Abstract
Mast cells (MCs) play an important role in allergic hyperresponsiveness and in defending microorganism infections. Recent studies of experimental animals and humans have suggested that MCs participate in obesity and diabetes. MC distribution and activities in adipose tissues may vary, depending on the locations of different adipose tissues. In addition to releasing inflammatory mediators to affect adipose tissue extracellular matrix remodeling and to promote inflammatory cell recruitment and proliferation, MCs directly and indirectly interact and activate adipose tissue cells, including adipocytes and recruited inflammatory cells. Plasma MC protease levels are significantly higher in obese patients than in lean subjects. Experimental obese animals lose body weight after MC inactivation. MC functions in diabetes are even more complicated, and depend on the type of diabetes and on different diabetic complications. Both plasma MC proteases and MC activation essential immunoglobulin E levels are significant risk factors for human pre-diabetes and diabetes mellitus. MC stabilization prevents diet-induced diabetes and improves pre-established diabetes in experimental animals. MC depletion or inactivation can improve diet-induced type 2 diabetes and some forms of type 1 diabetes, but also can worsen other forms of type 1 diabetes, at least in experimental animals. Observations from animal and human studies have suggested beneficial effects of treating diabetic patients with MC stabilizers. Some diabetic patients may benefit from enhancing MC survival and proliferation – hypotheses that merit detailed basic researches and clinical studies.
Highlights
Mast cells (MCs) are inflammatory cells similar to macrophages, neutrophils, and lymphocytes, but they localize near surfaces exposed to the environment – such as the skin, airway, and gastrointestinal tract, where pathogens, allergens, and other environment agents frequently reside (Metcalfe et al, 1997; Galli et al, 2005a)
We recently showed that CD8+ T cells and MCs localize together in mouse visceral white adipose tissue (WAT) (Xu and Shi, 2012)
We have shown that MC inactivation reduces macrophage infiltration to WAT (Liu et al, 2009)
Summary
Mast cells (MCs) are inflammatory cells similar to macrophages, neutrophils, and lymphocytes, but they localize near surfaces exposed to the environment – such as the skin, airway, and gastrointestinal tract, where pathogens, allergens, and other environment agents frequently reside (Metcalfe et al, 1997; Galli et al, 2005a). Obesity and diabetes are considered chronic inflammatory diseases, largely due to several recent seminal discoveries of inflammatory cells in WAT – including macrophages (Ochi et al, 1988; Weisberg et al, 2003; Xu et al, 2003), B cells (Winer et al, 2011), CD4+ T cells (Winer et al, 2009), CD8+ T cells (Nishimura et al., 2009), regulatory T cells (Treg; Feuerer et al, 2009), NK T cells (Ohmura et al, 2010), eosinophils (Wu et al, 2011), and MCs (Liu et al, 2009) These cells may interact directly through cell–cell contact, or indirectly by releasing cell mediators within adipose tissue. Mouse inguinal fat pads contain c-Kit+Thy1loLin−Sca+ cells, which can differentiate into other cell types in vitro, such as functional mucosal MCs (Poglio et al, 2010)
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