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Updated: Nov 7, 2025

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
Published on: February 19, 2019
RNA thermosensors facilitate Streptococcus pneumoniae and Haemophilus influenzae immune evasion
Hannes Eichner1, Jens Karlsson1, Laura Spelmink1
1Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Solna, Sweden.
Abstract:
Bacterial meningitis is a major cause of death and disability in children worldwide. Two human restricted respiratory pathogens, Streptococcus pneumoniae and Haemophilus influenzae, are the major causative agents of bacterial meningitis, attributing to 200,000 deaths annually. These pathogens are often part of the nasopharyngeal microflora of healthy carriers. However, what factors elicit them to disseminate and cause invasive diseases, remain unknown. Elevated temperature and fever are hallmarks of inflammation triggered by infections and can act as warning signals to pathogens. Here, we investigate whether these respiratory pathogens can sense environmental temperature to evade host complement-mediated killing. We show that productions of two vital virulence factors and vaccine components, the polysaccharide capsules and factor H binding proteins, are temperature dependent, thus influencing serum/opsonophagocytic killing of the bacteria. We identify and characterise four novel RNA thermosensors in S. pneumoniae and H. influenzae, responsible for capsular biosynthesis and production of factor H binding proteins. Our data suggest that these bacteria might have independently co-evolved thermosensing abilities with different RNA sequences but distinct secondary structures to evade the immune system.
Insights
Bacteria causing meningitis, Streptococcus pneumoniae and Haemophilus influenzae, sense temperature to evade immune defenses. This temperature sensing affects capsule and protein production, crucial for bacterial survival and disease.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Bacterial meningitis remains a significant global health threat, particularly for children.
- Streptococcus pneumoniae and Haemophilus influenzae are leading causes of bacterial meningitis, originating from the nasopharyngeal microflora.
- The transition from asymptomatic carriage to invasive disease is poorly understood, especially the role of host-pathogen interactions during infection.
Purpose of the Study:
- To investigate if Streptococcus pneumoniae and Haemophilus influenzae can sense environmental temperature to evade host immune responses.
- To determine the impact of temperature on the production of key virulence factors, including polysaccharide capsules and factor H binding proteins.
- To identify molecular mechanisms, specifically RNA thermosensors, involved in temperature-dependent regulation of virulence in these pathogens.
Main Methods:
- Culturing of Streptococcus pneumoniae and Haemophilus influenzae at varying temperatures.
- Quantification of polysaccharide capsule production and factor H binding protein expression under different temperature conditions.
- Identification and characterization of novel RNA thermosensors using molecular biology techniques, including sequence analysis and secondary structure prediction.
Main Results:
- Bacterial virulence factor production, specifically polysaccharide capsules and factor H binding proteins, is significantly influenced by temperature.
- The identified RNA thermosensors in both S. pneumoniae and H. influenzae regulate the biosynthesis of capsules and the production of factor H binding proteins.
- Temperature-dependent regulation of these virulence factors impacts the bacteria's ability to evade serum-mediated killing and opsonophagocytosis.
Conclusions:
- Streptococcus pneumoniae and Haemophilus influenzae possess thermosensing capabilities that allow them to modulate virulence factor expression in response to environmental temperature changes.
- Novel RNA thermosensors play a critical role in this temperature-dependent immune evasion strategy.
- These findings suggest independent co-evolution of thermosensing mechanisms in these distinct bacterial species to enhance survival against host immune defenses.
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