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Nomellini, V.

Publications and source records attributed to Nomellini, V..

2 recordsLinked to original sources

Lipid mobilization establishes metabolic tolerance and prevents autonomic collapse in infection

Survival during infection depends on both pathogen clearance and the ability to tolerate infection-induced physiological changes. Metabolic adaptations are a central component of this tolerance, but the mechanisms underlying these responses remain incompletely defined. Here, we identify white adipose tissue (WAT) lipolysis as a central regulator of metabolic tolerance to infection. In patients with sepsis, higher circulating non-esterified fatty acid (NEFA) levels were associated with reduced mortality. In mouse models of polymicrobial sepsis, infection induced robust adipose lipolysis and increased circulating NEFAs. Genetic ablation of adipose triglyceride lipase (ATGL) in adipose tissue impaired lipolysis, leading to hypothermia, bradycardia, and increased mortality without altering immune cell populations or pathogen burden, consistent with a defect in tolerance rather than resistance. Mechanistically, lipolysis-derived NEFAs, but not glycerol, were required for protection, as restoring circulating NEFAs rescued autonomic stability and survival in adipose tissue ATGL-deficient mice. Infection-induced lipolysis was redundantly regulated and did not depend on any single upstream signaling pathway. Both pharmacologic activation of lipolysis using a {beta}3-adrenergic agonist and exogenous fatty acid supplementation increased circulating NEFAs, improved survival, and promoted tolerance in mice. Consistent with these findings, analysis of real-world electronic health record data demonstrated that septic patients receiving FDA-approved {beta}3-adrenergic agonists had reduced mortality or hospice discharge in a propensity-matched cohort. Together, these results identify WAT lipolysis and circulating fatty acids as key mediators of tolerance to infection and support a therapeutic strategy based on repurposing clinically available {beta}3-adrenergic agonists to improve outcomes in sepsis. One Sentence SummaryWhite adipose tissue lipolysis promotes metabolic tolerance to infection through circulating fatty acids and is associated with improved survival in sepsis

physiology↗

Murine Neutrophil Chemotaxis Following Burn Injury with Poloxamer 188 Treatment in a Microfluidic Platform

This study investigates the effects of Poloxamer 188 (P188) on neutrophil chemotaxis following burn injury in male and female mice using a microfluidic system. Utilizing male and female CD1 mice, we evaluated neutrophil migration towards two chemoattractants, N-formyl-l-methionyl-l-leucyl-l-phenylalanine (fMLP) and Leukotriene B4 (LTB4), and FPR1 and BLT1 G protein-coupled receptors after administering P188. Our findings revealed that P188 significantly increased the migration toward LTB4 in both sexes. Additionally, our findings highlight the upregulation of BLT1 and FPR1 markers due to burn injury in both female and male mice in the Burn vs. Sham groups. These results demonstrate the potential of P188 in modulating neutrophil behavior post-burn injury in therapeutic strategies for inflammation management. This microfluidic platform offers a precise and controlled microenvironment for studying neutrophil chemotaxis post-burn injury with and without P188 treatment.

bioengineering↗