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Opinion: Tracheal Cytotoxin, pathogenic signal or microbial factor?

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This graphic displays whether LPS, PGN, or TCT induces the three main development factors of the squid's light organ. 

Ed Yong tells in his book “I Contain Multitudes”the mutualism relationship, studied by Margaret J. McFall-Ngai and her team, between the Hawaiian bobtail squid and the bacterium, which is main factor of its bioluminescence, Aliivibrio fischeri. He also explains it in a video with Margaret and her life partner and coworker Edward B. Ruby.

This bacteria goes into the light organ of the squid through pores, in which they allocate themselves inside the organ which selectively lets V. fischeri through, and the light organ responds to V. fischeri’s Pathogen-associated molecular pattern (PAMPs) to develop the light organ of the bobtail squid for counter-luminescence camouflage from predators.

This gave light to change the PAMPs concept to Microbial-associated molecular pattern (MAMPs). These factors are found in the gram-negative cell membrane of the V. fischeri; which are only, by Yong’s words, peptidoglycans (PGN) and lipopolysaccharides (LPS).

After analyzing the paper in which this excerpt is from, something quite interesting regarding this research came up.

The main factor related to the development of light organ is the monomer of V. fischeri’s PGN, tracheal cytotoxin (TCT). Besides the PGN and LPS, TCT by itself induces the three main factors that initiates the transformation of the organ: hemocytes infiltration (immune system cells, mainly recruited when there is an infection), apoptosis (programmed cell death, in this case induced by TCT) and regression of epithelial fields (process in which the epithelial cells in the light organ, are returned to a less developed state).

In the other side, only in one factor LPS and PGN induced these factors without needing to be complemented by the other. All these factors are accounted for the development of such light organ, which the squid uses for camouflage and evade predators.

Interestingly enough, TCT wasn't mention on that section of the book "I Contain Multitudes"; giving all the credit to PGN and LPS.

Which raises the question: Why Yong did not mention TCT as one of the factors that “develops” the light organ? A closer evaluation of TCT effect in other organisms could answer why.

TCT is known to play an important factor in whooping cough and gonorrhea, infectious diseases caused by Bordetella pertussis, another gram-negative bacteria that releases the toxin. All three factors that were initiated by TCT towards the light’s organ development are also describing pathogenic behaviors.

Let’s put it this way: TCT, released by V. fischeri, is literally telling the cells in the light organ to die; the squid is enabling their immune system, by recruiting the hemocytes, to fight the infection off; and after the recruitment of the bacteria is done, the light organ is quite different compared to its pre-infection look.

I'm merely a undergraduate student, and I'm sure McFall-Ngai, Yong and most likely any other microbiologist can prove me wrong at my point; but being induced apoptosis from TCT one of the factors for the light organ's development... is this organ development through adoption of what could be a pathogenic reaction towards this specific TCT signal?

I'm sure there are many other species that see benefit from this kind of interaction. They are being induced with a signal which can be damaging for their cells but that specie still uses it for its development, which is fascinating.

Maybe the reason that Yong didn't mention TCT was because it is signaling this pathogenic-like behaviors towards its hosts; and the host is, as mutualism describes, benefited from this interaction in which it develops its light organ for the desired function. Yes, there is mutualism involved, but raises from the TCT-signaled pathogenic behavior of V. fischeri towards its host’s epithelial cells.

In my humble, undergraduate-level perspective is something that needs to be further analyzed to comprehend the role of TCT in this situation and in other situations it is involved in as well. PGN and LPS are now classified as MAMPs, but where does TCT fall? As a pathogenic signal or just another microbial factor?