Title : Role of mast cells in infection and inflammation
Abstract:
Mast cells (MCs) originate from CD34+/CD117+/CD13+ pluripotent hematopoietic stem cells and they express the c-Kit receptor (c-Kit-R) which regulates their proliferation and sustains their survival, differentiation, and maturation. MCs are immune tissue cells derived from bone marrow that are present in all vascularized tissues and play active roles in processes and reactions relating to infection and inflammation. MCs are also involved in innate and adaptive immunity, autoimmunity, and cancer. These cells have a dual role in infection; they can be beneficial for infection by acting as immune cells, or they can cause harm by producing inflammatory cytokines such as tumor necrosis factor (TNF), IL-1, and IL-6. Since MCs release an exaggerated amount of pro-inflammatory cytokines in inflammation, inhibiting the production of MC compounds may represent a promising approach and a new therapeutic strategy that can be complementary to the traditional procedures used today. In infection, MCs can be activated through mRNA and release inflammatory cytokines, without degranulation. MCs can be recruited into inflamed tissue by diverse chemotactic molecules, including vascular endothelial growth factor (VEGF), stem cell factor (SCF), and several CC and CXC chemokines produced by activated immune cells. MCs are known to mediate endothelial cell activation, resulting in inflammatory disorders. The role of MCs in infectious diseases has been extensively studied and reported in the scientific literature and it is of great clinical interest. Here, we report the role of MCs and their generation of inflammatory cytokines in infections and suggest that blocking MC cytokine production by anti-inflammatory cytokines could be a new strategy for therapy.
