Search

Introduction. Hypoalimentation with the formation of protein-energy malnutrition can reduce the body’s resistance to acute respiratory infections (ARI). Soy and pumpkin can be a promising source of normalization of the diet.Aim. To study the effectiveness of the use of soybean-pumpkin products in the diet of healthy people to increase the resistance of the human body to ARI.Materials and methods. An open, randomized, parallel group study was conducted. Group 1 included 18 people who took a soy-pumpkin drink and dessert for 10 weeks in addition to their usual diet. Group 2 included 17 people on a regular diet. The concentration of vitamin E, cholesterol, α- and β-lipoproteins was determined in blood serum. Diene conjugates and unoxidized lipids were determined in the expired air condensate (EAC) by means of spectrophotometry. Lung function was assessed using spirometry.Results. According to the questionnaire survey, 50% of the participants in group 1 registered a positive dynamics from the regular use of soybean-pumpkin products. Only one participant underwent ARI. In the 2nd group, 7 people (41%) applied for medical help (χ2=4.43; p˂0.05), of which 6 (35%) had ARIs. At the end of the observation, an increase in vitamin E (from 34.1±0.68 to 36.4±0.55 μg/mL, p=0.0036), a decrease in total cholesterol (from 4.85±0.23 to 4.32±0.14 mmol/L, p=0.0013) and β-lipoproteins (from 2.92±0.24 to 2.31±0.18 mmol/L, p=0.0003). At the beginning of the study, in individuals of group 1, there was a relationship between age and the concentration of total cholesterol (r=0.50; p=0.036) and β-lipoproteins (r=0.47; p=0.048), as well as the weight and level of α-lipoproteins (r=-0.49; p=0.041), the concentration of unoxidized lipids (r=0.55; p=0.02), diene conjugates (r=0.48; p=0.043) in EAC. After regular use of soybean-pumpkin products, this correlation dependence was lost.Conclusion. Regular use of soy-pumpkin products for 10 weeks has a beneficial effect on the lipid profile of the blood, increases antioxidant defence, and reduces the susceptibility of a healthy person to ARI.

Since the beginning of the 50s of the last century, numerous classifications of sarcoidosis have been proposed, which to one degree or another satisfied specialists at certain stages of the development of medical technologies. Currently, sarcoidosis of the respiratory system is divided into five stages (from 0 to IV) based on the results of chest Xray examination. Active introduction into clinical practice of computed tomography and its more advanced version – lowdose multislice computed tomography (MSCT) – allows to carry out an effective diagnosis of sarcoidosis, including in outpatient practice, as well as when performing active screening and dynamic monitoring of the course of the disease. On the basis of the studies which were carried out, the dissonance between the progress in technology (from X-ray pattern to MSCT) and the stagnation of the conceptual issues of the classification of sarcoidosis is discussed, which urgently requires its reforming. Firstly, the category of patients with concomitant lesions of the intrathoracic lymph nodes (ITLN) and parenchyma (stage II) has sharply increased, which reflects the increased technological level of radiological diagnostics. As a result, the percentage of stages with isolated lymph node involvement (stage I) and isolated dissemination of the parenchyma (stage III) decreased. The classification based on MSCT data allows to more accurately determine the severity of the disease. This is of therapeutic and prognostic importance, since most patients of stage I generally do not need treatment, while symptomatic stage II requires hormone therapy. One should also take into account the possibility of spontaneous remission, which is observed more often in stage I. The main conclusion is that at present day the principle of staging in the classification of sarcoidosis can no longer satisfy the realities of modern clinics. It is more correct to single out the clinical and radiological forms of sarcoidosis: sarcoidosis of the ITLN, sarcoidosis of the ITLN and lungs, sarcoidosis of the lungs, as well as sarcoidosis of the respiratory system, combined with a single lesion of other organs.

