells; Cytokines - metabolism; Extracellular matrix; Fibroblasts; Fibrocytes; Fibrosis; Fibrosis - metabolism; Fibrosis - pathology; Humans; Immune system; Inflammation; Inflammation - metabolism; Inflammation - pathology; Leukocytes (basophilic); Leukocytes (eosinophilic); Lymphocytes - metabolism; Lymphocytes T; Lymphoid cells; Macrophages; Macrophages - metabolism; Mesenchyme; Monocytes; Regeneration; Signal Transduction; Tissue damage; Tissue engineering; CXCL; Tissue damage; IL; TSLP; Fibrocytes; Inflammation; CCL; TNF; PBMC; IFN; MMP; CCR; GM-CSF; PDGF; Fibrosis; CXCR
• ISSN: 0945-053X; 1569-1802
• DOI: 10.1016/j.matbio.2017.11.010

Tissue damage and inflammation are important triggers for regeneration and fibrosis. Tissue damage not only induces inflammation in general, it also determines the type and polarization of inflammation by recruiting and activating a variety of different cells types of the innate and adaptive immune system. This review focuses on the pathways leading from tissue damage to inflammation, from inflammation to fibrosis and from fibrosis to function. It covers the pro- and antifibrotic properties of immunological mediators released from T cells, monocytes/macrophages, innate lymphoid cells, basophils and eosinophils and takes into account that extracellular matrix proteins are not only produced by mesenchymal fibroblasts but also by other cell types, especially infiltrating hematopoietic cells. The special requirements for activation and recruitment of these so called fibrocytes are described in detail. •Covers the pathways from tissue damage to inflammation, from inflammation to fibrosis and from fibrosis to function•Covers the pro- and antifibrotic properties of immune cells and their mediators•Covers the special requirements for activation and recruitment of collagen-producing hematopoietic cells (fibrocytes)