Circumstantial evidence has suggested that C. burnetii is able to exert this control using proteins that are delivered via a mechanism called a Dot/Icm type IVB secretion system (T4BSS) which is critical for successful parasitism of macrophages by the organism.
Using new genetic tools, researchers from the National Institute of Allergy and Infectious Diseases and the University of Arkansas for Medical Science have finally verified that Dot/Icm function is in fact essential for productive infection of human macrophages by C. burnetii.
Protein Necessary for Bacteria to Produce Ulcers
When it comes to the ability of the bacterium Helicobacter pylori to effectively colonize the stomach and eventually cause ulcers it all comes down to a single protein.
H. pylori strains infect half of all humans worldwide and contribute to the development of peptic ulcers and gastric cancer. They cannot survive the harsh acidic environment inside stomach cavity and must therefore use their flagella to actively swim to and colonize the protective mucus and lining of the stomach. Researchers have discovered a novel protein, called ChePep, that the bacterium requires to swim properly.
Although H. pylori lacking ChePep have normal looking flagella and are mobile, when they swim they have a slight defect that can cause them to go backwards. If they cannot swim away from the acid and into the protective lining of the stomach, they die.
While ChePep is not unique to H. pylori it is unique to the class Epsilonproteobacteria, which includes the foodborne pathogen Campylobacter jejuni and the deep sea hydrothermal vent inhabitant Caminibacter mediatlanticus.
|Contact: Jim Sliwa|
American Society for Microbiology