IL-8 and the Activation of Eosinophils and Neutrophils following Nasal Allergen Challenge

Abstract

Background: A growing body of evidence suggests that proinflammatory cytokines play a role in allergic inflammation by attracting and activating inflammatory cells. In this study, we have investigated the relationship between interleukin-8 (IL-8) in nasal lavage fluid and the local activation of eosinophils and neutrophils following nasal allergen challenge of allergic patients. Methods: Nasal challenges were performed with grass pollen extract in 14 allergic patients and 5 nonallergic controls. Nasal lavage fluid was collected repeatedly for 10 h, and the levels of eosinophil cationic protein (ECP) and myeloperoxidase (MPO) were used as markers of eosinophil and neutrophil activation, respectively. The levels of these molecules were compared with that of IL-8 in nasal lavage fluid. Results: Allergen challenge of allergic patients produced a significant late-phase increase in the levels of ECP and MPO. Furthermore, the level of MPO showed a highly significant correlation with the level of IL-8 in lavage fluid (r = 0.8, p < 0.0001), whereas there was no significant relationship between the levels of ECP and IL-8. Conclusion: Interestingly, our findings suggest that both eosinophils and neutrophils are activated following nasal allergen challenge. In addition, our results are consistent with the hypothesis that IL-8 acts as a chemoattractant/activator of neutrophils during the late phase of the allergic inflammation. In contrast, we were not able to demonstrate any significant relationship between the level of IL-8 in lavage fluid and the activation of eosinophils.

Comparison of Allergen-Induced Late Inflammatory Reactions in the Nose and in the Skin in House Dust Mite-Allergic Patients with or without Asthma

“…The increase in nasal IL-5 and IL-8 and the subsequent influx of inflammatory cells accompanied by the increase in the soluble cell markers ECP and MPO as found in this study is in agreement with the results of other studies [12, 14, 23, 32, 33, 34, 35]. The association between increases in the chemoattractants IL-5 and IL-8 and the nasal influx of eosinophils and neutrophils, respectively, during the late phase, is in agreement with their reported role for the recruitment of these inflammatory cells.…”

“…Primary outcomes were levels of interleukin-5 (IL-5), IL-8, eosinophil cationic protein (ECP), myeloperoxidase (MPO) and cell differentials obtained during the phase of the late allergic reaction (4–24 h). Early protein leakage (α 2 -macroglobulin, A2M) and histamine levels were monitored as an indicator for early mast cell degranulation in the nose [12, 13, 14, 15]. The study was designed to detect a 25% difference in late skin reactivity and a 30% difference in log-normalized levels of soluble markers with a power of 0.80 and a 95% confidence level.…”

Levocetirizine better protects than desloratadine in a nasal provocation with allergen

“…43,44 An increase in IL-5, IL-8, eotaxin, and ECP levels was generally reported. 43,[45][46][47][48][49] A few studies only indicated an inhibition of IL-8 secretion by astemizole in a nasal challenge with allergen and of ECP and eosinophil influx by cetirizine, loratadine, or azelastine in seasonal trials. [50][51][52][53] In this single-dose trial, we could not demonstrate any effect of either levocetirizine or desloratadine at 5 mg on cytokine levels (IL-4 and IL-5), on chemokine levels (IL-8 and eotaxin), or on ECP secretion.…”

Characterisation of immune mediator release during the immediate response to segmental mucosal challenge in the jejunum of patients with food allergy

“…31 32 In our study, the absence of ECP increase after antigen challenge may be due to late phase release (more than six hours later) of this mediator during hypersensitivity reactions, as has been shown in faeces, tears, and nasal and bronchial fluids 2931 33-35 In contrast, non-atopic patients with intolerance to milk or patients with coeliac disease exhibited early increases in intestinal ECP release (20 minutes) after intraluminal antigen provocation 2736 However, the degranulation of eosinophils in these cases may have involved mechanisms other than IgE mediated hypersensitivity, such as IgA or IgG antibodies, which are also potent activating stimuli for the release of ECP 37…”