Differential Expression of Adhesion Molecules by Sinonasal Fibroblasts among Control and Chronic Rhinosinusitis Patients

Abstract

Sinonasal fibroblast expression of adhesion molecules in sinusitis varies by disease state and is selectively influenced by exposure to inflammatory cytokines.

Differential expression of tumor necrosis factor α, interleukin 1β, nuclear factor κB in nasal mucosa among chronic rhinosinusitis patients with and without polyps

“…rheumatoid arthritis, psoriasis) was reflected by successful attempts of their treatment with anti-TNF antibodies. Oyer et al [13] presented increased adhesion molecules (vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM)) expression on sinonasal fibroblast in chronic sinusitis patients with and without nasal polyposis. Our observation that both analyzed phenotypes of polyps showed stronger expressions of IL-1β than control nasal mucosa is consistent with current knowledge on the functioning of this cytokine [14].…”

Fibroblast levels are increased in chronic rhinosinusitis with nasal polyps and are associated with worse subjective disease severity

“…26,30,33 Additional ex vivo investigation demonstrated that sinonasal macrophages (as identified by Cluster of Differentiation 68 (CD68) and/or Antimacrophage antibody [MAC387]) were not FSP-positive (data not shown). Immunostaining and flow cytometric analysis of human sinonasal fibroblasts was conducted as described.…”

“…24,25 There is also increasing evidence that the fibroblast is at least partially responsible for recruitment of inflammatory cells in CRS. 26 In vitro studies have shown that fibroblasts can be proinflammatory and ex vivo studies have revealed fibroblasts' production of a broad array of matrix products. Although there appear to be proinflammatory changes in fibroblasts in CRS, the precise quantity of fibroblasts in CRS, their impact upon disease outcomes, or the impact of other factors such as smoke exposure or atopic status is unknown.…”

Editorial

“…Katotomichelakis et al 13 examined banked tissue specimens from Thai CRS patients with nasal polyps and observed an increasing prevalence of eosinophilic inflammation over the past 12 years, illustrating temporal variation in the cytology, and hence possibly the etiology, of this disease. The role of the fibroblast was further elucidated by Oyer et al 16 who showed increased expression of adhesion molecules by sinonasal fibroblasts in tissues from CRS patients. Park et al 15 described upregulated expression of YKL-40, a molecule potentially involved in fibroblast proliferation, migration, collagen production, and tissue remodeling, in nasal mucosa from patients allergic rhinitis.…”