Fine Reading: Autophagy & the Cytoskeleton—New Links Revealed By Intracellular Pathogens

by Elio

Life inside cells of the immune system presents a special challenge to pathogenic bacteria. Some are killed after being taken up, others survive. One favorite mechanism used by Shigella, Listeria, and Rickettsia, among others, is to escape from the phagocytic vacuole into the cytoplasm. This avoids the action of enzymes from the lysosomes that would otherwise fuse with the bacteria-containing vacuole. Once in the cytosol, the invaders enjoy what seems to be a rich and carefree existence.

But how do they infect new host cells? Instead of simply sitting idly, these bacteria recruit host actin, which in polymerizing pushes them around. When the moving bacteria hit the host cell membrane, they enter into protrusions that can penetrate into an adjacent cell. This has been the conventional story. The bug wins, or so it would seem. What does the host cell do about it? It has been discovered recently that the cells respond to these gymnastics by encasing the bacteria in cages of a cytoskeletal protein called septin. Now the bacteria can be dealt with by the autophagy system of the cell. The choreography between host and parasite continues.

One of the most satisfying aspects of current day Microbiology is how studying pathogens has contributed to our understanding of the host cell. Just like phages have helped understand bacteria, mammalian pathogens have helped elucidate the inner workings of their host.

Comments

[Mark O. Martin]

Elio, this is a fantastic post, and a great example of why microbiology is so vital to the undergraduate curriculum. I tell me students that "Cellular Microbiology" is a critical concept in our class, and the phrase does not mean learning how microbial cells work. Instead, as you point out (and have written about in some fine "thought articles"), it is about understanding how eukaryotic cells work by studying bacteria and their interactions with eukaryotic cells. It's just like reminding them how much we have learned about how ribosomes work due to antibiotics!

Much of this may garner a "I know" from microbiologists. But I promise you, this data is decidedly not well known by faculty and students at PUIs. So thank you for giving me yet more ammunition for my promotion of Microbial Supremacy!