Type III secretion system (T3SS) in Salmonella pathogenesis: Salmonella uses a T3SS to inject “effector” proteins; this system primarily helps the pathogen to…

Introduction / Context:
Gram-negative pathogens use Type III secretion systems (T3SS) as “molecular syringes” to deliver effector proteins into host cells. Salmonella encodes distinct T3SSs on pathogenicity islands that mediate invasion and intracellular survival—key steps in disease.

Given Data / Assumptions:

• Salmonella Pathogenicity Island-1 (SPI-1) aids epithelial invasion.
• Salmonella Pathogenicity Island-2 (SPI-2) supports survival inside phagocytes.
• Macrophages are central hosts for systemic Salmonella infection.

Concept / Approach:
SPI-2–encoded T3SS effectors remodel the Salmonella-containing vacuole, block phagosome–lysosome fusion, and alter vesicular trafficking, enabling intracellular survival and replication within macrophages. This differentiates T3SS action from toxin secretion into the lumen or direct T-cell activation.

Step-by-Step Solution:
Recognize T3SS as a translocation apparatus for effectors into host cell cytosol.Link Salmonella SPI-2 T3SS to macrophage intracellular survival mechanisms.Select the answer describing survival within macrophages.

Verification / Alternative check:
Mutants lacking SPI-2 T3SS exhibit impaired systemic infection and poor replication inside macrophages, validating the role of T3SS in intracellular survival rather than acid resistance or classic enterotoxin secretion.

Why Other Options Are Wrong:

• Acid survival: mediated by acid tolerance response, not T3SS.
• LT/ST secretion: characteristic of enterotoxigenic E. coli, not Salmonella T3SS.
• T-cell activation: not a direct T3SS role.
• Endospore formation: Salmonella does not form spores.

Common Pitfalls:
Conflating T3SS with general secretion of toxins into the lumen; ignoring distinct roles of SPI-1 vs SPI-2 systems.

Final Answer:
Survive and replicate within macrophages (intracellular survival).