Ascaris suum infection modulates inflammation: Implication of CD4+ CD25high Foxp3+ T cells and IL-10

Parasite Immunol. 2017 Sep;39(9). doi: 10.1111/pim.12453.


Helminth infections have the ability to modulate host's immune response through mechanisms that allow the chronic persistence of the worms in the host. Here, we investigated the mechanisms involved on the suppressive effect of Ascaris suum infection using a murine experimental model of LPS-induced inflammation. We found that infection with A. suum markedly inhibited leucocyte influx induced by LPS into air pouches, suppressed secretion of pro-inflammatory cytokines (IL-1β, TNF-α and IL-6) and induced high levels of IL-10 and TGF-β. Augmented frequency of CD4+ CD25high Foxp3+ T cells was observed in the mesenteric lymph nodes of infected mice. Adoptive transfer of purified CD4+ CD25+ T cells to recipient uninfected mice demonstrated that these cells were able to induce a suppressive effect in the LPS-induced inflammation in air pouch model. In addition, adoptive transfer of CD4+ CD25+ T cells derived from IL-10 knockout mice suggests that this suppressive effect of A. suum infection involves IL-10 cytokine. In conclusion, our results demonstrated that A. suum experimental infection was capable of suppressing LPS-induced inflammation by mechanisms, which seem to be dependent on responses of CD4+ CD25+ T cells and secretion of IL-10 cytokine.

Keywords: Ascaris suum; IL-10; immunomodulation; inflammation; regulatory T cells.

MeSH terms

  • Adoptive Transfer
  • Animals
  • Ascariasis / immunology*
  • Ascariasis / parasitology
  • Ascaris suum / immunology*
  • CD4 Antigens / metabolism
  • Cytokines / metabolism
  • Female
  • Forkhead Transcription Factors / metabolism
  • Inflammation / chemically induced
  • Interleukin-10 / metabolism
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Interleukin-6 / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • T-Lymphocytes / immunology
  • Transforming Growth Factor beta / metabolism
  • Tumor Necrosis Factor-alpha / metabolism


  • CD4 Antigens
  • Cytokines
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • IL10 protein, mouse
  • Il2ra protein, mouse
  • Interleukin-2 Receptor alpha Subunit
  • Interleukin-6
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Interleukin-10