Molecular Mechanisms of Palmitic Acid Augmentation in COVID-19 Pathologies.

The coronavirus disease 2019 (COVID-19) pandemic has claimed over 2.7 million lives globally. Obesity has been associated with increased severity and mortality of COVID-19.

Saturated Fatty Acids in Obesity-Associated Inflammation.

Obesity is a major risk factor for the development of various pathological conditions including insulin resistance, diabetes, cardiovascular diseases, and non-alcoholic fatty liver disease (NAFLD). Central to these conditions is obesity-associated chronic low-grade inflammation in many tissues including adipose, liver, muscle, kidney, pancreas, and brain. There is increasing evidence that saturated fatty acids (SFAs) increase the phosphorylation of MAPKs, enhance the activation of transcription factors such as nuclear factor (NF)-κB, and elevate the expression of inflammatory genes.

Postnatal development of lipopolysaccharide-induced inflammatory response in the brain.

Objective: This study aimed to characterize postnatal development of lipopolysaccharide (LPS)-induced inflammatory response in the brain.

Methods: Postnatal day (P)1, P21 and P70 Sprague-Dawley(®) rats were treated with saline or 0.25 mg/kg LPS for 2 h, and the mRNA expression of neuroinflammatory mediators in the brain was determined using reverse transcriptase-polymerase chain reaction (RT-PCR).

Altered hepatic inflammatory response in the offspring following prenatal LPS exposure.

There is increasing evidence that maternal immune activation has a significant impact on the offspring's immune function. In this study, we examined the effects of maternal immune activation on the offspring's hepatic inflammatory response. We treated pregnant rats with 500 microg/kg LPS or saline on day 18 of pregnancy, subsequently stimulated the offspring with 250 microg/kg LPS or saline at postnatal day (P) 21, and then examined the expression of LPS cell surface receptors, namely toll-like receptor (TLR)-4 and CD14, and cytokines, namely tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6, as well as the activation of key intracellular mediators of the TLR-4 signaling cascade, namely p38 MAPK and p42/44 MAPK, in the offspring liver.