IP-10 in occupational asthma: review of the literature and case-control study.

Abstract

T-helper (Th)2 cytokines are thought to mediate most of the allergic inflammatory responses associated with atopic asthma. But the Th1-related chemokine, interferon (IFN)-γ-induced protein 10 (IP-10)/chemokine (C-X-C motif) ligand (CXCL)10, was the predominant chemokine measured during human allergic pulmonary late-phase reaction. Viral infection and allergens can exacerbate asthma by inducing the accumulation of these chemokines and inflammatory cells in the airway. Short-acting β2-adrenoreceptor agonists, budesonide and formoterol (all important relievers in asthma exacerbation), such as vitamin D3, vitamin C, have been shown to inhibit airway cells inflammatory responses by modulating these chemokines. Furthemore it has been suggested that Th1-related IP-10 and monokine induced by IFN-γ (MIG)/CXCL9 may be useful inflammatory markers of asthma exacerbation. In this study we have evaluated serum levels of the Th1-related CXC chemokine IP-10, in 8 patients with occupational asthma (OA) during exacerbation due to occupational exposure, and after 2-3 months, when patients were in stable conditions, in comparison with 8 age and gender matched healthy subjects. A significant increase in the serum levels of IP-10 were found in OA patients with an acute exacerbation in contrast to healthy controls (p<0.01), and in comparison with same OA patients after 2-3 months, when they were without any respiratory symptoms or disorders. These results suggest that the Th1-related CXC chemokines IP-10 is an useful inflammatory marker of OA exacerbation. However, other studies in larger number of patients are needed.