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Clostridium difficile binary toxin (CDT) is recognized by the TLR2/6 heterodimer to induce an NF-κB response

By Morgan Simpson, Alyse Frisbee, Pankaj Kumar, Carsten Schwan, Klaus Aktories, William A Petri

Posted 09 Sep 2020
bioRxiv DOI: 10.1101/2020.09.08.288209

Clostridioides difficile infection (CDI) represents a significant burden on the health care system, one that is exacerbated by the emergence of binary toxin (CDT)-producing hypervirulent C. difficile strains. Previous work from our lab has shown that TLR2 recognizes CDT to induce inflammation. Here we explore the interactions of CDT with TLR2 and the impact on host immunity during CDI. We found that the TLR2/6 heterodimer, not TLR2/1, is responsible for CDT recognition, and that gene pathways including NF-κB and MAPK downstream of TLR2/6 are upregulated in mice with intact TLR2/6 signaling during CDI. ### Competing Interest Statement Dr. Petri is a consultant for TechLab, Inc, outside the submitted work

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