Localization of il‐1β mrna and cell adhesion molecules in the maxillary sinus mucosa of patients with chronic sinusitis

Abstract

Interleukin-1 beta (IL-1 beta) is a predominant cytokine in retained paranasal sinus fluid of chronic sinusitis where infiltration by polymorphonuclear neutrophils (PMNs) of nasal and paranasal mucosa is characteristic. The authors investigated the localization of IL-1 beta messenger RNA (mRNA) in the maxillary sinus mucosa of patients with chronic sinusitis, using digoxigenin-labeled oligonucleotide probes. IL-1 beta mRNA was detected in some extravascular PMNs and small numbers of mononuclear leukocytes but was not detected in other tissue cells or intravascular leukocytes. The expression and distribution of the cell adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1), were also studied in cultured human mucosal microvascular endothelial cells and in the maxillary sinus mucosa in chronic sinusitis by immunohistochemistry using monoclonal antibodies against these cell adhesion molecules. Only ICAM-1 was expressed on cultured human mucosal microvascular endothelial cells without IL-1 beta stimulation. With IL-1 beta activation of these cells, ELAM-1 was expressed strongly and the expression of ICAM-1 was enhanced. In the maxillary sinus mucosa, ICAM-1 was strongly and universally expressed on endothelial cells of all small vessels, whereas ELAM-1 was expressed only in the subepithelial region. These findings suggest that IL-1 beta, one of mediators in chronic sinusitis, is produced by PMNs, induces the expression of ICAM-1 and ELAM-1 on endothelial cells, and, thereby, stimulates PMN infiltration in chronic sinusitis.

Inflammatory mechanisms and remodeling in chronic rhinosinusitis and nasal polyps

“…In general, although nonallergic patients show some evidence for neutrophilic infl ammatory process, allergic patients tend to show fewer neutrophils and somewhat more eosinophils in the infl ammatory process [ 16 , 22 ]. The relative abundance of eosinophils and fewer numbers of neutrophils in those patients with CRS and coexisting asthma suggest that this type of infl ammatory response may be independent of infection and may represent an allergic infl ammation [23][24][25][26]. However, it is also likely that infection impacts upon this disease process.…”

Influence of interleukin-13 on β-catenin levels ineosinophilic chronic rhinosinusitis cell culture

“…In the establishment of nonallergic CRS, IL-8, which is generated by neutrophils and mucosal epithelia, has been reported to play a pivotal role (6). Tokushige et al proposed that IL-1 production by neutrophils induced the expression of the intercellular adhesion molecule (ICAM-1) on endothelial cells, leading to neutrophil infiltration in CRS (7). It has been demonstrated that the peripheral blood mononuclear cells (PBMCs) of patients suffering from CRS produced large amounts of IL-13 when exposed in vitro to Alternaria species (8).…”

Expression of Adhesion Molecules in Cultured Human Nasal Mucosal Microvascular Endothelial Cells Activated by Interleukin–1â or Tumor Necrosis Factor–·: Effects of Dexamethasone

“…Nonallergic chronic sinusitis is characterized by purulent paranasal sinus effusion and persistent nasal discharge with numerous emigrated neutrophils [2, 3, 4, 5, 6, 7, 8, 9], in additon to the accumulation of eosinophils in the tissue [5, 10, 11, 12, 13]. Tokushiga et al [14]proposed that IL–1β induces the expression of both intercellular adhesion molecule–1 (ICAM–1) and E–selectin on ECs, presumably leading to neutrophil infiltration. The increased adhesion of neutrophils to cultured human nasal microvascular endothelial cells (HNMECs) induced by sinus effusion was significantly inhibited by anti–IL–1β antibody [3].…”