Camping advice from Helicobacter pylori

Given the environmental stresses experienced by H. pylori, tight regulation of cellular processes is vital. Researchers in the United States have shown that knowing when to keep biofilm formation suppressed is a key factor for survival.

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In an interesting study published in the Journal of Bacteriology last week, researches investigating acid stress in H. pylori made an unexpected discovery. They found that knocking out a key acid regulator drastically increased biofilm formation.

H. pylori cells must navigate the harsh environment and changing pH's of the stomach in order to reach epithelial surface where they can attach and eventually form biofilm. If extracellular matrix production is not tightly regulated and H. pylori goes into biofilm production too early, then cells may form biofilms before they have reached the safety of the stomach epithelium and will be stranded in the stomach lumen where they will eventually die.

So what is the moral of the story? Well, biofilms are like camping equipment, essential for survival but you have to deploy them at the right time. If you start trying to put your tent up when you are at a particularly dangerous point in your trek, you may regret it.

Thanks for the tip Helicobacter pylori.

Article Info


Helicobacter pylori must be able to rapidly respond to fluctuating conditions within the stomach. Despite this need for constant adaptation, H. pylori encodes few regulatory proteins. Of the identified regulators, Fur (ferric uptake regulator), NikR (nickel response regulator), and ArsRS (two-component acid response system), are each paramount to the success of this pathogen. While numerous studies have individually examined these regulatory proteins, little is known about their combined effect. Therefore, we constructed a series of isogenic mutant strains that contained all possible single, double and triple regulatory mutations in Fur, NikR and ArsS. Growth curve analysis revealed minor variation in growth kinetics across the strains; these were most pronounced in the triple mutant and in strains lacking ArsS. Visual analysis showed that strains lacking ArsS formed large aggregates and a biofilm-like matrix at the air liquid interface. Biofilm quantification using crystal violet assays and visualization via scanning electron microscopy (SEM) showed that all strains lacking ArsS or containing a non-phosphorylateable form of ArsR (ArsR-D52N) formed significantly more biofilm than the wild-type strain. Molecular characterization of biofilm formation showed that strains containing mutations in the ArsRS pathway displayed increased levels of cell aggregation and adherence, both of which are key to biofilm development. Furthermore, SEM analysis revealed prevalent coccoid cells and extracellular matrix formation in the ArsR-D52N, ΔnikRΔarsS, and ΔfurΔnikRΔarsS strains, suggesting that these strains may have an exacerbated stress response that further contributes to biofilm formation. Thus, H. pylori ArsRS has a previously unrecognized role in biofilm formation.


Despite a paucity of regulatory proteins, adaptation is key to the survival of H. pylori within the stomach. While prior studies have focused on individual regulatory proteins such as Fur, NikR and ArsRS, few studies have examined the combined effect of these factors. Analysis of isogenic mutant strains that contained all possible single, double and triple regulatory mutations in Fur, NikR and ArsS revealed a previously unrecognized role for the acid responsive two-component system, ArsRS, in biofilm formation.

Stephanie L. Servetas, Beth M. Carpenter, Kathryn P. Haley, Jeremy J. Gilbreath, Jennifer A. Gaddy, and Scott Merrell. 18 July 2016. Characterization of key H. pylori regulators identifies a role for ArsRS in biofilm formation. Journal of Bacteriology. doi:10.1128/JB.00324-16.

Ben Libberton

Science Communicator, Freelance

I'm a freelance science communicator, formerly a Postdoc in the biofilm field. I'm interested in how bacteria cause disease and look to technology to produce novel tools to study and ultimately prevent infection.