Abstract
Introduction.
Respiratory viruses are the primary trigger for asthma exacerbations, and their initial detection by the body depends on pattern recognition receptors (PRRs) of the mucosa. The upper respiratory tract is the first to contact both infection and cold air; however, the impact of local cooling on PRR expression in asthma patients remains unstudied.
Aim.
To evaluate changes in the gene expression of PRRs (TLR3, TLR7, TLR8, TLR9, DDX58/RIGI, IFIH1/MDA5, and DHX58/LGP2) at the messenger ribonucleic acid (mRNA) level in the nasal epithelium of asthma patients in response to local cooling, and to determine the relationship between PRR expression levels and the frequency of acute respiratory viral infection episodes.
Materials and methods.
A total of 48 individuals were examined, including 30 asthma patients (aged 39.0 [23.0; 50.0] years, 53.3 % male), predominantly with mild persistent asthma (50 %), and 18 individuals without chronic diseases, with the exception of allergic rhinitis (aged 40.0 [30.0; 49.0] years, 38.9 % male). Inferior turbinate epithelium was collected by brush biopsy before and after a 3-minute nasal inhalation of cold air (-20 ºC), followed by RNA extraction from the obtained samples. The assessment of PRR gene expression was performed using quantitative reverse transcription PCR (RT-qPCR).
Results.
The baseline PRR profile of the nasal epithelium was characterized by high expression of TLR3, DHX58/LGP2, and IFIH1/MDA5, with no differences found between the groups. Local cooling was not accompanied by any significant changes in the expression of the studied PRRs across all subjects. More frequent respiratory viral infections were associated with decreased DHX58/LGP2 (ρ = -0.45, p = 0.01) and IFIH1/MDA5 (ρ = -0.42, p = 0.02) expression.
Conclusion.
Asthma patients are not characterized by any specific features in the mRNA expression of the studied PRR genes in the nasal epithelium. Short-term local cooling of the nasal cavity does not lead to changes in the PRR profile, whereas more frequent respiratory viral infections are associated with reduced expression of IFIH1/MDA5 and DHX58/LGP2.