Abstract

Abstract Sepsis is characterized by a dysregulated response to infection that is initiated by recognition of pathogen-associated molecular patterns from invasive microorganisms by pathogen recognition receptors to trigger an immune response. The goal is to establish regulatory mechanisms governing sepsis-induced cell death and correlate cell death mechanisms with clinical biochemistry pre- and post- antibiotic treatment. Towards this end, we present a case report of a 48-year-old male patient with a clinical history of adenocarcinoma, colostomy, chronic kidney disease and suspected sepsis admitted to emergency department. Patient was on an antibiotic treatment regimen (Monocef 1 g single dose and Flucloxacillin 1 g single dose for three days). Among several promising biomarkers for sepsis, the role of cell death marker p62/SQSTM1 was evaluated for its prognostic role in this particular case of sepsis. Flow cytometry and ELISA analysis of septic patient’s peripheral blood mononuclear cells (PBMCs) and serum samples were performed and correlated with serum electrolyte and serum biochemistry values pre- and post- antibiotic dose. Flow cytometry data analysis of PBMC samples from septic patient showed significantly lower p62 post- antibiotic when compared to pre- antibiotic dose [p < 0.05]. Notably, comparison of pre- and post- antibiotic treatment regimen showed significant modulation of serum ELISA levels of autophagy marker, p62/SQSTM1, that correlated with alteration in serum potassium levels [p < 0.05]. Our current study demonstrates the impact of serum potassium levels on autophagy in a patient’s case of sepsis.

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