PURPOSE: Asthma in the elderly has different clinical features including more severe phenotypes with higher comorbidities. Epithelial cells are known to initiate innate/adaptive immune responses in asthmatic airways. We investigated clinical features and epithelial derived cytokine levels in elderly asthmatics compared to non-elderly asthmatics in a cross-sectional cohort of adult asthmatics in order to further understand its pathogenic mechanisms. METHODS: A total of 1,452 adult asthmatics were enrolled from a single tertiary hospital and were classified into 2 groups: 234 elderly (≥ 60 years at initial diagnosis) and 1,218 non-elderly (< 60 years at initial diagnosis) asthmatics. Asthma-related clinical parameters were compared between the 2 groups. Serum levels of epithelial cell-derived cytokines including interleukin (IL)-31, IL-33, IL-8, eotaxin-2, transforming growth factor beta 1 (TGF-β1) and periostin were measured by enzyme-linked immunosorbent assay. RESULTS: Significantly higher prevalence rates of late-onset asthma (onset age ≥ 40 years) and severe asthma, as well as the lower rate of atopy, blood/sputum eosinophil counts, total immunoglobulin E and eosinophil cationic protein levels were noted in elderly asthmatics compared to non-elderly asthmatics (P < 0.05, respectively). The forced expiratory volume in 1 second (FEV1, % predicted) level tended to be lower in elderly asthmatics (P = 0.07). In addition, serum IL-33 and IL-31 levels were significantly lower in elderly asthmatics, while no differences were found in the serum level of IL-8, eotaxin-2, TGF-β1 or periostin. Among elderly asthmatics, subjects with severe asthma had lower FEV1 (% predicted) value, but showed significantly higher serum levels of eotaxin-2 and TGF-β1, than those with non-severe asthma (P < 0.05 for each). CONCLUSIONS: These findings suggest that age-related changes of epithelial cell-derived cytokines may affect clinical phenotypes and severity of elderly asthma: decreased levels of IL-33 and IL-31 may contribute to less Th2 phenotype, while increased levels of eotaxin-2 and TGF-β1 may contribute to severity.
Adult ; Aged* ; Asthma* ; Chemokine CCL24 ; Cohort Studies ; Comorbidity ; Cytokines* ; Enzyme-Linked Immunosorbent Assay ; Eosinophil Cationic Protein ; Eosinophils ; Epithelial Cells ; Forced Expiratory Volume ; Humans ; Immunoglobulin E ; Immunoglobulins ; Interleukin-33 ; Interleukin-8 ; Interleukins ; Phenotype* ; Prevalence ; Tertiary Care Centers ; Transforming Growth Factor beta

Asthma is a chronic disease associated with airway constriction due to inflammation caused by eosinophils, mast cells, and T lymphocytes, leading to serious chronic illness in children. The eotaxin gene family has been shown to play an important role in the pathogenesis of asthma. We hypothesized that the distinctive variations among the four seasons in Korea may affect the expression of eotaxin polymorphisms, especially in children. We examined the possible effects of birth season (spring, March-May; summer, June-August; fall, September-November; and winter, December-February) on the phenotype of asthma in children. All SNP data sets of the eotaxin-2 and eotaxin-3 genes were collected from 78 asthma patients and 101 controls. Here, we investigated the effects of birth season on the expression of eotaxin-2 and eotaxin-3 in Korean children. Using the HAPLOTYPE procedure with the HTR method in SAS/Genetics, we showed that children born in spring and summer show significant haplotypes in both the eotaxin-2 and eotaxin-3 genes. Thus, the expression of polymorphisms in eotaxin-2 and eotaxin-3 may vary by season.
Asthma ; Chemokine CCL24 ; Child ; Chronic Disease ; Constriction ; Eosinophils ; Haplotypes ; Humans ; Inflammation ; Korea ; Mast Cells ; Parturition ; Phenotype ; Seasons ; T-Lymphocytes

OBJECTIVE: To study the expression of Eotaxin and Eotaxin-2 in nasal polyp and observe the effects of steroids on Eotaxin and Eotaxin-2 in nasal polyps. METHOD: The SP immunohistochemical method was applied to explore the expression of Eotaxin and Eotaxin-2 in nasal polyps before and after systemic corticosteroids therapy; the optical density of positive cells were measured by using HPIAL-2000 image-conduct system. RESULT: The expression of Eotaxin and Eotaxin 2 were positive in mucosal epithelia, vascular endothelial, glandular epithelium, and inflammatory cells. After corticosteroids use, the number of eosinophils, the expression of Eotaxin in mucosal epithelia, inflammatory cells and vascular endothelial, and the expression of Eotaxin-2 in mucosal epithelia were significantly decreased (P<0.05). The steroids affected the expression of on Eotaxin-2 in mucosal epithelia of nasal polyps mostly. CONCLUSION 1) The expression of Eotaxin and Eotaxin-2 in nasal polyp are positive. 2) The effects of steroid on the nasal polyps may depend on decreasing the infiltration of eosinophils and the expression of Eotaxin and Eotaxin-2.
Adrenal Cortex Hormones ; pharmacology ; Adult ; Chemokine CCL11 ; metabolism ; Chemokine CCL24 ; metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Mucosa ; drug effects ; metabolism ; Nasal Polyps ; drug therapy ; metabolism ; Young Adult

OBJECTIVE: To study the expression of Eotaxin and Eotaxin-2 in nasal polyposis and nasal polyp and explore the different mechanism between polyposis and polyp. METHOD: Fifteen cases of nasal polyposis, thirteen cases of polyp and eight cases of normal middle turbinate were studied with immunohistochemical SP method to detect the expression of Eotaxin and Eotaxin-2. RESULT: There were significant differences between either two groups about the expression of Eotaxin-2 (P < 0.05). The expression of Eotaxin in nasal polyposis and polyp were dramatically higher than in controls (P < 0.05), the expression of Eotaxin between nasal polyposis and polyp was no remarkable difference (P > 0.05). CONCLUSION Both of Eotaxin and Eotaxin-2 likely play key roles in the inflammatory reaction process of nasal polyposis and polyp. The different expression of Eotaxin-2 between nasal polyposis and polyp demonstrates it may be one of the main causes in the different mechanism of the two diseases.
Adolescent ; Adult ; Chemokine CCL11 ; metabolism ; Chemokine CCL24 ; metabolism ; Child ; Female ; Humans ; Male ; Middle Aged ; Nasal Polyps ; metabolism ; pathology ; Young Adult