A research team from UConn's Center of Excellence in Vaccine Research (CEVR) has made a huge leap in experimentations for vaccine development. Finding a vaccine for Mycoplasma pneumoniae has been a struggle for scientists since they have found that vaccines previously tested for the pathogen caused rebound effects.
In the new study, the researchers have found that cytokines play an important role in vaccine protection in similar pneumonia-causing bacteria. Through cytokines, they were able to get rid of the hurdle of vaccine-enhanced disease (VED) with the pneumonia-provoking pathogen.
Although the journey to finding a safe and efficient vaccine is still far from over, the research team is excited with the contribution of their findings. The complete details of their research paper were published in the clinical journal Nature Partner Journal, Vaccines.
Diseases Made Worse by Vaccines
Vaccine research for Mycoplasma pneumoniae was stalled since the 1960s after it was found to cause VED. During this time, community-acquired pneumonia (CAP) was becoming a widespread disease in closed community settings such as prisons, college dormitories, military bases, ships, and hospitals. There was a dire need for a vaccine at the time because of these circumstances.
According to Steven Szczepanek, an assistant professor in Pathobiology and Veterinary Science from the facility, the NIH developed two vaccines to address the problem. In most people vaccinated, protection from the disease was evident, and they showed no symptoms. On the other hand, there were instances wherein symptoms got worse for people who were vaccinated and already infected.
He said their symptoms were even worse than those who did not get the vaccine. Experts have concluded that the course of VED for pneumonia was terrible. VED is paradoxical to the reason behind vaccination. To cure the disease, scientists deduce that they need to come up with a vaccine that strikes a balance.
Furthermore, Steven Geary, the department head of Pathobiology and Veterinary Science, and the director of CERVED said that VED has also been detected in other pathogens. Dengue fever and respiratory syncytial virus (RSV), in particular, also displayed the phenomenon in animal models in SARS vaccine research.
On Cytokines and Lipoproteins
Szczepanek explains that trends in research reveal that cytokines play an important part in vaccine protection to Streptococcus pneumoniae. The bacteria is another known pneumonia-causing pathogen. They were able to determine that the same cytokines with it were driving VED with M. pneumoniae.
To determine the cause of VED with M. pneumoniae vaccination, the researchers broke down the building blocks of the bacteria. They each examined its proteins, lipids, and lipoproteins to check if they gave off an immune response.
Later on, they were able to pinpoint that membrane-bound surface lipoprotein was the cause of VED in pneumonia. They found that the chemical expulsion of the lipid portion of purified M. pneumoniae lipoproteins erased VED. Furthermore, it even caused some level of protection from infection.
Although more work and research have to be done to enhance the efficacy of a vaccine formulation fully, the researchers are confident that their findings will be helpful in future researchers.
They claim to have identified and eliminated the cause of VED that halted the field for research on the disease for over half a century. Finally, they conclude that safety concerns are no longer a problem for M. pneumoniae vaccines.