Field of Science

Bacterial needles and their role in infection

This post was chosen as an Editor's Selection for ResearchBlogging.orgI spent ages over the title of this post. The original paper "Injecting for infection" was my favorite but it isn't wonderfully clear. It sounds like something about dirty needles; bacterial colonies over the surface of injections. In reality it's about something far more amazing, the little needles that bacteria make themselves, in order to inject toxins into the cells that they destroy.

Officially these are called Type III secretion systems, as they allow the secretion of toxins (and other things for that matter) from the cell. They occasionally fall off the bacteria allowing very detailed electron microscope pictures to be taken, showing that, whatever their official name, they do look a lot like little needles.

Image A shows the imprint of the needle on the bacterial cell surface. Image B shows the isolated needles, showing their structures (which are wonderfully detailed and quite beautiful). Image C shows a drawing of the proteins involved in the structure within the cell membrane. Scale bar is 100nm.

In infectious organisms this secretion system is vital for survival, but it's interesting to see how it's used in organisms that are only opportunistically infective, such as Pseudomonas aeruginosa. P aeruginosa is an opportunistic pathogen, it can survive fine outside the human body, but in cases where it gets a chance to invade (particularly in the lungs of people with cystic fibrosis) it will go for it. Where it inherited the needle complex from is not clear, although it is thought to have distantly evolved from flagella and been passed to the pseudomonas by horizontal gene transfer from another bacteria.

Removal of the needle complex does not prevent P aeruginosa from invading and infecting an organism, but it does make the infection slightly less virulent. Work on acute pneumonia has started to build up a model of how the needle works, and what role it plays in infection. The bacterial cells invade the epithelial tissue in the human host at points where it is damaged (i.e by cystic fibrosis). As non-damaged epithelial cells are usually quite resistant to the bacterial colonization, it is only when the lung tissue is already injured that the Pseudomonas can take hold.

Once P. aeruginosa has colonized the damaged tissue surrounding macrophages and neutrophils will gather at the site of infection. These merely further damage the surrounding tissue, without harming the bacteria allowing it to settle and grow. Only then does the needle start pumping out damaging toxins, which lead to the symptoms of pneumonia. In a severe infection this can lead to a breach of the tissue barrier between the lungs and the blood stream, which goes on to cause systemic bacteria infection and rapid septic shock. The removal of the needle complex can therefore stop some of these more extreme reactions, but does not prevent the infection starting in the first place.

Hauser, A. (2009). The type III secretion system of Pseudomonas aeruginosa: infection by injection Nature Reviews Microbiology, 7 (9), 654-665 DOI: 10.1038/nrmicro2199


Anonymous said...

Wow ... all these years and I never knew that bacteria were shooting up their hosts.

That's amazing!

Psi Wavefunction said...

Ah so that's what TC-S was talking about in his epic novel of doom (2006 Biol Direct); been meaning to look it up eventually - thanks for scratching one more item off my 'chore list' (ie random tidbits I needed to read up on)!

I really do like "Injecting for infection" =D

Perplexed by the LGT idea though - even if all the necessary genes were transferred (already unlikely), would it also require cytoplasmic transfer of the apparatus itself? Do you happen to know how the 'needles' replicate -- do they self-assemble or is there directed-assembly (sensu Grimes & Aufderheide 1991) based on existing needles?

Lab Rat said...

@Psi: The apparatus builds itself! The base proteins are inserted into the membrane after being produced, just like normal membrane-proteins and then the filament proteins that form the injecting bit are moved through that pore and assemble themselves on the outside. Flagella do a similar sort of thing.

I haven't actually looked it up, but I get the feeling that once you transfer the necessary genes over, the thing builds itself fairly happily.

Bacteria don't share needles :p As far as I'm aware there is no transfer of the membrane proteins, just the genes for them.

diseaseoftheweek said...

"although it is thought to have distantly evolved from flagella and been passed to the pseudomonas by horizontal gene transfer from another bacteria"

It was my understanding that flagella were most likely evolved from faulty T3SS. Is this not the case anymore?

Also the wholesale transfer of T3SS's happens/ed a lot. Presumably because half a T3SS is useless so the genes are quite closely linked. As for assembly T3SS are really no different from any other large multi-component membrane complex, chaperones and self assembly do the job.

Lab Rat said...

@disease: There is definitely a link between T3SS and flagella, I'm not sure if it's quite certain which one came from which. The paper put it down as a speculation, and I think it's more likely that T3SS came from flagella than the other way around.

Thanks for the comment and extra information!