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Pinto, S. N.

Publications and source records attributed to Pinto, S. N..

2 recordsLinked to original sources

Ceramide Connects TNF-α Signaling to Organelle Biophysical Remodeling

Ceramides are essential bioactive lipids involved in cell physiology and stress responses, yet the mechanisms linking their biophysical effects on membranes to downstream cellular outcomes remain incompletely understood. Here, we demonstrate that endogenous ceramide generation in response to TNF--induced stress results in the rapid remodeling of the plasma membrane, triggering a cascade of cellular events. Ceramide accumulation increases membrane order and drives the formation of internalizing vesicles enriched in ceramides, which traffic through the endolysosomal system. These vesicles act as carriers that transmit membrane remodeling signals to intracellular compartments, altering their biophysical properties and function. In parallel, ceramide production reprograms lipid droplet metabolism, decreasing polarity and modifying gene expression related to lipid storage. Our findings provide direct evidence that ceramides function as biophysical integrators of the TNF- stress response, coupling membrane order, vesicle trafficking, and lipid metabolic adaptation. This work reveals how localized lipid remodeling at the plasma membrane propagates intracellularly to support cellular adaptation and homeostasis under inflammatory stress.

biophysics↗

A Metabolite-Based Resistance Mechanism Against Malaria

Whether jaundice, a common presentation of Plasmodium (P.) falciparum malaria (1-3) arising from the accumulation of circulating bilirubin, represents an adaptive or maladaptive response to Plasmodium spp. infection is not understood (1-3). We found that asymptomatic P. falciparum infection was associated with a >10-fold higher ratio of unconjugated bilirubin over parasite burden, compared to symptomatic malaria. Genetic suppression of bilirubin synthesis by biliverdin reductase A (BVRA) (4) increased parasite virulence and malaria mortality in mice. Accumulation of unconjugated bilirubin in plasma, via genetic inhibition of hepatic conjugation by UDP glucuronosyltransferase family 1 member A1 (UGT1A1) (5), was protective against malaria in mice. Unconjugated bilirubin inhibited P. falciparum proliferation in red blood cells (RBC) via a mechanism that suppressed mitochondrial pyrimidine synthesis. Moreover, unconjugated bilirubin inhibited hemozoin (Hz) crystallization and compromised the parasites food vacuole. In conclusion, jaundice represents a metabolic response to Plasmodium spp. infection that limits malaria severity.

immunology↗