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. 2022 Sep 17;12(9):1316.
doi: 10.3390/biom12091316.

Expression of Major Lipid Raft Protein Raftlin in Chronic Rhinosinusitis with Nasal Polyps in Smoking and Non-Smoking Patients Correlated with Interleukin-17 and Tumor Necrosis Factor-α Levels

Yu-Tsai Lin  1   2   3 , Ming-Hsien Tsai  1   2   3 , Yan-Ye Su  1   2 , Wei-Chih Chen  1   2 , Shun-Chen Huang  4 , Chih-Yen Chien  1   2
Affiliations

Expression of Major Lipid Raft Protein Raftlin in Chronic Rhinosinusitis with Nasal Polyps in Smoking and Non-Smoking Patients Correlated with Interleukin-17 and Tumor Necrosis Factor-α Levels

Yu-Tsai Lin et al. Biomolecules. .

Abstract

Raftlin, as an inflammatory biomarker, has been previously reported in chronic inflammatory diseases. This study investigates the expression of Raftlin in cigarette smokers and in chronic rhinosinusitis with nasal polyps (CRSwNP), as well as evaluating its correlation with interleukin-17 (IL-17) and tumor necrosis factor-α (TNF-α) levels. A total of 30 CRSwNP non-smoking and 16 CRSwNP + SK (smoking) patients undergoing endoscopic sinus surgery were enrolled, while 20 middle turbinate tissue pieces were examined and performed as the control group. In nasal mucosa epithelial staining, Raftlin levels were elevated in the columnar cells and were stained much more intensely in the CRSwNP and CRSwNP + SK groups. Raftlin was located more closely to the apical region of the epithelium in the CRSwNP + SK group; however, the Raftlin levels from whole nasal tissue pieces, according to ELISA data, showed that there was no significant difference between the three different study groups. A positive relationship by Pearson correlation was found between IL-17 or TNF-α levels and Raftlin levels. Taken together, these data indicate that increasing Raftlin expression in columnar cells might involve nasal epithelial remodeling in smokers with CRSwNP.

Keywords: Raftlin; chronic rhinosinusitis; interleukin-17; nasal polyps; smoking; tumor necrosis factor-α.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Theexpressionof Raftlinin nasal tissues. (A) The Raftlin levels from whole nasal tissue pieces in the control (n = 20), CRSwNP (n = 30), and CRSwNP + SK (n = 16) groups were analyzed byELISA assay. (B) Representative photomicrograph of nasal epithelium staining of Raftlin expression and its corresponding normal rabbit immunoglobulin G (IgG) as the isotype control for three different study groups. Yellow arrows: basal cells staining and red arrows: columnar cells staining. Scale bar = 50 μm. The quantitative intensity of staining for (C) the basal cells and (D) columnar cells was measured by Image-Pro Plus 6.0. * p < 0.05 vs. control; ** p < 0.01 vs. control. SK: smoking.
Figure 2
Figure 2
Theexpressionof IL-17 and TNF-αin nasal tissues. ELISA data from (A) IL-17 and (B) TNF-α expression from the whole nasal tissue pieces for the control (n = 20), CRSwNP (n = 30), and CRSwNP + SK (n = 16) groups. ** p < 0.01 vs. control. SK: smoking. (C) IHC images of IL-17 and TNF-α expression in nasal tissues. The nasal mucosae as a control and nasal polyps as of group CRSwNP and CRSwNP + SK were stained by hematoxylin and eosin (H&E) staining (top panels) and IL-17 (middle panels) and TNF-α (bottom panels) staining. Scale bar = 50 μm.
Figure 2
Figure 2
Theexpressionof IL-17 and TNF-αin nasal tissues. ELISA data from (A) IL-17 and (B) TNF-α expression from the whole nasal tissue pieces for the control (n = 20), CRSwNP (n = 30), and CRSwNP + SK (n = 16) groups. ** p < 0.01 vs. control. SK: smoking. (C) IHC images of IL-17 and TNF-α expression in nasal tissues. The nasal mucosae as a control and nasal polyps as of group CRSwNP and CRSwNP + SK were stained by hematoxylin and eosin (H&E) staining (top panels) and IL-17 (middle panels) and TNF-α (bottom panels) staining. Scale bar = 50 μm.
Figure 3
Figure 3
The correlation between IL-17 or TNF-α and the three measurable Raftlin levels (66 samples in total) was analyzed by Pearson R test. (A) Correlation between levels of IL-17 and Raftlin from whole nasal tissues, (B) between IL-17 and Raftlin from IHC intensity of basal cells, (C) between IL-17 and Raftlin from IHC intensity of columnar cells, (D) between levels of TNF-α and Raftlin from whole nasal tissues, (E) between TNF-α and Raftlin from IHC intensity of basal cells, and (F) between TNF-α and Raftlin from IHC intensity of columnar cells in all study subjects. IL: Interleukin; TNF-α: Tumor necrosis factor alpha; p < 0.05 was considered a statistically significant difference.
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Grants and funding

This research was funded by the Kaohsiung Chang Gung Memorial Hospital, Taiwan, grant number CMRPG8J0681 and CMRPG8G0792.
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