Abstract
Human fibrocytes are bone marrow-derived mesenchymal progenitor cells that express a variety of markers related to leukocytes, hematopoietic stem cells and a diverse set of fibroblast phenotypes. Fibrocytes can be recruited from the circulation to the tissue where they further can differentiate and proliferate into various mesenchymal cell types depending on the tissue niche. This local tissue niche is important because it modulates the fibrocytes and coordinates their role in tissue behaviour and repair. However, plasticity of a niche may be co-opted in chronic airway diseases such as asthma, idiopathic pulmonary fibrosis and obliterative bronchiolitis. This review will therefore focus on a possible role of fibrocytes in pathological tissue repair processes in those diseases.
Highlights
Tissue repair and remodelling are ongoing processes in all types of wound healing
Tissue repair in lung disorders Today, both fibrocytes and fibroblasts are known to be important in wound healing as extracellular matrix (ECM)-producing cells that function in response to injury
In idiopathic pulmonary fibrosis (IPF), there is a correlation between the number of fibrocytes in the tissue and the number of fibroblastic foci
Summary
Tissue repair and remodelling are ongoing processes in all types of wound healing. In healthy subjects, the primary role of the extracellular matrix (ECM) is to provide tissues with specific mechanical properties and to serve as a structural framework for cell attachment and migration. The CXCR4-expressing fibrocytes are recruited from the circulation to the tissue by a gradient of stromal cell-derived factor (SDF)-1/CXCL12. Tissue repair in lung disorders Today, both fibrocytes and fibroblasts are known to be important in wound healing as ECM-producing cells that function in response to injury. The tissue process starts with lymphocyte infiltration in the submucosa and injury of the mucosa and epithelial cell layer, and that results in recruitment of ECM-producing fibroblasts or their progenitor cells, such as fibrocytes. The remodelled vessels, with enlarged lumen and greater endothelial cell area, that are identified in patients with OB after lung or bone marrow transplantation could be a result of local hypoxia. It is possible that this cell population is of fibrocytic origin but has differentiated because of the local environment in the IPF lung, and for this reason does not express CXCR4 (Figure 1). The pathophysiological obliteration of the small airways probably makes it difficult for fibrocytes to migrate to the lumen, at least in the occluded part of the lung
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