Free radical damage to the respiratory tract in patients with asthma leads to the destruction of the bronchial parenchyma and the generation of signaling molecules of inflammation by parenchymal cells. Objective: to study the role of the structural and functional status of granulocytes in the development of epithelial destruction and oxidative lipid modification in the bronchi of asthma patients with airway hyperresponsiveness to cold and hyperosmolar stimuli. Material and methods. In 48 asthma patients, the level of asthma control was assessed according to the Asthma Control Test (ACT) questionnaire; lung function; bronchial response to 3-minute isocapnic hyperventilation with cold (- 20 °C) air (IHCA) and with ultrasonic inhalation of hypertonic (4.5 %) NaCl solution (IHS). The cellular composition and the degree of cellular destruction in induced sputum (IS) were measured. Reaction products for enzymes from the group of heme-containing peroxidases (myeloperoxidase in neutrophils, peroxidase in eosinophils) with the calculation of the average cytochemical coefficient were studied. The content of lipid peroxidation products in according to ultraviolet absorption spectra of lipid extracts in exhaled breath condensate (EBC) was assessed. Results. Patients of group 1 (n=15) with airway hyperresponsiveness to IHCA and IHS in relation to group 2 (n=33) with a negative reaction had lower ACT (14.7±1.4 vs. 18.4±0.8 points, p=0.017). In sputum, the number of neutrophils in groups 1 and 2 was 41.8±6.4 vs. 33.6±3.4 %, eosinophils – 23.5±3.5 vs. 14.9±2.6 %; average cytochemical coefficient of peroxidase 117.5±12.5 vs. 88.8±8.9 pixels (p=0.07), cell destruction index (CDI) of bronchial epithelium 0.56±0.04 vs. 0.39±0.02 r.u. (p =0.0002). The content of diene conjugates (E233) in EBC in group 1 was higher than in group 2 (0.07±0.008 vs. 0.05±0.005 optical units, p˂0.05). A correlation was found between peroxidase level and CDI, the number of totally destroyed cells (IV class of cell destruction), between the number of neutrophils in IS and E233, as well as the ratio of E233 to E206 (non-oxidized lipids) in EBC. Conclusion. In asthma patients with airway hyperresponsiveness to cold and hyperosmolar stimuli, changes in the structure of the epithelium and the structural and functional profile of granulocytes are associated with the activation of the peroxidase function of granulocytes and are interrelated with lipid peroxidation.

Background: Airway hyperresponsiveness is related to the intensification of the lipid peroxidation (LP) in asthma. We aimed to study the effect of smoking on the LP status of asthma patients with EIB. Methods: 62 subjects (36.2±1.3 years) with EIB (drop of FEV1 -21.9±2.0%) were divided into 2 groups: the 1st included 30 non-smokers, the 2nd - 32 smokers (8.2±1.5 pack/year). The contents of conjugated dienes and non-oxidized lipids in the exhaled breath condensate were analyzed before and after 6-minute submaximal exercise on treadmill, using ultraviolet spectra of lipid extracts absorption and evaluated in terms of optical density at 233 nm (E233) and 206 nm (E206), respectively. Results: In group 2, FEV1 was lower (84.6±2.7 vs. 92.0±2.5%; p 0.05) in the2nd group led to a change in E233/E206 after exercise: 0.39±0.09 (p>0.05) vs. 0.38±0.05 (p Conclusion: Smoking in asthmatics with EIB leads to changes in the LP, which is accompanied by a deterioration of airway patency and a decrease of the response to dosed exercise.

Background: Features of bronchial inflammation that contribute to the development of cold airway hyperresponsiveness in patients with asthma have been poorly studied. We aimed to investigate the correlation between the neutrophils and airway response to cold stimulus. Methods: In 116 patients with uncontrolled asthma (mean age 43.2±0.8 years), the lung function (FEV1,%), airway response to 3-minute isocapnic hyperventilation with cold air (IHCA), the cell composition of induced sputum (IS, %), the activity of myeloperoxidase (MPO, in pixels), and the degree of structural integrity of cells using the destruction index (DI, relative units) were studied. Asthma control was assessed by ACT questionnaire. Results: The patients were divided into 2 groups based on the number of neutrophils in IS: group 1 (n=52) less than 40%, and group 2 (n=64) more than 40%. The number of eosinophils in IS was 21.2±1.4 vs. 14.3±1.4%, respectively (p=0.001). The baseline FEV1 was 87.3±1.7 and 84.3±2.6% (p>0.05); the FEV1 drop in response to IHCA was -10.9±1.3 and -10.9±1.6%. The level of ACT in group 1 was higher (13.7±0.33 vs. 12.4±0.44 points, p=0.026), the MPO content of granulocytes was lower (81.7±3.6 vs. 135.9±12.1 pixels, p=0.00001), as well as neutrophil DI (0.47±0.02 vs. 0.56±0.04, p=0.047) and DI of the bronchial epithelium (0.52±0.02 vs. 0.63±0.06, p=0.05). The correlation was found between the content of neutrophils in IS and the airway response to IHCA (r=-0.18, p=0.047). Conclusion: An increase in the number of neutrophils with an escalation of their functional activity in patients with uncontrolled asthma is related to the severity of the airway response to the IHCA.

