Fibrinogen is increased in the spleen over the course of murine endotoxemia

Abstract The fibrinogen protein is composed of three subunits encoded for by the genes Fga, Fgb, and Fgg. This trimer a main component blood clots. Irregular clotting contributes to low pressure during septic shock, which eventually leads death from total system organ failure. A previously published data set finds Fgg be dysregulated sepsis in serum both wildtype (WT) toll-like receptor 4 (TLR4) deficient mice. Deficiency innate immune TLR4 models ataxia that occurs patients who recover surviving have an increased risk mortality due secondary infection. We hypothesize symptoms shock independent pathway. In this study we confirm transcriptionally upregulated liver WT TLR4−/− mice over course LPS induced endotoxemia. Western blots were completed using lysates liver, spleen, kidney, brain 0, 6, 12, 18 hours after induction endotoxemia with intraperitoneal injection 30 mg/kg lipopolysaccharide (LPS). show control express similar amounts organs, there more than consistent current literature. conducted endotoxemic samples disease mice, levels are but increase spleen. Continued experiments will determine level TLR4-independent activation provide evidence use modulators recovered shock. supported Towson University FDRC grant awarded EMH, Fisher College Science Mathematics undergraduate research award KEN, 2022 Linda Sweeting Summer fellowship KEN Department Chemistry.