Antibiotics promote susceptibility to C. difficile infection through a CCR5-dependent immune response
Md Jashim Uddin 1,§,#, Nick R Natale 1,2,3,4,#, Farha Naz 1, Jiayi Tian 1,4, Rachel McMillan 1,4, Duncan J Hart 1,4, Shelby L Schenck 1,4, William A Petri Jr
https://pmc.ncbi.nlm.nih.gov/articles/PMC13345209/
"ABX treatment enriched the colon with type I immunity-associated leukocytes, including CCR5+ ILC1s and CCR5+ Th1 cells, prompting us to investigate the role of CCR5 in orchestrating the immune response during CDI. Both partial genetic deletion of CCR5 and pharmacological inhibition of CCR5 ameliorated disease severity, suggesting that a CCR5-dependent immune circuit drives CDI susceptibility. Collectively, these findings unveil a CCR5-reliant type I immune response as an underappreciated mechanism by which ABXs prime the host for severe CDI"
Md Jashim Uddin 1,§,#, Nick R Natale 1,2,3,4,#, Farha Naz 1, Jiayi Tian 1,4, Rachel McMillan 1,4, Duncan J Hart 1,4, Shelby L Schenck 1,4, William A Petri Jr
https://pmc.ncbi.nlm.nih.gov/articles/PMC13345209/
"ABX treatment enriched the colon with type I immunity-associated leukocytes, including CCR5+ ILC1s and CCR5+ Th1 cells, prompting us to investigate the role of CCR5 in orchestrating the immune response during CDI. Both partial genetic deletion of CCR5 and pharmacological inhibition of CCR5 ameliorated disease severity, suggesting that a CCR5-dependent immune circuit drives CDI susceptibility. Collectively, these findings unveil a CCR5-reliant type I immune response as an underappreciated mechanism by which ABXs prime the host for severe CDI"
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