Among the maladies that affect the human brain, meningitis is amongst the most lethal. Shedding more light on the potency of the inflammatory condition, a new study has found that two meningitis-causing bacteria can evade the immune system by slipping past the fever response of the body to infections.
According to researchers from Karolinska Institutet, Streptococcus pneumoniae and Haemophilus influenza—two bacteria that cause meningitis—can mount countermeasures to protect themselves from increasing temperatures of the body. The study published in the journal PLoS Pathogens stated that this evasive safeguard can improve their action against the immune system and boost their chances of survival in the body.
"This discovery helps to increase our understanding of the mechanisms these bacteria use to evade our normal immune defenses. It could be an important piece of the puzzle in examining what turns this usually harmless bacterium into a lethal killer," said Edmund Loh, co-corresponding author of the study, in a statement.
A Neurological Disaster
Meningitis is the severe inflammation of the protective membranes known as meninges that surround the brain and the spinal cord. Several pathogens such as bacteria, fungi, parasites, and viruses can cause the often life-threatening condition. Nearly 10.6 million cases of meningitis were reported worldwide in 2017 alone, with around 288,000 deaths resulting from them.
Bacterial meningitis is among the adverse forms of the condition and is a major cause of disability and death among children across the world. Around 200,000 deaths are attributed to bacterial meningitis annually, including those caused by Streptococcus pneumoniae and Haemophilus influenza.
The two mentioned bacteria are often present in the throat and nose of healthy individuals without causing any illness in them. They are transmitted from person to person via droplets of throat or respiratory secretions. Some of the common symptoms of the condition include stiff neck, high fever, severe headache, seizures, and skin rashes among others. Therapeutic interventions depend on the causative pathogen and the condition itself can be prevented through specific vaccinations.
Countering Increasing Temperatures
One of the prominent indications of an infection in the body is sharply rising temperatures and fever. The aim of the response is to generally amplify the immune system's capacity to combat the infection. Through the study, the authors sought to examine the link between changes in temperature and the rate of survival of S. pneumoniae and H. influenzae under laboratory conditions.
Interestingly, the team discovered that both the bacteria initiated stronger protective measures against the body's immune system when presented with higher temperatures. The current study was also informed by recent findings that found a connection between the abilities of the Neisseria meningitides bacteria to sense temperature and the meningococcal disease that it causes.
Protection Bestowed By RNA Molecules
The authors explained that this mechanism of the bacteria involved four specific temperature-sensitive non-coding RNA molecules known as RNA thermosensors (RNATs). These RNATs enabled the heightened production of larger protective capsules and Factor H binding proteins—components that protect these pathogens from the immune system's onslaught.
"Our results indicate that these temperature sensing RNATs create an additional layer of protection that helps the bacteria colonize their normal habitat in the nose and throat," noted Hannes Eichner, first author of the study. He illustrated: "Interestingly, we saw that these RNATs do not possess any sequence similarity, but all retain the same thermosensing ability, which indicates that these RNATs have evolved independently to sense the same temperature cue in the nasopharynx to avoid immune killing."
Nevertheless, the authors admitted that additional research was required to glean the exact triggers that lead to the bacteria invading the bloodstream and deeper parts of the brain from the mucous membrane. They also called for studies involving in vivo infection models for understanding the role of the specific RNATs during the course of the pathogens' colonization and invasion process.
