The endogenous neurosteroid (3α,5α)-3-hydroxypregnan-20-one (3α,5α-THP) modulates inflammatory and neuroinflammatory signaling through toll-like receptors (TLRs) in human and mouse macrophages, human blood cells and alcohol-preferring (P) rat brains. Although it is recognized that 3α,5α-THP inhibits TLR4 activation by blocking interactions with MD2 and MyD88, the comprehensive molecular mechanisms remain to be elucidated. This study explores additional TLR4 activation sites, including TIRAP binding to MyD88, which is pivotal for MyD88 myddosome formation, as well as LPS interactions with the TLR4:MD2 complex.
View Article and Find Full Text PDFA novel framework has been developed which summarizes the efficacy of treatment technologies for emerging contaminants (ECs) based on the general mitigation mechanisms of Removal, Inactivation/Degradation, and Destruction (i.e., RIDD).
View Article and Find Full Text PDFBackground: Pathogenesis of seborrheic dermatitis involves lipid secretion by sebaceous glands, Malassezia colonization, and an inflammatory response with skin barrier disruption. Each of these pathways could be modulated by diet, obesity, and nutritional supplements. Current treatment options provide only temporary control of the condition; thus, it is essential to recognize modifiable lifestyle factors that may play a role in determining disease severity.
View Article and Find Full Text PDFAntimicrob Agents Chemother
August 2024