The Interleukin (IL) 17R/IL-22R Signaling Axis Is Dispensable for Vulvovaginal Candidiasis Regardless of Estrogen Status. J Infect Dis 2020 Apr 07;221(9):1554-1563
Date
12/06/2019Pubmed ID
31805183Pubmed Central ID
PMC7137889DOI
10.1093/infdis/jiz649Scopus ID
2-s2.0-85078761600 (requires institutional sign-in at Scopus site) 46 CitationsAbstract
Candida albicans, a ubiquitous commensal fungus that colonizes human mucosal tissues and skin, can become pathogenic, clinically manifesting most commonly as oropharyngeal candidiasis and vulvovaginal candidiasis (VVC). Studies in mice and humans convincingly show that T-helper 17 (Th17)/interleukin 17 (IL-17)-driven immunity is essential to control oral and dermal candidiasis. However, the role of the IL-17 pathway during VVC remains controversial, with conflicting reports from human data and mouse models. Like others, we observed induction of a strong IL-17-related gene signature in the vagina during estrogen-dependent murine VVC. As estrogen increases susceptibility to vaginal colonization and resulting immunopathology, we asked whether estrogen use in the standard VVC model masks a role for the Th17/IL-17 axis. We demonstrate that mice lacking IL-17RA, Act1, or interleukin 22 showed no evidence for altered VVC susceptibility or immunopathology, regardless of estrogen administration. Hence, these data support the emerging consensus that Th17/IL-17 axis signaling is dispensable for the immunopathogenesis of VVC.
Author List
Peters BM, Coleman BM, Willems HME, Barker KS, Aggor FEY, Cipolla E, Verma AH, Bishu S, Huppler AH, Bruno VM, Gaffen SLAuthor
Anna Huppler MD Associate Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCandida albicans
Candidiasis, Oral
Candidiasis, Vulvovaginal
Disease Models, Animal
Estrogens
Female
Interleukin-17
Mice
Mice, Inbred C57BL
Mucous Membrane
Receptors, Interleukin
Receptors, Interleukin-17
Signal Transduction
Vagina
