PCN033 infection triggered systemic inflammation, characterized by elevated pro-inflammatory cytokines (IL-1β, TNF-α) and suppressed anti-inflammatory cytokine TGF-β across in affected tissues, correlating with histopathologically confirmed pulmonary and cerebral lesions, consistent with the typical pathogenesis of ExPEC, which manifests as pneumonia, meningitis and septicemia [27,51]. This evidence concerns the gene IL1B and Sepsis.