Researchers at the Karolinska Institute in Sweden have discovered a mechanism by which bacteria that cause meningitis can escape our immune system. In lab tests, they found that Streptococcus pneumoniae and Haemophilus influenzae respond to rising temperatures by producing protective measures that prevent them from getting killed. This can prime their defenses against our immune system and increase their chances of survival, researchers say. The results are published in the journal PLoS pathogens.
“This discovery helps us better understand the mechanisms these bacteria use to escape our normal immune defenses,” says co-correspondent author Edmund Loh, researcher in the Department of Microbiology, Tumor and Cell Biology at the Karolinska Institute. “It could be an important piece of the puzzle for examining what turns this generally harmless bacteria into a deadly killer.”
Meningitis is an inflammation of the membranes surrounding the brain and spinal cord. It can be caused by viruses, bacteria, fungi and parasites.
Bacterial meningitis is one of the most serious types and a leading cause of death and disability in children worldwide. Several types of bacteria can cause infection, including the respiratory pathogens Streptococcus pneumoniae and Haemophilus influenzae, which can be attributed to some 200,000 meningitis deaths each year.
These two bacteria often reside in the nose and throat of healthy people without making them sick. In some cases, they spread through the bloodstream and cause invasive disease, but the reasons are largely unknown.
In this study, the researchers set out to investigate the link between changes in temperature and the survival of these bacteria in the laboratory. The experiments were prompted by another recent discovery that linked the temperature sensing capabilities of N. meningitidis bacteria to invasive meningococcal disease.
One of the signs of an infection is a high temperature and fever, which usually increase the ability of our immune system to fight off the disease. In this study, however, researchers found that S. pneumoniae and H. influenzae activated stronger immune protections when faced with higher temperatures.
They did this through mechanisms involving four specific RNA Temperature Sensors (RNATs), which are temperature-sensitive, non-coding RNA molecules. These RNATs helped stimulate the production of larger protective capsules and immunomodulatory factor H binding proteins, both of which help protect these bacteria from attack by the immune system.
“Our results indicate that these temperature-sensing RNATs create an additional layer of protection that helps bacteria colonize their normal habitat in the nose and throat,” explains the first author of the article, Hannes Eichner, a doctoral student in the same. department. “Interestingly, we saw that these RNATs do not have any sequence similarity, but all retain the same thermodetection ability, indicating that these RNATs have independently evolved to detect the same temperature signal in the nasopharynx to avoid immune destruction. . “
More research is needed to understand exactly what triggers the rupture of these mucous membrane pathogens into the bloodstream and further into the brain. Future studies encompassing the in vivo infection model are warranted to characterize the role of these RNATs during colonization and invasion, the researchers say.
The work was supported by grants from the Knut and Alice Wallenberg Foundation, the Swedish Foundation for Strategic Research, the Swedish Research Council, Stockholm County Council and the Karolinska Institute.
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