Human Tumor Necrosis Factor (TNF superfamily, member 2), TNF ELISA Kit

Microglia are phagocytic cells involved in homeostasis of the brain and are key players in the pathogenesis of multiple sclerosis (MS). A hallmark of MS diagnosis is the presence of IgG Abs, which appear as oligoclonal bands in the cerebrospinal fluid. In this study, we demonstrate that myelin obtained post mortem from 8 out of 11 MS brain donors is bound by IgG Abs. Importantly, we show that IgG immune complexes strongly potentiate activation of primary human microglia by breaking their tolerance for microbial stimuli, such as LPS and Poly I:C, resulting in increased production of key proinflammatory cytokines, such as TNF and IL-1 beta. We identified Fc gamma RI and Fc gamma RIIa as the two main responsible IgG receptors for the breaking of immune tolerance of microglia. Combined, these data indicate that IgG immune complexes potentiate inflammation by human microglia, which may play an important role in MS-associated inflammation and the formation of demyelinating lesions.

Inflammation is an essential biological process for maintaining homeostasis in the body. However, excessive inflammatory response is closely related to many chronic diseases. Ammonia is a known environmental pollutant and a main harmful gas in the environment of livestock house. It causes deterioration of air quality and poses a threat to human and animal health. Chickens are very sensitive to ammonia. In order to assess the toxicity of ammonia to the heart, the pathology, ATPase activities, markers of oxidative stress, inflammatory pathways and inflammation markers were investigated in the hearts of chickens exposed to ammonia. The results showed that the cardiac pathological structure, oxidative stress index, and ATPase activity changed significantly in ammonia-treated chickens. In addition, the inflammation pathways (JAK/STAT and MAPK) were activated in the ammonia group, and the inflammatory markers (COX-2, TNF-alpha, NF-kappa B and PPAR-gamma) were significantly altered at both mRNA and protein levels. In conclusion, excess ammonia can activate inflammatory pathways through oxidative stress and abnormal energy metabolism, and induce cardiac inflammatory injury. Our findings will provide a new insight for better assessing the toxicity mechanism of ammonia on the heart. (C) 2020 Elsevier B.V. All rights reserved.