Abstract
BackgroundNew therapeutic approaches with biologic agents such as anti-cytokine antibodies are currently on trial for the treatment of asthma, rhinosinusitis or allergic diseases necessitating patient selection by biomarkers. Allergic rhinitis (AR), affecting about 20 % of the Canadian population, is an inflammatory disease characterised by a disequilibrium of T-lymphocytes and tissue eosinophilia. Aim of the present study was to describe distinct cytokine patterns in nasal secretion between seasonal and perennial AR (SAR/PAR), and healthy controls by comparing cytokines regulating T-cells or stimulating inflammatory cells, and chemokines.MethodsNasal secretions of 44 participants suffering from SAR, 45 participants with PAR and 48 healthy controls were gained using the cotton wool method, and analysed for IL-1β, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IL-17, GM-CSF, G-CSF, IFN-γ, MCP-1, MIP-1α, MIP-1β, eotaxin, and RANTES by Bio-Plex Cytokine Assay as well as for ECP and tryptase by UniCAP-FEIA.ResultsParticipants with SAR or PAR presented elevated levels of tryptase, ECP, MCP-1, and MIP-1β, while values of GM-CSF, G-CSF, IL-1β, and IL-6 did not differ from the controls. Increased levels of IL-5, eotaxin, MIP-1α, and IL-17 and decreased levels of IFN-γ, IL-12 and IL-10 were found in SAR only. RANTES was elevated in SAR in comparison to PAR. Interestingly, we found reduced levels of IL-4 in PAR and of IL-13 in SAR.ConclusionsElevated levels of proinflammatory cytokines were seen in both disease entities. They were, however, more pronounced in SAR, indicating a higher degree of inflammation. This study suggests a downregulation of TH1 and Treg-lymphocytes and an upregulation of TH17 in SAR. Moreover, the results display a prominent role of eosinophils and mast cells in AR. The observed distinct cytokine profiles in nasal secretion may prove useful as a diagnostic tool helping to match patients to antibody therapies.
Highlights
New therapeutic approaches with biologic agents such as anti-cytokine antibodies are currently on trial for the treatment of asthma, rhinosinusitis or allergic diseases necessitating patient selection by biomarkers
The late-phase is characterised by the secretion of chemokines like eosinophil chemotactic protein, “regulated on activation, normal T cell expressed and secreted” (RANTES), and macrophage inflammatory protein-1α (MIP-1α) [9], which induce the recruitment of eosinophils and other inflammatory cells
We analysed the levels of cytokines and other inflammatory mediators in the nasal fluid of participants suffering from SAR or PAR, focusing on three main topics: cytokines (1) regulating TH1 (interferon-γ (IFN-γ), IL-12), TH2 (IL-4, IL-13), Treg (IL10), and TH17 (IL-17) cells, or (2) stimulating and activating inflammatory cells like granulocytes and mast cells (granulocyte colony-stimulating factor (G-CSF), granulocyte–macrophage colonystimulating factor (GM-CSF), IL-1β, IL-5, and IL-6), and (3) chemokines such as eotaxin, RANTES, monocyte chemotactic protein-1 (MCP-1), or MIP-1α/β
Summary
New therapeutic approaches with biologic agents such as anti-cytokine antibodies are currently on trial for the treatment of asthma, rhinosinusitis or allergic diseases necessitating patient selection by biomarkers. TH2-lymphocytes secrete cytokines which promote the differentiation of B cells as well as induce immunoglobulin (Ig) synthesis and regulate Ig isotype switching. This results in increased levels of specific IgE, both local and systemic [8]. In the early-phase of allergic reaction, mast cells, coated with specific IgE, recognise the allergen and release several mediators such as histamine and tryptase. The late-phase is characterised by the secretion of chemokines like eosinophil chemotactic protein (eotaxin), “regulated on activation, normal T cell expressed and secreted” (RANTES), and macrophage inflammatory protein-1α (MIP-1α) [9], which induce the recruitment of eosinophils and other inflammatory cells. Whereas the early-phase response to allergen exposure leads to acute symptoms, the late-phase reaction is held responsible for persisting inflammation
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