Childhood Overweight is Associated with Increased Monocyte Concentration and Altered Subset Distribution

Childhood obesity rates have nearly tripled in the last 30 years. Obesity increases risk for chronic disease. While monocytes, cells of the innate immune system that are altered with obesity, are purported to play an integral role in the development of these chronic diseases, no research has focused on early phenotypic changes in monocytes of overweight children. Two monocytes subsets exist, classic and pro-inflammatory; alterations in number and distribution may be implicated in disease development in obesity. The purpose of this study was to examine the concentration and relative distribution of monocytes among “normal weight” (N=66) and “at risk for being overweight/overweight” (N=56) Mexican American children. Blood samples were collected and analyzed for total monocyte concentration and monocyte subset concentration via flow cytometry. Total monocyte concentration, as well as the concentration of both classic and pro-inflammatory monocyte subsets was significantly greater in the “at risk for overweight/overweight” children (P\u3e0.05). Understanding early alterations in monocyte populations will be the first step in the development of early diagnosis and treatment techniques

Neutrophil Extracellular Traps in Inflammatory Bowel Disease: Pathogenic Mechanisms and Clinical Translation

The Inflammatory Bowel Diseases (IBD), Ulcerative Colitis (UC) and Crohn’s Disease (CD) are characterised by chronic non-resolving gut mucosal inflammation involving innate and adaptive immune responses. Neutrophils, usually regarded as first responders in inflammation, are a key presence in the gut mucosal inflammatory milieu in IBD. Here, we review the role of neutrophil extracellular trap (NET) formation as a potential effector disease mechanism. NETs are extracellular webs of chromatin, microbicidal proteins and oxidative enzymes that are released by neutrophils to contain pathogens. NETs contribute to the pathogenesis of several immune-mediated diseases such as systemic lupus erythematosus and rheumatoid arthritis; and recently, as a major tissue damaging process involved in the host response to severe acute respiratory syndrome coronavirus 2 infection. NETs are pertinent as a defence mechanism at the gut mucosal interphase exposed to high levels of bacteria, viruses and fungi. On the other hand, NETs can also potentiate and perpetuate gut inflammation. In this review, we discuss the broad protective vs. pathogenic roles of NETs, explanatory factors that could lead to an increase in NET formation in IBD and how NETs may contribute to gut inflammation and IBD-related complications. Finally, we summarise therapeutic opportunities to target NETs in IBD