Acute exposure to methamphetamine alters TLR9-mediated cytokine expression in human macrophage

Ariel Burns, Pawel Ciborowski

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Recent studies show that methamphetamine (Meth) use leads to higher susceptibility to and progression of infections, which suggests impairment of the immune system. The first line of defense against infections is the innate immune system and the macrophage is a key player in preventing and fighting infections. So we profiled cytokines over time in Meth treated THP-1 cells, as a human macrophage model, at a relevant concentration using high throughput screening to find a signaling target. We showed that after a single exposure, the effect of Meth on macrophage cytokine production was rapid and time dependent and shifted the balance of expression of cytokines to pro-inflammatory. Our results were analogous to previous reports in that Meth up-regulates TNF-α and IL-8 after two hours of exposure. However, global screening led to the novel identification of CXCL16, CXCL1 and many other up-regulated cytokines. We also showed CCL7 as the most down-regulated chemokine due to Meth exposure, which led us to hypothesize that Meth dysregulates the MyD88-dependent Toll-like receptor 9 (TLR9) signaling pathway. In conclusion, altered cytokine expression in macrophages suggests it could lead to a suppressed innate immunity in people who use Meth.

Original languageEnglish (US)
Pages (from-to)199-207
Number of pages9
JournalImmunobiology
Volume221
Issue number2
DOIs
StatePublished - Feb 1 2016

Keywords

  • CCL7
  • Cytokine
  • Inflammation
  • Macrophage
  • Methamphetamine
  • Toll-like receptor signaling

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Hematology

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