The causative agent of anthrax is the bacterium Bacillus anthracis. Like other organisms of the Bacillus genera, the bacterium can exist in the spore state (which allows it to survive unfavorable conditions) as well as the vegetative state (which it needs to be in to reproduce). This different physiological state appears to be critical for understanding how the immune system responds to an infection. New research shows that the human body’s immune system is efficient at initially detecting the presence of anthrax spores, which is through recognizing the RNA molecules that coat the spores’ surface. However, this also hinders the body’s fight against anthrax once the spores germinate.
The disease anthrax occurs occur in four forms: skin, inhalation, intestinal, and injection. A skin infection appears in the form of blisters which can become ulcers with black centers. The inhalation type leads to fever, chest pain, and shortness of breath; whereas the intestinal form results in nausea, vomiting, diarrhea, or abdominal pain. The final form, injection, causes fever and an abscess at the site of injection (this form is associated with some drug addicts).
Although risks of anthrax are better controlled, the disease remains prevalent in various regions of the world and combating the disease remains a matter of medical importance. One such study has been initiated by Professor Jin Mo Park from the Massachusetts General Hospital and Harvard Medical School. Professor Park gas discovered that it is the spores of the bacterium that stimulate the body’s immune system into action and this leads to the switching on of a set of immune sensors. However, the weakness with the immune response is that when the spore generate the body fails to recognize the organism.
This phenomena has been shown from studies using mice. Commenting on the research, which partly explains why anthrax infections are so deadly, Professor Park said: “We postulate that Bacillus anthracis has evolved to use spore-associated RNA to…evade host immunity. Our findings suggest that spore-associated RNA triggers early host responses to anthrax infection, but that type I interferon signaling serves to misguide host immunity and impair the body’s defense against the vegetative form of the bacterium at later stages of infection.”
The next phase of the research is to investigate if the spores of other bacterial pathogens use similar strategies to misdirect the host immune response.
The research has been published in The Journal of Experimental Medicine where the study is called “TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects.”