Mesothelium derives from the embryonic mesoderm cell layer, that lines the coelom in the embryo. It develops into the layer of cells that covers and protects most of the internal organs of the body.
The mesothelium is composed of an extensive monolayer of specialized cells that line the body's serous cavities and internal organs. The main purpose of these cells is to produce a lubricating fluid that is released between layers, providing a slippery, non-adhesive, and protective surface to facilitate intracoelomic movement. The mesothelium is also implicated in the transport and movement of fluid and particulate matter across the serosal cavities, leukocytemigration in response to inflammatory mediators, synthesis of pro-inflammatory cytokines, growth factors, and extracellular matrix proteins to aid in serosal repair, and the release of factors to promote the disposition and clearance of fibrin. Mesothelial cells are capable of phagocytosis and are antigen-presenting cells. Furthermore, the secretion of glycosaminoglycans and lubricants may protect the body against infection and tumor dissemination.
Role in disease
Mesothelioma: is a disease in which cells of the mesothelium become abnormal and divide without control or order. They can invade and damage nearby tissues and organs. Cancer cells can also metastasize from their original site to other parts of the body. Most cases of mesothelioma begin in the pleura or peritoneum. More than 90% of mesothelioma cases are linked to asbestos exposure.
Mesothelial hyperplasia
Intra-abdominal adhesions: Normally, the mesothelium secretes plasminogen, which removes fibrin deposits. During surgical procedures, the mesothelium may be damaged. Its fibrinolytic capacity becomes insufficient and fibrin accumulates, causing fibrous adhesions between opposing surfaces. These adhesions cause intestinal obstruction and female infertility if it occurs in the abdomen, and may impair cardiac and lung function in the thorax.
Ultrafiltration failure: The peritoneal mesothelium is implicated in the long-term development of ultrafiltration failure in peritoneal dialysis patients. The presence of supra-physiological glucose concentrations, acidity, and glucose degradation products in peritoneal dialysis fluids contribute to the fibrosis of the peritoneal mesothelium, either by epithelial–mesenchymal transition or increased proliferation of existing fibroblasts. A fibrosed peritoneum results in the increased passage of solutes across the peritoneum and ultrafiltration failure.
