Abnormal M1 polarization of placental macrophage induced by IL-15/STAT5 activation in VVC may lead to adverse pregnancy outcomes

Microbes Infect. 2024 Jan-Feb;26(1-2):105232. doi: 10.1016/j.micinf.2023.105232. Epub 2023 Oct 5.

Abstract

Pregnant women with vulvovaginal candidiasis (VVC) may experience adverse pregnancy outcomes such as premature delivery, intrauterine infection, abortion, and neonatal infection. Therefore, finding new treatments for VVC in pregnancy is a public health priority. We aimed to study the adverse consequences of Candida albicans (C. albicans) vaginal infection in pregnant mice and explore the mechanisms by which C. albicans affects macrophages. Our findings contribute to the development of new approaches to treat VVC during pregnancy. We established an animal model of vaginal infection by C. albicans in pregnant mice and observed adverse pregnancy outcomes such as decreased body weight, reduced implantation number, and increased abortion rates. Additionally, we infected mouse macrophage line RAW264.7 cells with C. albicans and established a cell model. We employed RT-qPCR, Western blot, and immunofluorescence staining to verify the changes in the IL-15/STAT5 signaling pathway and the role it played on the M1 polarization of C. albicans-infected macrophages at both the gene and protein levels. Our results indicate that the adverse pregnancy outcomes in VVC may be linked to changes in the IL-15/STAT5 pathway induced by C. albicans, which could impact macrophage M1 polarization.

Keywords: Candida albicans; IL-15; M1 polarization; Pregnancy; STAT5; Vulvovaginal candidiasis.

MeSH terms

  • Animals
  • Antifungal Agents / pharmacology
  • Antifungal Agents / therapeutic use
  • Candida albicans
  • Candidiasis, Vulvovaginal* / drug therapy
  • Female
  • Humans
  • Interleukin-15
  • Macrophages
  • Mice
  • Placenta
  • Pregnancy
  • Pregnancy Outcome
  • STAT5 Transcription Factor
  • Signal Transduction

Substances

  • Antifungal Agents
  • Interleukin-15
  • STAT5 Transcription Factor
  • STAT5A protein, human
  • Stat5a protein, mouse
  • IL15 protein, human