Dimethyl sulfoxide decreases interleukin-8-mediated neutrophil recruitment in the airways

Abstract

In this study, we investigated the role of dimethyl sulfoxide (DMSO) in inhibiting interleukin-8 (IL-8)-mediated neutrophil recruitment induced by Pseudomonas aeruginosa (PA) bacterial supernatant. First, we tested whether DMSO could inhibit IL-8 production induced by PA in human bronchial epithelial (16-HBE) cells in vitro. In these cells, exposure to PA or H2O2 induced IL-8 production dose dependently, an effect that was inhibited by 1% DMSO at both the protein and RNA level. Second, we tested whether DMSO could block the recruitment of neutrophils induced by PA in a bypassed segment of dog trachea in vivo. PA supernatant was placed in the tracheal segment for 6 h in four dogs, and neutrophil recruitment and IL-8 concentrations were measured in the superfusate. DMSO prevented the recruitment of neutrophils and IL-8 production induced by PA time dependently. The results suggest that DMSO may play an anti-inflammatory role in the airway by inhibiting IL-8 production in epithelial cells.

Neutrophilic airway inflammation and IL‐17

“…These radicals can increase the transcription of IL-8 mRNA, leading to IL-8 protein production, subsequent neutrophil recruitment and bronchial hyperresponssiveness in canine airways (29)(30)(31). This also supports the idea that neutrophils have a functional impact in the airways and lungs.…”

Neutrophils, interleukin-17A and lung disease

“…This is of interest as there is experimental evidence in mammals that reactive oxygen species can induce the transcription of the mRNA encoding neutrophil-recruiting cytokines, such as the functionally important neutrophil chemoattractant IL-8, leading to subsequent release of IL-8 and more neutrophil recruitment [94,95]. Hypothetically, these events might contribute to altered lung function, since reactive oxygen species contribute to nonspecific bronchial hyperresponsiveness and this phenomenon may involve neutrophils in the lungs in vivo, as indicated by studies in cats, dogs and guinea pigs [64,[96][97][98][99].…”

“…Thus, neutrophils themselves have the capacity to recruit even more neutrophils; this mechanism probably normally serves to mobilise large numbers of neutrophils to sites of infection. TNF-a probably also causes additional neutrophil recruitment via the stimulation of IL-8 release from bronchial epithelial cells [94,110,111]. In addition, there is evidence that IL-8 prolongs neutrophil survival, by delaying cell death through apoptosis [112,113].…”

“…Thus, bronchial epithelial cells, bronchial smooth muscle cells, fibroblasts, monocyte-derived cells, neutrophils and even eosinophils bear the potential of contributing to neutrophil recruitment by releasing IL-8 and other CXC chemokines in diseases such as asthma and chronic bronchitis [5,94,110,111,[116][117][118][119][120].…”

Airway neutrophils and interleukin-17

“…The recruitment and activation of neutrophils in the airways may therefore contribute to excacerbations of obstructive airways disease. This also means that factors controlling the mediators affecting neutrophil recruitment, such as CXC chemokines or tachykinins [12,13,20], may play a role in triggering exacerbations of obstructive airways disease.…”