In septic shock caused by Gram-negative infection, which cytokine is most likely to contribute to fever, hypotension, and DIC?

In septic shock caused by Gram-negative infection, which cytokine is most likely to contribute to fever, hypotension, and DIC?

• A. IL-2
• B. TNF
• C. IL-12
• D. IL-7

Answer: (B)

In septic shock from Gram-negative infection, the outbreak of fever, low blood pressure, and DIC is chiefly driven by TNF-alpha released from macrophages in response to endotoxin (LPS). TNF-alpha acts to raise body temperature and promote fever, and it causes profound vasodilation and increased capillary permeability, leading to hypotension. It also activates the coagulation system by upregulating tissue factor on endothelial cells and monocytes, pushing the body toward disseminated intravascular coagulation. While IL-1 also contributes to fever and hypotension, TNF-alpha is the primary mediator tied to the severe hemodynamic instability and coagulopathy seen in septic shock. The other cytokines listed are not central drivers of these features: IL-2 and IL-7 are mainly lymphocyte growth factors, and IL-12 drives Th1 responses rather than septic shock pathophysiology.

In septic shock from Gram-negative infection, the outbreak of fever, low blood pressure, and DIC is chiefly driven by TNF-alpha released from macrophages in response to endotoxin (LPS). TNF-alpha acts to raise body temperature and promote fever, and it causes profound vasodilation and increased capillary permeability, leading to hypotension. It also activates the coagulation system by upregulating tissue factor on endothelial cells and monocytes, pushing the body toward disseminated intravascular coagulation. While IL-1 also contributes to fever and hypotension, TNF-alpha is the primary mediator tied to the severe hemodynamic instability and coagulopathy seen in septic shock. The other cytokines listed are not central drivers of these features: IL-2 and IL-7 are mainly lymphocyte growth factors, and IL-12 drives Th1 responses rather than septic shock pathophysiology.