Previously characterized as a purely immune mediated disease, sepsis is now recognized as a dysregulated multisystem response against a pathogen. Recognition of the infectious agent by pathogen recognition receptors (PRRs) can initiate activation of the NF-κB signaling pathway and promote the secretion of proinflammatory cytokines. During sepsis, the activation of NF-κB is dysregulated and results in cytokine storm, or the pathologic release of cytokines.

Sepsis is highly prevalent, and is one of the main causes of mortality among hospitalized patients. Ethanol consumption in large quantities compromises the normal functioning of the body, leading to dysfunction of multiple different organ systems. The association between sepsis and ethanol is not fully understood, but it is well accepted that ethanol

Bacillus anthracis (Ba) is a gram-positive, rod-shaped, spore- and toxin-forming bacterium. While mainly an herbivore pathogen, human infection with Ba spores can occur through a number of routes including cutaneous, gastrointestinal, injectional, or inhalational. The deadliest form of anthrax exposure is through inhalation of Ba spores, leading to systemic dissemination of the bacteria, with mortality ranging from 45% to 90%. 

Sepsis is a key driver of worldwide mortality, representing close to 20% of global deaths in 2017 [1]. Approximately half of patients hospitalized with sepsis are 65 years and older [2]. Delivery of 30ml/kg of crystalloid fluid bolus within three hours of diagnosing sepsis remains a cornerstone of the Surviving Sepsis Campaign (SSC)

Background: Sepsis remains a critical global health challenge with high mortality. This review summarizes current understanding of the intricate molecular mechanisms governing sepsis pathogenesis and highlights emerging therapeutic approaches.