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Bacterial pathogenesis

Meningococcus warms up to immune evasion

Nature Reviews Microbiology volume 11, page 818 (2013)Cite this article

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Loh, Kugelberg et al. show that a temperature increase triggers immune evasion by Neisseria meningitidis owing to the control of gene expression by three independent RNA thermosensors. RNA thermosensors are located in the 5′ UTRs of mRNAs and, at low temperatures, form stable hairpin structures that prevent ribosome binding and thereby inhibit translation. At higher temperatures, the hairpin melts and gene expression is restored. The authors found that these thermosensors are upstream of genes that are involved in capsule biosynthesis, lipopolysaccharide sialylation and factor H-binding protein expression, all of which are required for immune evasion. They conclude that increases in temperature function as an alarm signal for meningococci to upregulate immune defence genes. As temperature increases during the inflammatory response to other pathogens, this adaptive mechanism could provide these bacteria with an advantage during co-infections.

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References

  1. Loh, E., Kugelberg, E. et al. Temperature triggers immune evasion by Neisseria meningitidis. Nature 502, 237–240 (2013)

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  1. Christina Tobin Kåhrström
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Kåhrström, C. Meningococcus warms up to immune evasion. Nat Rev Microbiol 11, 818 (2013). https://doi.org/10.1038/nrmicro3171

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