fucoxanthin and Sepsis

Fucoxanthin (FX) has been reported to reduce mortality in mouse models of sepsis, but its exact cause remains to be determined. In the present study, we evaluated the immunomodulatory properties of FX in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Our results showed that FX could not only suppress the immune activation responses caused by LPS primary stimulation, but also antagonize LPS restimulation-induced immunosuppression in macrophages. The immunomodulatory capabilities of FX was mainly demonstrated by regulating the production of the inflammatory mediator under different LPS stimuli. Furthermore, we found that adenosine monophosphate-activated protein kinase (AMPK) activation was required for FX's anti-inflammatory and anti-immunosuppressive activities. Our results complement existing data supporting the clinical potential for FX in treating sepsis.

Topics: Animals; Immunosuppression Therapy; Inflammation; Lipopolysaccharides; Macrophages; Mice; Sepsis

Suppression of excessive inflammatory responses improves the survival of patients with sepsis. We previously illustrated the anti-inflammatory effects of fucoxanthin (FX), a natural carotenoid isolated from brown algae; nevertheless, the underlying mechanism remains unknown. In this study, we examine the mechanism of the action of FX by targeting interferon regulatory factor 3 (IRF3) to inhibit inflammatory response. We observed that FX regulated innate immunity by inhibiting IRF3 phosphorylation

Topics: Animals; Inflammation; Interferon Regulatory Factor-3; Mice; Sepsis; Xanthophylls

To improve patient survival in sepsis, it is necessary to curtail exaggerated inflammatory responses. Fucoxanthin (FX), a carotenoid derived from brown algae, efficiently suppresses pro-inflammatory cytokine expression via IRF3 activation, thereby reducing mortality in a mouse model of sepsis. However, the effects of FX-targeted IRF3 on the bacterial flora (which is disrupted in sepsis) and the mechanisms by which it impacts sepsis development remain unclear. This study aims to elucidate how FX-targeted IRF3 modulates intestinal microbiota compositions, influencing sepsis development. FX significantly reduced the bacterial load in the abdominal cavity of mice with cecal ligation and puncture (CLP)-induced sepsis via IRF3 activation and increased short-chain fatty acids, like acetic and propionic acids, with respect to their intestines. FX also altered the structure of the intestinal flora, notably elevating beneficial Verrucomicrobiota and

Topics: Animals; Cytokines; Gastrointestinal Microbiome; Humans; Interferon Regulatory Factor-3; Mice; Microbiota; Sepsis; Xanthophylls