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Association between cigarette smoking and interleukin-17A expression in nasal tissues of patients with chronic rhinosinusitis and asthma

View Article: PubMed Central - PubMed

ABSTRACT

Cigarette smoke plays a substantial role in the development of airway inflammatory diseases, including asthma and chronic rhinosinusitis (CRS). Interleukin (IL)-17A might contribute to cigarette smoke-related inflammation of the airway. This study aimed to investigate the association between cigarette smoking and IL-17A expression in the nasal tissues of patients with CRS and asthma.

We prospectively recruited 24 patients (13 smokers, 11 nonsmokers) with CRS and asthma and 6 patients with asthma but without CRS (control group) in a tertiary medical center. Nasal mucosa was obtained as part of the nasal surgery. Protein and mRNA levels of IL-17A in the nasal tissues were determined by immunostaining and real-time polymerase chain reaction.

The number of unexpected emergency clinic visits for acute asthma attacks were higher among smokers than among nonsmokers. Interleukin-17A protein and mRNA levels in the nasal tissues of smokers were greater compared to those in the nasal tissues of nonsmokers (P = 0.02 both) and control patients (P = 0.05 and 0.04, respectively).

Cigarette smoking was associated with an increase in the number of unexpected emergency clinic visits due to acute asthma attack and in the expression of IL-17A in the nasal tissues of patients with airway inflammatory diseases.

No MeSH data available.


Comparison of interleukin (IL)-12A (A), IL-4 (B), IL-5 (C), IL-13 (D), and IL-17A (E) mRNA levels in nasal tissues among smokers (n = 13), nonsmokers (n = 11), and control subjects (n = 6) based on the real-time polymerase chain reaction findings. The IL-17A mRNA levels in smokers were significantly higher compared to those in nonsmokers and control subjects (E). aAnalyzed by the Kruskal–Wallis test among the 3 groups. ∗Significance was considered at P < 0.05, analyzed by the Mann–Whitney U test. IL = interleukin.
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Figure 2: Comparison of interleukin (IL)-12A (A), IL-4 (B), IL-5 (C), IL-13 (D), and IL-17A (E) mRNA levels in nasal tissues among smokers (n = 13), nonsmokers (n = 11), and control subjects (n = 6) based on the real-time polymerase chain reaction findings. The IL-17A mRNA levels in smokers were significantly higher compared to those in nonsmokers and control subjects (E). aAnalyzed by the Kruskal–Wallis test among the 3 groups. ∗Significance was considered at P < 0.05, analyzed by the Mann–Whitney U test. IL = interleukin.

Mentions: There were no significant differences in the mRNA levels of Th1- and various Th2-driven cytokines including IL-12A, IL-4, IL-5, and IL-13 among the smoker, nonsmoker, and control groups (Fig. 2A–D). However, the levels of IL-17AmRNA in the nasal tissues of smokers were significantly higher compared to those in the nasal tissues of nonsmokers and control subjects (P = 0.02 and 0.04, respectively, Fig. 2E).


Association between cigarette smoking and interleukin-17A expression in nasal tissues of patients with chronic rhinosinusitis and asthma
Comparison of interleukin (IL)-12A (A), IL-4 (B), IL-5 (C), IL-13 (D), and IL-17A (E) mRNA levels in nasal tissues among smokers (n = 13), nonsmokers (n = 11), and control subjects (n = 6) based on the real-time polymerase chain reaction findings. The IL-17A mRNA levels in smokers were significantly higher compared to those in nonsmokers and control subjects (E). aAnalyzed by the Kruskal–Wallis test among the 3 groups. ∗Significance was considered at P < 0.05, analyzed by the Mann–Whitney U test. IL = interleukin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5134879&req=5

Figure 2: Comparison of interleukin (IL)-12A (A), IL-4 (B), IL-5 (C), IL-13 (D), and IL-17A (E) mRNA levels in nasal tissues among smokers (n = 13), nonsmokers (n = 11), and control subjects (n = 6) based on the real-time polymerase chain reaction findings. The IL-17A mRNA levels in smokers were significantly higher compared to those in nonsmokers and control subjects (E). aAnalyzed by the Kruskal–Wallis test among the 3 groups. ∗Significance was considered at P < 0.05, analyzed by the Mann–Whitney U test. IL = interleukin.
Mentions: There were no significant differences in the mRNA levels of Th1- and various Th2-driven cytokines including IL-12A, IL-4, IL-5, and IL-13 among the smoker, nonsmoker, and control groups (Fig. 2A–D). However, the levels of IL-17AmRNA in the nasal tissues of smokers were significantly higher compared to those in the nasal tissues of nonsmokers and control subjects (P = 0.02 and 0.04, respectively, Fig. 2E).

View Article: PubMed Central - PubMed

ABSTRACT

Cigarette smoke plays a substantial role in the development of airway inflammatory diseases, including asthma and chronic rhinosinusitis (CRS). Interleukin (IL)-17A might contribute to cigarette smoke-related inflammation of the airway. This study aimed to investigate the association between cigarette smoking and IL-17A expression in the nasal tissues of patients with CRS and asthma.

We prospectively recruited 24 patients (13 smokers, 11 nonsmokers) with CRS and asthma and 6 patients with asthma but without CRS (control group) in a tertiary medical center. Nasal mucosa was obtained as part of the nasal surgery. Protein and mRNA levels of IL-17A in the nasal tissues were determined by immunostaining and real-time polymerase chain reaction.

The number of unexpected emergency clinic visits for acute asthma attacks were higher among smokers than among nonsmokers. Interleukin-17A protein and mRNA levels in the nasal tissues of smokers were greater compared to those in the nasal tissues of nonsmokers (P&#8202;=&#8202;0.02 both) and control patients (P&#8202;=&#8202;0.05 and 0.04, respectively).

Cigarette smoking was associated with an increase in the number of unexpected emergency clinic visits due to acute asthma attack and in the expression of IL-17A in the nasal tissues of patients with airway inflammatory diseases.

No MeSH data available.