Measurement of adolescent psychological wellbeing: A test of factor structure and measurement invariance.

Gains in holistic approaches to adult mental health have been associated with increasing interest in understanding psychological wellbeing (PWB) among adolescents. Empirical examination of measurement models for PWB in adolescence is lacking. Thus, the current study examined PWB in a longitudinal, diverse sample of 433 adolescents (non-Latinx Black: 37.6%; non-Latinx White: 25.9%; Latinx: 36.5%; Male adolescents: 50.1%). A one-factor, correlated six-factor and hierarchical models were examined across racial/ethnic (White, Black, and Hispanic) and gender (female, male) identities, after which the best fitting model was selected to undergo invariance testing. A one-factor structure was superior, and exhibited strict invariance across racial/ethnic and gender identities at each wave of the study, as well as longitudinal invariance within the entire sample.

Anti-Inflammatory Action of an Antimicrobial Model Peptide That Suppresses the TRIF-Dependent Signaling Pathway via Inhibition of Toll-Like Receptor 4 Endocytosis in Lipopolysaccharide-Stimulated Macrophages.

Antimicrobial peptides (AMPs), also called host defense peptides, particularly those with amphipathic helical structures, are emerging as target molecules for therapeutic development due to their immunomodulatory properties. Although the antimicrobial activity of AMPs is known to be exerted primarily by permeation of the bacterial membrane, the mechanism underlying its anti-inflammatory activity remains to be elucidated. We report potent anti-inflammatory activity of WALK11.3, an antimicrobial model peptide with an amphipathic helical conformation, in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. This peptide inhibited the expression of inflammatory mediators, including nitric oxide, COX-2, IL-1ß, IL-6, INF-ß, and TNF-α. Although WALK11.3 did not exert a major effect on all downstream signaling in the MyD88-dependent pathway, toll-like receptor 4 (TLR4)- mediated pro-inflammatory signals were markedly attenuated in the TRIF-dependent pathway due to inhibition of the phosphorylation of STAT1 by attenuation of IRF3 phosphorylation. WALK11.3 specifically inhibited the endocytosis of TLR4, which is essential for triggering TRIF-mediated signaling in macrophage cells. Hence, we suggest that specific interference with TLR4 endocytosis could be one of the major modes of the anti-inflammatory action of AMPs. Our designed WALK11 peptides, which possess both antimicrobial and anti-inflammatory activities, may be promising molecules for the development of therapies for infectious inflammation.