Elevated Toll-Like Receptor-Induced CXCL8 Secretion in Human Blood Basophils from Allergic Donors Is Independent of Toll-Like Receptor Expression Levels

PLoS One. 2016 Feb 12;11(2):e0149275. doi: 10.1371/journal.pone.0149275. eCollection 2016.

Abstract

Human blood basophils have recently gained interest in addition to their function as allergic effector cells. Previous work suggests the involvement of innate immune mechanisms in the development and exacerbation of allergic responses, which might be mediated by basophils. We assayed the expression levels of Toll-like receptor (TLR) 1, 2, 4 and 6 on purified basophils from birch pollen-, house dust mite-, and non-allergic individuals. Additionally, we compared cytokine and chemokine secretion upon TLR stimulation in these basophil donor groups. Expression of TLR4 on the basophils of the allergic donor groups was decreased and CXCL8 secretion was elevated upon stimulation of TLR1/2 and TLR2/6 compared to the non-allergic donors. Decreased TLR expression and elevated CXCL8 secretion may represent possible mechanisms for aggravation of allergic symptoms in case of parasitic infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Basophils / immunology*
  • Basophils / pathology
  • Child
  • Female
  • Humans
  • Hypersensitivity / immunology*
  • Hypersensitivity / pathology
  • Interleukin-8 / analysis
  • Interleukin-8 / immunology*
  • Male
  • Middle Aged
  • Toll-Like Receptor 1 / analysis
  • Toll-Like Receptor 1 / immunology
  • Toll-Like Receptor 2 / analysis
  • Toll-Like Receptor 2 / immunology
  • Toll-Like Receptor 4 / analysis
  • Toll-Like Receptor 4 / immunology
  • Toll-Like Receptor 6 / analysis
  • Toll-Like Receptor 6 / immunology
  • Toll-Like Receptors / analysis
  • Toll-Like Receptors / immunology*
  • Young Adult

Substances

  • Interleukin-8
  • Toll-Like Receptor 1
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4
  • Toll-Like Receptor 6
  • Toll-Like Receptors

Grant support

This work was supported by grant P18820-B13 of the Austrian Science Fund (FWF). Buehlmann Laboratories AG did not play a role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript and only provided financial support in the form of authors' salaries (Michael Schneider) and/or research materials (stimulation buffer for basophils).