Correct option is A
Explanation:
(A) Invasin and β1 Integrins → Zipper Mechanism
- Certain bacteria (e.g., Yersinia spp.) produce invasins, which bind β1 integrins on host cells.
- This induces cytoskeletal rearrangement leading to bacterial internalization.
- This process follows a "zipper" mechanism, where bacteria closely interact with the host cell membrane.
(B) Actin Polymerization and Clathrin Assembly → Zipper Mechanism
- Bacterial uptake via the zipper mechanism requires actin polymerization at the site of bacterial attachment.
- Example: Listeria monocytogenes and Yersinia spp. use this pathway.
- Clathrin coating is not typically involved in bacterial entry but is essential for endocytosis, which bacteria exploit.
(C) Type III Secretion System (T3SS) → Trigger Mechanism
- Salmonella enterica, Shigella, and Pseudomonas use the trigger mechanism for invasion.
- The T3SS injects effector proteins into host cells, inducing membrane ruffling and cytoskeletal changes.
- This results in bacterial engulfment and internalization.
(D) Ca²⁺ Elevation and Lysosomal Fusion → Not a Typical Entry Mechanism
- Ca²⁺ elevation plays a role in intracellular trafficking and phagosome maturation.
- However, fusion with lysosomes is NOT a mechanism for bacterial invasion into non-phagocytic cells.
- Instead, bacteria avoid lysosomal fusion to prevent degradation.
Information Booster:
- Zipper Mechanism (Used by Yersinia & Listeria):
- Involves tight receptor-ligand interactions.
- Uses β1 integrins & cadherins to mediate actin polymerization.
- Trigger Mechanism (Used by Salmonella & Shigella):
- Bacteria inject effectors via T3SS, causing membrane ruffling.
- Leads to macropinocytosis-like uptake of bacteria.
- Actin Cytoskeleton Remodeling:
- Required for both zipper & trigger mechanisms.
- Pathogens manipulate actin polymerization to enter cells.
- Role of Calcium (Ca²⁺) in Infection:
- Intracellular Ca²⁺ regulates vesicular trafficking, but it is not a direct invasion strategy.
- Some bacteria manipulate Ca²⁺ signaling to disrupt host immune responses.