Antibodies Trick Bacteria into Killing Each Other
The dominant theory about antibodies is that they directly target and kill disease-causing organisms. In a surprising twist, researchers from the Albert Einstein College of Medicine have discovered that certain antibodies to Streptococcus pneumoniae actually trick the bacteria into killing each other.
Pneumococcal vaccines currently in use today target the pneumococcal capsular polysaccharide (PPS), a sort of armor that surrounds the bacterial cell, protecting it from destruction. Current thought hold that PPS-binding antibodies protect against pneumococcus by inducing opsonic killing, a process in which pathogens are coated with a substance called opsonin, marking the pathogen out for destruction by the immune system.
While such antibodies are an important part of how pneumococcal vaccines protect against disease, there are PPS-specific antibodies that do not promote opsonic killing but are protective nonetheless. In the study, Masahide Yano and his colleagues identify one of mechanisms these non-opsonic antibodies use. They increase the rate of communication between the bacterial cells as well as competence-induced killing, or fratricide, where the bacteria naturally kill each other off because of overconcentration.
"These findings reveal a novel, previously unsuspected mechanism by which certain PPS-specific antibodies exert a direct effect on pneumococcal biology that has broad implications for bacterial clearance, genetic exchange and antibody immunity to pneumococcus," says Yano.
Why Do Some Influenza Virus Subtypes Die Out?
Every so often we hear about a new strain of influenza virus which has appeared and in some cases may sweep across the globe in a pandemic, much as the H1N1 virus did last year. What happens to the old seasonal viruses? In an opinion piece in the current issue of mBio Peter Palese and Taia Wang of the Mount Sinai School of Medicine in New York City postulate one theory.
"The emergence of novel viruses, historically, has often been coupled with the disappearance of existing seasonal virus strains," they write. "Here, we propose that the elimination seasonal strains during virus pandemics is a process mediate, at the population level, by humoral immunity."
Specifically, Palese and Wang think the reason may be that the new strain retains a critical characteristic of the old strains: the stalks that holds up the hemagglutinin blobs on the surface of the virus (i.e. the 'H' in H1N1).
They suggest that infection with the new influenza virus in people who have been previously infected with influenza virus elicits an anti-stalk antibody response. These antibodies are not strong enough to prevent infection but can recognize a wide variety of influenza viruses. When the immune system confronts the new flu virus, these broadly-neutralizing anti-stalk antibodies are deployed to fight it, lessening the severity of the novel virus, but also eliminating the old virus. Palese and Wang say antibodies against another surface protein, viral neuraminidase (i.e. the 'N' in H1N1), can act in much the same way.
"The present discussion suggests that the induction of a large-scale humoral immune response against conserved hemagglutinin stalk epitopes and/or against the neuraminidase protein results in the clearance of old seasonal influenza virus strains," they write.
Triple Threat: One Bacterium, Three Plasmids
Researchers from Australia found something completely new while conducting a genetic study of the pathogenesis of an enteric disease in birds. They report what is believed to be the first bacterial strain to carry three closely related but independently conjugative plasmids.
The authors were researching the pathogensis of avian necrotic enteritis, a disease caused by the bacterium Clostridium perfringens which causes necrotic lesions in the small intestines of infected birds. This disease is economically important to the poultry industry as acute clinical disease leads to increased mortality of birds and subclinical disease leads to decreased weight and loss of productivity.
In order to cause disease, the bacterium must be capable of producing the toxin netB. In this study the researchers examined the location of netB gene within the Australian necrotic enteritis isolate EHE-NE18, a strain that was also resistant to tetracycline. They found the gene was encoded on a plasmid, a piece of DNA which exists inside the bacterium but is separate from the chromosomal DNA. Plasmids can also replicate independently and can be transferred to other bacteria.
Additional research identified two other plasmids that shared a similar DNA sequence but coded for different processes. One encoded a different toxin, called beta2, and the other coded for the tetracycline resistance.
"To our knowledge, this is the first report of a bacterial strain that carries three closely related by different independently conjugative plasmids. These results have significant implications for our understanding of the transmission of virulence and antibiotic resistance genes in pathogenic bacteria," write the authors.
|Contact: Jim Sliwa|
American Society for Microbiology