The complexity of the pathogenetic mechanisms of the development of chronic inflammation in asthma determines its heterogeneity and insufficient treatment effectiveness. Nuclear transcription factors, which include peroxisome proliferator-activated receptors, that is, PPARs, play an important role in the regulation of initiation and resolution of the inflammatory process. The ability of PPARs to modulate not only lipid homeostasis but also the activity of the inflammatory response makes them an important pathogenetic target in asthma therapy. At present, special attention is focused on natural (polyunsaturated fatty acids (PUFAs), endocannabinoids, and eicosanoids) and synthetic (fibrates, thiazolidinediones) PPAR ligands and the study of signaling mechanisms involved in the implementation of their anti-inflammatory effects in asthma. This review summarizes current views on the structure and function of PPARs, as well as their participation in the pathogenesis of chronic inflammation in asthma. The potential use of PPAR ligands as therapeutic agents for treating asthma is under discussion.

Asthma is a widespread chronic disease of the bronchopulmonary system with a heterogeneous course due to the complex etiopathogenesis. Natural-climatic and anthropogenic factors play an important role in the development and progression of this pathology. The reception of physical and chemical environmental stimuli and the regulation of body temperature are mediated by thermosensory channels, members of a subfamily of transient receptor potential (TRP) ion channels. It has been found that genes encoding vanilloid, ankyrin, and melastatin TRP channels are involved in the development of some asthma phenotypes and in the formation of exacerbations of this pathology. The review summarizes modern views on the role of high and low temperatures in airway inflammation in asthma. The participation of thermosensory TRP channels (vanilloid, ankyrin, and melastatin TRP channels) in the reaction to high and low temperatures and air humidity as well as in the formation of bronchial hyperreactivity and respiratory symptoms accompanying asthma is described. The genetic aspects of the functioning of thermosensory TRP channels are discussed. It is shown that new methods of treatment of asthma exacerbations caused by the influence of temperature and humidity should be based on the regulation of channel activity.

Background: Role of interferon-gamma (IFNγ) in asthma remains controversial. While certain studies found association of this cytokine with severe asthma and bronchial hyperresponsiveness, the other ones established its rather beneficial effect on mucin secretion and asthma development. Objectives: The aim of the study was to investigate IFNγ levels in exhaled breath condensate (EBC) of asthma patients. Methods: The study included 46 patients with asthma (mostly newly diagnosed - 52% and moderate - 30%) and 23 patients with chronic bronchitis. Mean age of patients was 38.1±1.60 years. Among asthma patients, 78% had uncontrolled disease according to ACQ5. Lung function was tested by spirometry. IFNγ was measured in EBC by BD cytometric bead array method with enhanced sensitivity. Results: Asthma patients had higher level of IFNγ than patients of control group (2654 (1328.9; 3123.9) fg/ml vs. 1872 (1707.8; 2506.3) fg/ml) but the difference was not significant. IFNγ was increased in moderate asthma (2199 (1764.8; 2519) fg/ml) compared to newly diagnosed asthma (1666 (928.8; 2048.5), p=0.01). Moreover, IFNγ was positively correlated with ACQ5 score (R=0.39, p=0.01). In uncontrolled asthma concentration of the cytokine was more than two times higher compared to patients with partially or fully controlled disease (2807 (1512.9; 3123.9) fg/ml vs. 1158 (995.5; 1589.6) fg/ml, p=0.02). 10-days treatment with oral glucocorticoids decreased IFNγ from the initial (2654 (1328.9; 3123.9) fg/ml) to “normal” values (1790 (1124.4; 3070.1) fg/ml, p=0.08). Conclusions: Our observations suggest detrimental effect of IFNγ in asthma pathogenesis. The study was supported by RFBR (#18-54-53019).

