Clearance of Pneumocystis murina infection is not dependent on MyD88

Microbes Infect. 2014 Jun;16(6):522-7. doi: 10.1016/j.micinf.2014.03.005. Epub 2014 Mar 25.

Abstract

To determine if myeloid differentiation factor 88 (MyD88), which is necessary for signaling by most TLRs and IL-1Rs, is necessary for control of Pneumocystis infection, MyD88-deficient and wild-type mice were infected with Pneumocystis by exposure to infected seeder mice and were followed for up to 106 days. MyD88-deficient mice showed clearance of Pneumocystis and development of anti-Pneumocystis antibody responses with kinetics similar to wild-type mice. Based on expression levels of select genes, MyD88-deficient mice developed immune responses similar to wild-type mice. Thus, MyD88 and the upstream pathways that rely on MyD88 signaling are not required for control of Pneumocystis infection.

Keywords: Innate immunity; MyD88; PCP; Pneumocystis; TLR.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Mice
  • Mice, Inbred C57BL
  • Myeloid Differentiation Factor 88 / genetics
  • Myeloid Differentiation Factor 88 / immunology*
  • Myeloid Differentiation Factor 88 / metabolism
  • Pneumocystis / pathogenicity*
  • Pneumocystis Infections / genetics
  • Pneumocystis Infections / immunology*
  • Receptors, Interleukin-1 / genetics
  • Receptors, Interleukin-1 / metabolism
  • Signal Transduction*

Substances

  • Myeloid Differentiation Factor 88
  • Receptors, Interleukin-1