Regulation and characterization of IL-17A expression in patients with chronic rhinosinusitis and its relationship with eosinophilic inflammation

Abstract

be immunogenic in this age group, with all infants enrolled in the study capable of producing adequate serotype-specific IgG to at least 9 of the 23 serotypes at 12 months of age.Nevertheless, there are several issues concerning the use of 23vPPV in children younger than 2 years that require further clarification. It will be important to monitor the kinetics of the immune response over time, because recent studies and our own data raise the possibility that early administration of full-dose 23vPPV may result in immune hyporesponsiveness to subsequent challenge with polysaccharide antigens. 9 Further investigations including disease incidence and nasopharyngeal carriage data are required to clarify this issue.

Interleukin‐9 and interleukin‐17C in chronic rhinosinusitis

“…16 Another study revealed significantly higher level of IL-17A in CRSwNP than CRSsNP with a higher number of subjects. 17 There was 1 study showing increased IL-17C expression in CRSwNP. 5 No study has yet compared IL-17C levels in CRSwNP and CRSsNP nor their correlation with allergy and asthma.…”

Characterization of IL-18 Expression and Release in the Pathogenesis of Chronic Rhinosinusitis

“…To determine IL-18 expression, double immunohistochemistry was performed using a previously described method [7]. Briefly, sections were incubated with murine antibodies directed against markers of mast cells, eosinophils, neutrophils, B cells, macrophages, T cells, epithelial cells, vascular endothelial cells and fibroblasts, or against control mouse IgG1 (Dako), together with either rabbit anti-human IL-18 antibody or normal rabbit immunoglobulin fraction (Dako) overnight at 4°C (table 2).…”

“…It is currently thought that NP formation affects between 1 and 4% of the population [2]. While the precise etiology and pathophysiology underlying CRS remains poorly understood, it has been proposed that networks of Th1, Th2, Th17, and Treg-associated cytokines might be involved [4,5,6,7]. …”

“…We compared the local expression of IL-18 among the various CRS phenotypes and examined the characterization of IL-18 expression in the pathogenesis of CRS. We further investigated not only the regulation of the local IL-18 release but also the regulatory effect of IL-18 on Th1/Th2/Th17-associated cytokine production in NPs using a recently developed ex vivo system [5,7]. The present findings provide novel insights into the pathogenesis of chronic eosinophilic airway diseases regulated by IL-18, in addition to providing a basis for the role of danger signals in IL-18 release in the airways [25].…”

Advances in upper airway diseases and allergen immunotherapy

“…We start with the key advances in upper airway diseases which are summarized in Table I. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] …”