Effects of Acetone on the CrdRS Pathway of H. pylori

Hey everyone!

My name is Yusheng Qin. I’m a rising Junior and a Biology major at the College of William and Mary. For the past year, I’ve been working in Dr. Mark Forsyth’s lab on signal transduction in Helicobacter pylori. H. pylori (HP) is a bacterium that causes many gastric diseases in humans such as gastric ulcers and gastric cancers. In order to thrive in the highly acidic environment in the stomach, HP has evolved complex mechanisms for resistance to environmental changes in the stomach such as pH fluctuations. One way the gastric pathogen achieve this is through the use of two-component signal transduction (TCST) systems. This summer I will be studying one of these TCST systems named CrdRS.

There is relatively little research about the environmental stimuli CrdRS detects and mediates in the human stomach. Previous research in Dr. Forsyth’s lab pointed to acetone as a possible signal triggering the CrdRS pathway. I plan to test acetone’s effects on CrdRS with a two-stage research design. The first stage is the growing stage. I will first grow HP J99 wild-type and null mutant strains on blood agar plates for 48 hours and then transfer to SFBB broth for 17 hours. Next I will do a one-hour experimental acetone treatment with the broth. Afterwards, I will spin the J99 cells down using centrifuge technique and then extract mRNA from the cell pellets using the MagMax protocol. The second stage of the experiment is quantitative analysis. For this stage, I will perform quantitative real-time polymerase chain reaction (qRT-PCR) on all of my RNA samples. If my hypothesis is correct, then the expression of acxA in null mutant strains exposed to acetone will be significantly higher than the acxA expression in control null mutant strains with no acetone, as well as in wild-type strains with or without acetone.  Since H. pylori only has three TCST pathways, studying their roles in adapting to host environmental conditions and mediating bacterial metabolism can help us understand how HP is able to establish chronic association with the host and enable us to find novel targeted treatments to HP infections.

Comments

  1. scgilliand says:

    This sounds like a really interesting project! It’s amazing that HP has developed such a resistance to conditions in the human stomach, and with such harmful consequences. And it’s a shame that it would take so long for humans to in turn evolve a defense against this process, if it were even possible. But since we can’t do it ourselves, it’s vital that people investigate how to treat HP infections. I don’t know exactly how this all works, but if your results show that acetone is indeed a trigger for the pathway, it would be great to then look into how to block this pathway in humans.

  2. Are there any safety concerns when studying HP? Is there a risk that you could get infected by HP using your lab practices, and if so, what measures do you take to prevent infection?