Background: Airway hyperresponsiveness (AHR) to osmotic stimuli is common and clinically relevant in asthma. AQP5 is a membrane water channel that may be functionally implicated in airway inflammation and hypersecretion. Objectives: The aim was to assess the effect of AQP5 SNPs on osmotic AHR in asthma patients. Methods: The study enrolled 274 patients with mild-to-moderate asthma, mean age 36.2±0.67 years. The patients underwent bronchoprovocation with 3-min inhalation of distilled water (hypoosmotic stimulus) and hypertonic saline aerosol (hyperosmotic stimulus). Lung function was measured by spirometry before and after each challenge. AQP5 SNPs (rs3759129, rs3736309, rs296756, rs1964676) were genotyped by LATE-PCR. Results: Association with hypoosmotic AHR was found for rs3759129 and rs296756. C allele of rs3759129 was protective against hypoosmotic AHR as AC heterozygotes had less profound response to the challenge compared to AA carriers (ΔFEV1 -1.4 (-6.3; 2.33)% vs. -5.4 (-12.0; -1.0)%, p=0.001; ΔFEF25-75 -1.0 (-18.0; 14.0)% vs. -9.1 (-21.1; 1.2)%, p=0.009). G allele of rs296756 in homozygous state also had protective effect. AA and AG (but not GG) carriers showed marked reduction in airway patency (ΔFEV1 -5,5 (-12,0; -0,8)% vs. -0,2 (-4,5; 3,4)%, p=0.004; ΔFEF25-75 -9,6 (-22,0; 2,3)% vs. 2,0 (-8,9; 9,0)%, p=0.008, for AA and GG genotypes, respectively). rs3759129 also influenced hyperosmotic AHR: all patients with the AHR had AA genotype while 27% of patients without the AHR had AC genotype (p=0.006). Conclusions:AC genotype of rs3759129 and GG genotype of rs296756 exert a protective effect on hypoosmotic AHR. AC genotype of rs3759129 also protects asthma patients from hyperosmotic AHR.

The aim of the research was to study the state of the bronchial mucosa epi-thelium in relation to the severity of clinical manifestations in severe uncon-trolled asthma depending on the pattern of inflammation and the presence of cold airway hyperresponsiveness. Materials and methods. In 48 patients with severe uncontrolled asthma, there were assessed asthma symptoms, clinical signs of cold airway hyperre-sponsiveness, and lung function; the samples of slides were analyzed in the cytological examination of the sputum; the degree of damage to epithelial cells and granulocytes was estimated using the total cell destruction index (CDI). Results. According to the analysis of sputum cytograms, the patients were divided into two groups: group I (22 patients) included persons with eosin-ophilic inflammation pattern (31.0±3.1% of eosinophils and 22.0±2.2% of neutrophils), group II (26 patients) was with mixed inflammation pattern (7.2±1.4 and 71.8±4.2%, respectively). The patients of group II had lower disease control according to Asthma Control Test (ACT; 12.1±0.7 and 17.8±0.2 points, respectively; р

Background. Pneumococcal infection being one of the dominant causes of acute respiratory diseases and exacerbation of chronic ones is a serious problem for human health and society. The flood in the Amur river basin in the summer of 2013 created a special zone and risk conditions for the formation of respiratory pathology in the Far-Eastern region of Russia. We aimed to give clinical and epidemiological assessment of the effectiveness of vaccination programs of respiratory viral and pneumococcal infections and generalization of regional experience in the organization of a set of measures aimed at their prevention in the postflood period in the Far-Eastern region. Methods. The monitoring program includes children aged 2 to 5 years in the amount of 4988 with risk factors for pneumococcal infection. The pneumococcal conjugate vaccine Prevenar-13 was used for immunization. Data on the incidence of ARVI and pneumonia in children in pre- and postvaccination periods were to be recorded. The indicators and special criteria were used to assess the effectiveness of vaccination. To study the circulation of serovariants of pneumococcus in inflammatory diseases of the respiratory tract and nasopharyngeal carrier, bacteriological and molecular genetic methods (RT-PCR in the mode of multiprime detection) were used. Results. Differences in the frequency and range of serovariants of circulating isolates of pneumococcus in the postvaccinal period and in unvaccinated children, elimination of a number of serotypes, and appearance of circulation of nonvaccinated strains were revealed. The incidence of acute respiratory diseases and pneumonia among the vaccinated population for 2 years in the region decreased by 2.5 times. The coefficient of effectiveness of vaccination according to the indicator of morbidity of children with pneumonia reaches 75-100% with direct dependence on the age of children (r=0.98). Conclusion. Comparative statistical analysis revealed a high degree of effectiveness of regional programs with the methods of immunoprophylaxis of pneumococcal infections.

