In conclusion, we present the first evidence that patients with MASLD have different cytokine and chemokine responses during community-acquired bacterial sepsis, including increase in biomediators which have already been implicated in MASLD progression, IL-17, IL-23, IL-33, CXCL10 and TGF-β1, and linked with early sepsis outcomes and prolonged immunosuppressive state in sepsis survivals. Here, IL33 is linked to metabolic dysfunction-associated steatotic liver disease.