Publications by authors named "Katie L Styer"
A large body of evidence indicates that metazoan innate immunity is regulated by the nervous system, but the mechanisms involved in the process and the biological importance of such control remain unclear. We show that a neural circuit involving npr-1, which encodes a G protein-coupled receptor (GPCR) related to mammalian neuropeptide Y receptors, functions to suppress innate immune responses. The immune inhibitory function requires a guanosine 3',5'-monophosphate-gated ion channel encoded by tax-2 and tax-4 as well as the soluble guanylate cyclase GCY-35.
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- Yersinia pestis, the bacteria responsible for plague, needs to survive in blood and evade the immune system to spread effectively via fleas.
- The study identified four Ail/Lom family proteins in the Y. pestis genome, with Ail being crucial for resisting immune attacks at body temperatures but not at cooler ones.
- Deleting the Ail protein made Y. pestis highly vulnerable to the immune response from most mammals, except mice, and tests were conducted to understand Ail's role in infecting mice, worms, and fleas.
CCR5 is a chemokine receptor used by HIV-1 to enter cells and has recently been found to act as a pathogen associated molecule pattern receptor. Current positive selection for the high frequency of a CCR5-Delta32 allele in humans has been attributed to resistance to HIV, smallpox, and plague infections. Using an intranasal mouse model of Y.
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- Yersinia pestis, the bacterium responsible for the plague, can kill the roundworm Caenorhabditis elegans (C. elegans) through different mechanisms, including a biofilm-dependent one and a newly discovered biofilm-independent one.
- Research using a specific mutant strain of Y. pestis lacking biofilm-forming genes revealed that the bacteria can still kill C. elegans by accumulating in its intestine, highlighting the complexity of its pathogenic mechanisms.
- The study identified both known and previously unknown virulence-related genes essential for Y. pestis's effectiveness, including a novel gene linked to reduced virulence in mice, suggesting that this model system could help uncover new virulence factors relevant to mammalian infections