Acute or chronic cold exposure exacerbates chronic inflammatory airway diseases, such as chronic obstructive pulmonary disease (COPD) and asthma. Cold-inducible RNA-binding protein (CIRP) is a cold-shock protein and is induced by various environmental stressors, such as hypothermia and hypoxia. In this study, we showed that CIRP gene and protein levels were significantly increased in patients with COPD and in rats with chronic airway inflammation compared with healthy subjects. Similarly, inflammatory cytokine production and MUC5AC secretion were up-regulated in rats following cigarette smoke inhalation. Cold temperature-induced CIRP overexpression and translocation were shown to be dependent on arginine methylation in vitro. CIRP overexpression promoted stress granule (SG) assembly. In the cytoplasm, the stability of pro-inflammatory cytokine mRNAs was increased through specific interactions between CIRP and mediator mRNA 3'-UTRs; these interactions increased the mRNA translation, resulting in MUC5AC overproduction in response to cold stress. Conversely, CIRP silencing and a methyltransferase inhibitor (adenosine dialdehyde) promoted cytokine mRNA degradation and inhibited the inflammatory response and mucus hypersecretion. These findings indicate that cold temperature can induce an airway inflammatory response and excess mucus production via a CIRP-mediated increase in mRNA stability and protein translation.

The effect of single nucleotide polymorphisms (SNP) of TRPV4 gene on the development of airway hyperresponsiveness (39.7% of cases) in response to the decrease in osmolarity under inspiration of distilled water aerosol was studies in 189 patients with uncontrolled bronchial asthma. rs6606743 SNP was found to significantly contribute to the development of osmotic airway hyperresponsiveness. Analysis of the dominant genetic model revealed substantial prevalence of AG + GG genotype frequency in the group of patients with asthma with osmotic hyperresponsiveness in comparison with the patients who had negative response to bronchoprovocation. In addition, carriers of GG or AG genotypes had significantly more profound decrease of lung function parameters in relation to A homozygous patients.

Mucin 5AC (MUC5AC) is a highly O-glycosylated mucin secreted by human bronchial epithelial cells during pulmonary inflammatory diseases. T antigen, a component of the MUC5AC glycans, is the product of the O-glycosylation transferase T-synthase and its chaperone Cosmc. Since the expression of Cosmc is mediated by signaling pathways and inflammatory factors affecting mucin O-glycosylation, we analyzed the impact of neutrophil elastase (NE)-mediated Cosmc and T antigen expression in BEAS-2B cells derived from human bronchial epithelial cells. The expression of Cosmc and T antigen in human lung tissue was analyzed by immunohistochemistry. Cellular immunohistochemistry and western blot analysis demonstrated elevated expression of T antigen in BEAS-2B cells after NE stimulation. Altered Cosmc expression in BEAS-2B cells after NE stimulation was analyzed by confocal microscopy, western blot analysis and quantitative RT-PCR. To assess the biological implications of Cosmc function for T-synthase activity and T antigen synthesis after NE stimulation, BEAS-2B cells were transfected with shRNA to silence the expression of Cosmc. The changes in signaling pathways were analyzed by western blotting. The expression of Cosmc and T antigen increased in lung tissue exposed to chronic inflammation. The expression of Cosmc and T antigen increased in NE-stimulated BEAS-2B cells. NE induced increases in T antigen expression and T-synthase transferase activity in BEAS-2B cells expressing Cosmc, highlighting the importance of Cosmc in the relationship between NE and T antigen. Cosmc and phosphatidylinositol-3-kinase (PI3K) played important roles in the signaling pathway that stimulated hyperexpression of T antigen.

Background: The definition of the personality traits involved in the formation of patients’ adherence is practically important. Aim: to determine the influence of personal characteristics of patients with asthma on their medication adherence. Methods: 93 patients with mild (n=60) and moderate (n=33) asthma at the age of 18-58 years were examined with the help of Minnesota Multiphasic Personality Inventory (MMPI). 85% of them were women. Results: 54 patients were adherent to the medication (group 1), and 39 patients didn’t fully perform medical prescription or change the therapeutic regimen by themselves. Analyzing the data of psychological tests, significantly higher values of the average ratings of MMPI scores De (depression), Pt (psychasthenia), Sc (schizophrenia) and Si (social introversion) (p 70 T-points). Soreness and individuality of patients of the 2nd group makes it difficult to predict their speech and behavior. Conclusion: The presence of anxiety and depressive disorders, introversion and soreness tendency and personal identity of asthma patients have a negative influence on their medication adherence. To achieve the asthma control it should be taken into account when predicting the clinical course and then it should be corrected on time.

