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Keywords:

  • adrenergic antagonists;
  • adrenergic receptors;
  • chemokines;
  • intestinal epithelial cells;
  • norepinephrine;
  • stress;
  • Toxoplasma gondii

Summary

Infection with Toxoplasma gondii induces chemokine up-regulation in several cell types. Here, we investigated the role of stress products (norepinephrine, NE) on chemokine production in mouse intestinal epithelial cells (IECs). Purified IECs were used to determine the expression levels of chemokines by real-time PCR. There was significantly increased expression in CCL2, CCL3, CCL5, CXCL2, CXCL9 and CXCL10 in IECs following peroral infection with T. gondii (INF) on day eight post-infection (PI) compared to infected mice subjected to cold-water stress (INF+CWS). In vitro studies using the MODE-K cell line showed increased chemokine mRNA and protein expression in infected but not in cells exposed to parasite antigen. Down-regulation of chemokine expression was more pronounced when active infection was used in combination with NE. Chemokine receptor expression was increased in IECs isolated from INF and decreased in the INF+CWS group. In MODE-K cells, there was decreased mRNA expression of chemokine receptors when incubated with β-adrenergic antagonists. Neither, adrenergic antagonists blocked the effect of infection on chemokine receptor expression. Cold-water stress was able to decrease expression of chemokines and their receptors in IECs in vivo and in vitro. Cold-water stress-mediated modulation of innate intestinal responses are beneficial in C57BL/6 mice during T. gondii infection.