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Infect Immun. 2017 July; 85(7): e00348-17.
Published online 2017 June 20. doi:  10.1128/IAI.00348-17
PMCID: PMC5478952

Articles of Significant Interest Selected from This Issue by the Editors

Pneumocystis murina Induces Th1 and Th17 Responses in Immunocompetent Mice but Does Not Require Interleukin-17A for Clearance

Pneumocystis causes life-threatening pneumonia in immunosuppressed hosts but also infects immunocompetent hosts; CD4+ T cells are critical to clearing infection. In a mouse model that utilizes cohousing to transmit Pneumocystis infection by the respiratory route, Ripamonti et al. (e00434-16) demonstrate that pulmonary CD4+ Th1 and Th17 responses predominated and coincided with clearance of infection, while Th2 responses were minimal. However, interleukin-17A knockout mice cleared infection with kinetics similar to wild-type mice. Since prior studies have shown that gamma interferon knockout mice also clear infection, these studies suggest that redundant CD4+ Th cell pathways play a role in controlling Pneumocystis infection.

The Common Anesthetic Propofol Exacerbates Staphylococcus aureus Infections

Propofol is a widely used anesthetic induction agent, and recent evidence indicates that propofol sedation can increase host susceptibility to microbial infection. Visvabharathy and Freitag (e00097-17) find that 5 minutes of propofol sedation significantly increased kidney pathology in mice infected with methicillin-resistant Staphylococcus aureus (MRSA). Propofol sedation reduced the numbers of mature immune effector cells and expanded myeloid-derived suppressor cell-like populations. When coadministered with vancomycin, propofol dramatically increased kidney abscess formation and bacterial dissemination. Propofol sedation thus exacerbates the severity of bloodstream MRSA infection even with vancomycin prophylaxis, a finding with potentially important implications for patient care.


Articles from Infection and Immunity are provided here courtesy of American Society for Microbiology (ASM)