Background: Cold airway hyperresponsiveness (CAH) is common in asthma. However, it is not clear, if any changes in the expression of particular mucins are induced by cold air inhalation in vivo. Objectives: The aim of the study was to investigate MUC5AC and MUC5B expression in nasal epithelium of asthma patients under cold temperature. Methods: The study enrolled 33 patients with mild-to-moderate asthma and mean age 37.9±1.89. Isocapnic (5% CO2) cold air (-20°C) hyperventilation was performed through the nose and the mouth during 3-min. Nasal epithelium was obtained by superficial scrape biopsy before and after the hyperventilation. Expression of mucins was evaluated by qRT-PCR and 2-ΔΔCT method. Results: Basal expression of MUC5AC in nasal epithelium was 3-times higher in patients with CAH when compared to patients without the hyperresponsiveness. After the cold air hyperventilation MUC5AC expression in CAH patients remained increased up to 2.3-fold. Generally, cold air produced 1.6-fold increase in MUC5AC expression with slightly higher response in patients without CAH (1.7-fold) and lower – in patients with CAH (1.4-fold). At the same time, CAH was associated with down-regulation of MUC5B before (0.8-fold) and after (0.05-fold) the challenge. Interestingly, cold air inhalation resulted in decrease of MUC5B expression (0.2-fold) in patients with CAH, while in patients without CAH it increased (3.4-fold). Conclusions: The obtained results suggest that cold air may produce differential response in terms of mucins expression. Cold airway hyperresponsiveness is associated with increased MUC5AC and decreased MUC5B expression, what is typical for asthma. This study was supported by RFBR (project 17-54-53162).

Background and objective Cold-induced airway hyperresponsiveness (CAH) is common in bronchial asthma (BA) patients and represents a problem for those living in cold climate. Transient receptor potential melastatin 8 (TRPM8) channel is the main cold temperature sensor in humans that could mediate cold response in asthmatics with CAH. No associations between TRPM8 gene polymorphisms and CAH have been reported. Methods The present study involved 123 BA patients. CAH was assessed by 3-min isocapnic (5% CO2) cold air (−20°C) hyperventilation challenge. The c.750G > C (rs11562975), c.1256G > A (rs7593557), c.3048C > T (rs11563208) and c.3174C > G (rs11563071) polymorphisms of TRPM8 gene were genotyped by allele-specific polymerase chain reaction (PCR) and PCR with subsequent restriction fragment length polymorphism analysis. Results: GC genotype and C allele carriers of the c.750G > C (rs11562975) polymorphism were more frequently observed to exhibit CAH. The estimated odds ratio for the GC genotype was 3.73 95%CI (1.48; 9.37), P = 0.005. Furthermore, GC heterozygotes had a prominent decrease in forced expiratory volume in 1 s after the challenge as compared to GG homozygotes (−12% (−16; −8.1) vs −6.45% (−11; −2.1), P C (rs11562975) polymorphism is associated with CAH in patients with BA, which suggests a potential role of TRPM8 in CAH development.

Background/Aim: Increased mucin secretion is a characteristic feature of many chronic airway diseases, particularly during periods of exacerbation; however, the exact mechanism of mucin secretion remains unclear. Ezrin, which is a specific marker of apical membranes, is predominantly concentrated in exocyst-rich cell surface structures, crosslinking the actin cytoskeleton with the plasma membrane. In the present study, we examined whether Ezrin is involved in mucin 5AC (MUC5AC) secretion after neutrophil elastase (NE) attack, and we investigated the role of the exocyst complex docking protein Sec3 in this process. Methods: NE was used as a stimulator in a 16HBE14o- cell culture model. The expression and location of Ezrin and Sec3 were investigated, and the interaction between Ezrin and Sec3 in 16HBE14o-cells was assayed after treatment with NE, Ezrin siRNA, Sec3 siRNA, neomycin or PIP2-Ab. Results: We found that Ezrin was highly expressed in the bronchi of humans with chronic airway diseases. NE induced robust MUC5AC protein secretion. The Ezrin siRNA, Sec3 siRNA, and neomycin treatments led to impaired MUC5AC secretion in cells. Both Ezrin and Sec3 were recruited primarily to the cytoplasmic membrane after NE stimulation, and the neomycin and PIP2-Ab treatments abrogated this effect. Immunoprecipitation analysis revealed that Ezrin and Sec3 combined to form complexes; however, these complexes could not be detected in Ezrin∆1-333 mutant-transfected cells, even when PIP2 was added. Conclusions: These results demonstrate that Ezrin/Sec3 complexes are essential for MUC5AC secretion in NE-stimulated airway epithelial cells and that PIP2 is of critical importance in the formation of these complexes.