Nasal levels of soluble IL‐33R ST2 and IL‐16 in allergic rhinitis: inverse correlation trends with disease severity

  title={Nasal levels of soluble IL‐33R ST2 and IL‐16 in allergic rhinitis: inverse correlation trends with disease severity},
  author={Ralf Baumann and Matthaeus Rabaszowski and Igor Stenin and Lisa Tilgner and Maria Gaertner-Akerboom and Kathrin Scheckenbach and Jens Wiltfang and Adam M. Chaker and J{\"o}rg Schipper and Martin Wagenmann},
  journal={Clinical \& Experimental Allergy},
  pages={1134 - 1143}
Serum levels of IL‐16, IL‐33 and the decoy receptor of IL‐33, soluble ST2, are elevated in allergic rhinitis. Recent studies show that IL‐16, soluble ST2 or anti‐IL‐33 reduce type 2 cytokines (such as IL‐5) and eosinophilia in murine models of allergic asthma or allergic rhinitis respectively. 

Synergistic relationship between TSLP and IL‐33/ST2 signaling pathways in allergic rhinitis and the effects of hypoxia

The aim of this study was to explore the relationship and expressions and biologic functions of TSLP and IL‐33/ST2 in AR, and also to determine the effects of hypoxia on these cytokines.

Plasma IL‐33 in atopic patients correlates with pro‐inflammatory cytokines and changes cholesterol transport protein expression: a surprising neutral overall impact on atherogenicity

  • I. VoloshynaT. Mucci A. Reiss
  • Biology, Medicine
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 2015
The effect of physiological and elevated IL‐33 levels in plasma from atopic patients (AP) on cholesterol metabolism in human macrophages as compared to plasma from healthy controls (HC) is examined.

Interleukin-33: Its Emerging Role in Allergic Diseases

The mobilization and biological function of IL-33 in allergic disorders is reviewed, providing novel insights for addressing these hypersensitive conditions.

Serum levels of interleukin 33 and its receptor ST2 in patients treated with subcutaneous allergen immunotherapy in intermittent allergic rhinitis

Increase in serum levels of IL-33 after the first course of immunotherapy may suggest it is too short period to prevent the expected raise in serum IL- 33 levels in the pollen season, and longer treatment is required to observe significant changes of this cytokine.

Interleukin‐16 aggravates ovalbumin‐induced allergic inflammation by enhancing Th2 and Th17 cytokine production in a mouse model

It is confirmed that IL‐16 enhances the lung allergic inflammatory response and suggest a mechanism possibly associated with the up‐regulation of IgE and the promotion of Th2 and Th17 cytokine production that provides a new target for the clinical treatment of asthma.

Cytokine Profiles in Allergic Rhinitis

  • G. Scadding
  • Medicine, Biology
    Current Allergy and Asthma Reports
  • 2014
Evidence for the involvement of different cytokines and cytokine groups in allergic rhinitis is considered.

Role of interleukin 33 in chronic rhinosinusitis

An emphasis on defining CRS endotypes based on distinct functional or pathobiological mechanisms of disease may be more effective at identifying patient groups that would respond to therapeutic interventions targeting specific proinflammatory mediators or infectious agents that trigger the disease pathology.

The nasal mucosal late allergic reaction to grass pollen involves type 2 inflammation (IL-5 and IL-13), the inflammasome (IL-1β), and complement

The study shows that the LAR to grass pollen involves a range of inflammatory pathways and suggests potential new biomarkers and therapeutic targets, and the marked variation in mucosal inflammatory events between different patients suggests that in the future precision mucosal sampling may enable rational specific therapy.

Notch‐1 signaling activation sustains overexpression of interleukin 33 in the epithelium of nasal polyps

Alterations in the nasal epithelial barrier homeostasis and increased interleukin 33 (IL‐33) expression contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP).

Evidence for the induction of Th2 inflammation by group 2 innate lymphoid cells in response to prostaglandin D2 and cysteinyl leukotrienes in allergic rhinitis

Group 2 innate lymphoid cells (ILC2s) play important roles in allergic inflammation. However, their roles in the pathophysiology of allergic rhinitis (AR) are poorly understood.



Association of serum interleukin‐33 level and the interleukin‐33 genetic variant with Japanese cedar pollinosis

  • M. SakashitaT. Yoshimoto M. Tamari
  • Medicine, Biology
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 2008
Serum levels of IL‐33 and the genetic influences of the polymorphisms ofIL‐33 in human allergic diseases are unclear and type 2 T helper responses are studied.

Exogenous interleukin‐16 inhibits antigen‐induced airway hyper‐reactivity, eosinophilia and Th2‐type cytokine production in mice

This data indicates that prolonged exposure to high levels of IL‐16 for prolonged periods of time increases the likelihood that the substance will act as a ‘spatially aggregating force’ to drive immune responses in vivo.

Adenovirus‐mediated delivery of soluble ST2 attenuates ovalbumin‐induced allergic asthma in mice

  • H. YinX. Li J. Zhu
  • Biology, Medicine
    Clinical and experimental immunology
  • 2012
Histopathological examination of the lungs revealed that sST2‐Fc over‐expression markedly suppressed allergen‐induced peribronchial inflammation and disruption of the alveolar architecture, and suggested that administration of Ad‐sST2-Fc gene transfer may have therapeutic potential for the immunomodulatory treatment of OVA‐mediated allergic pulmonary diseases.

Contribution of IL-33 to induction and augmentation of experimental allergic conjunctivitis.

In vivo IL-33 treatment significantly increased the capacity of T cells in the cervical lymph nodes of RW-immunized mice to produce IL-4, IL-5 and IL-13 upon challenge with anti- CD3 and anti-CD28 antibodies in vitro.

IL-16 Variability and Modulation by Antiallergic Drugs in a Murine Experimental Allergic Rhinitis Model

IL-16 was both systemically and locally upregulated in the murine allergic rhinitis model and that IL-16 changed in parallel to allergic state by treatment with the drugs.

Expression and function of the ST2 gene in a murine model of allergic airway inflammation

It is reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation, and the role, function, and kinetics of soluble ST1 expression in asthma remain unclear.

Nasal IL-16 and MIP-1 alpha in late-phase allergic response.

The data demonstrate that IL-16 and MIP-1 alpha are expressed in the late-phase response in allergic rhinitis in a more or less similar kinetic like IL-5 and ECP.

Expression of Interleukin-16 in Allergic Rhinitis

The data indicate that one of the sources of elevated serum IL-16 in allergic patients may be gland cells and lymphocytes in allergic nasal mucosa, which may be strongly associated with the developmental mechanism of allergic rhinitis.

Human basophils and eosinophils are the direct target leukocytes of the novel IL-1 family member IL-33.

It is demonstrated that basophils and eosinophils are the only direct target leukocytes for IL- 33, suggesting that IL-33 promotes allergic inflammation and Th2 polarization mainly by the selective activation of these specialized cells of the innate immune system.

Interleukin‐16 inhibits interleukin‐13 production by allergen‐stimulated blood mononuclear cells

IL‐16 may play an important immunoregulatory role in allergic states in response to allergen, and its modulatory effect on cytokine synthesis was mediated by interferon‐γ (IFN‐γ), IL‐10, IL‐12 or IL‐18,allergen‐stimulated PBMC.