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If you have any questions, you are always welcome to contact us. We'll get back to you as soon as possible, withing 24 hours on weekdays.
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All questions about your order, return and delivery must be sent to our customer service team by e-mail at yourstore@yourdomain.com
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Epidemiological and genetic studies showed that severity of invasive group A streptococcal (GAS) sepsis is influenced by interactions of genetic factors of both bacteria and host. Systems biology approaches presented shed light on host mechanisms of differential response to invasive GAS sepsis. Using genomewide association studies, we found association between differential susceptibility to GAS sepsis and quantitative trait loci (QTL) on mouse Chr 2 and X. Genes within these QTLs were prioritized based on bioinformatics and qPCR to explore mechanisms of host differential susceptibility. Collectively, data suggested that prostaglandin and interleukin 1 signaling pathways act as key modulators of a network of genes involved in immune responses to GAS sepsis. In addition, genomewide transcriptome studies showed that pathways involving activation of interleukin 10 production and signaling are likely to be associated with resistance to infection. Despite differences between mouse and human immune systems, systems biology approaches results using mice corresponded well with results obtained from human studies demonstrating the power of this approach and better translation to humans.
⚠️ WARNING (California Proposition 65):
This product may contain chemicals known to the State of California to cause cancer,
birth defects, or other reproductive harm.
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