Endotoxemia mortality results exclusively from a systemic inflammatory response characterized by an acute increase in circulating inflammatory cytokine levels (e.g. TNF, IL-6, and IL-1β) from splenocytes and myeloid-derived innate immune cells (Lewis et al., 2016; Wang et al., 2016; Radzyukevich et al., 2021; Zhang et al., 2012). Here, IL1B is linked to serum lipopolysaccharide activity.