Animals ; Chemokine CCL11 ; metabolism ; Guinea Pigs ; Respiratory Mucosa ; metabolism ; Rhinitis, Allergic, Seasonal ; metabolism

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

PURPOSE: Aspirin-intolerant asthma (AIA) is characterized by moderate to severe asthma that is aggravated by aspirin or other non-steroidal anti-inflammatory drugs. Affected patients frequently have chronic rhinosinusitis and nasal polyposis due to persistent upper and lower airway inflammation with marked eosinophilia. IL-13 plays a crucial role in the development of allergic asthma by inducing airway eosinophilia and hyper-reactivity and it has been correlated with an increased eosinophil count. METHODS: Two promoter polymorphisms of the IL-13 gene (-1510 A>C and -1055C>T) and one coding nonsynonymus Arg110Gln (110G>A) polymorphism were genotyped using primer extension methods in 162 patients with AIA, 301 patients with aspirin-tolerant asthma (ATA), and 430 normal healthy controls (NC). RESULTS: There was no significant difference in the genotype, allele, and haplotype frequencies of the three polymorphisms among the three groups. AIA patients with the AA genotype -1510A>C (P=0.012) and CC genotype -1055C>T (P<0.001) had a significantly higher frequency of rhinosinusitis, as compared to those with the minor alleles of these two single nucleotide polymorphisms. AIA patients with the GG genotype had a higher peripheral eosinophil count (P=0.025) and a higher serum eotaxin-1 level (P=0.044), as compared to patients with the AA genotype IL-13 Arg110Gln (110G>A). CONCLUSIONS: These findings suggest that the IL-13 polymorphisms at -1510A>C and 1055C>T are associated with the development of rhinosinusitis in AIA patients. IL-13 Arg110Gln may be associated with an increased eosinophil count and eotaxin-1 level and could increase eosinophilic inflammation in the upper and lower airways of patients with AIA.
Alleles ; Aspirin ; Asthma ; Chemokine CCL11 ; Clinical Coding ; Eosinophilia ; Eosinophils ; Genotype ; Haplotypes ; Humans ; Inflammation ; Interleukin-13 ; Polymorphism, Single Nucleotide

PURPOSE: Aspirin-intolerant asthma (AIA) is characterized by moderate to severe asthma that is aggravated by aspirin or other non-steroidal anti-inflammatory drugs. Affected patients frequently have chronic rhinosinusitis and nasal polyposis due to persistent upper and lower airway inflammation with marked eosinophilia. IL-13 plays a crucial role in the development of allergic asthma by inducing airway eosinophilia and hyper-reactivity and it has been correlated with an increased eosinophil count. METHODS: Two promoter polymorphisms of the IL-13 gene (-1510 A>C and -1055C>T) and one coding nonsynonymus Arg110Gln (110G>A) polymorphism were genotyped using primer extension methods in 162 patients with AIA, 301 patients with aspirin-tolerant asthma (ATA), and 430 normal healthy controls (NC). RESULTS: There was no significant difference in the genotype, allele, and haplotype frequencies of the three polymorphisms among the three groups. AIA patients with the AA genotype -1510A>C (P=0.012) and CC genotype -1055C>T (P<0.001) had a significantly higher frequency of rhinosinusitis, as compared to those with the minor alleles of these two single nucleotide polymorphisms. AIA patients with the GG genotype had a higher peripheral eosinophil count (P=0.025) and a higher serum eotaxin-1 level (P=0.044), as compared to patients with the AA genotype IL-13 Arg110Gln (110G>A). CONCLUSIONS: These findings suggest that the IL-13 polymorphisms at -1510A>C and 1055C>T are associated with the development of rhinosinusitis in AIA patients. IL-13 Arg110Gln may be associated with an increased eosinophil count and eotaxin-1 level and could increase eosinophilic inflammation in the upper and lower airways of patients with AIA.
Alleles ; Aspirin ; Asthma ; Chemokine CCL11 ; Clinical Coding ; Eosinophilia ; Eosinophils ; Genotype ; Haplotypes ; Humans ; Inflammation ; Interleukin-13 ; Polymorphism, Single Nucleotide

OBJECTIVE: To observe the effects of systemic corticosteroids on the expression of Eotaxin in nasal polyps. METHOD: The SP immunohistochemical methods were applied to detected the expression of Eotaxin in nasal polyps before and after corticosteroids therapy. The optical density of positive cells in mucosal epithelia, vascular endothelia, inflammatory cells was measured by using HPIAS-2000 image-conduct system. RESULT: The expression of Eotaxin was positive in the cytoplasm of the mucosal epithelia,the inflammatory cells and the vascular endothelia in nasal polyps. The expression of Eotaxin was significantly reduced in the mucosal epithelia, the inflammatory cells and the vascular endothelia of nasal polyps after treated with corticosteroids compared with pre-treated. CONCLUSION Inhibiting the expression of Eotaxin in mucosal epithelia, inflammatory cells and vascular endothelia of nasal polyps, reducing recruitment and activation of eosinophil and relieving eosinophil inflammatory reaction in nasal polyps may be one of mechanisms of systemic corticosteroids therapy on the nasal polyps.
Adrenal Cortex Hormones ; therapeutic use ; Chemokine CCL11 ; metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Polyps ; drug therapy ; metabolism

OBJECTIVE: To explore the expression and significance of Eotaxin and RANTES in the rat model of allergic rhinitis (AR). METHOD: 20 female SD rats in 6-7 weeks were randomly divided into control group and AR group (n = 10, respectively). AR rat model was made with ovalbumin stimulation. To detect pathological changes in mucosa and chemokine Eotaxin, RANTES in their nasal and lung tissues after execution. RESULT: Compared with the control group, Lung EOS cell counted higher in AR group and the difference was significant (P < 0.01); the AR rats nasal mucosa and lung tissue of Eotaxin, RANTES expression was significantly increased (P < 0.01). CONCLUSION There exist high expression of Eotaxin, RANTES, infiltration of eosinophils in nasal and lung tissue of model rats with allergic rhinitis, inferring that the upper and lower respiratory tract inflammatory response has obvious consistency.
Animals ; Chemokine CCL11 ; metabolism ; Chemokine CCL5 ; metabolism ; Disease Models, Animal ; Female ; Lung ; metabolism ; Nasal Mucosa ; metabolism ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic ; metabolism

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 investigate the distribution of mast cells in nasal polyps. METHOD: Biopsy specimens from patients with nasal polyps (n = 20) and control patients (n = 8) were obtained and included in this study. The distribution of mast cells in nasal polyps and the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8, IL-6) in the epithelial cells of normal nasal mucosa and nasal polyps was determined by immunohistochemistry. RESULT: Mast cells migrate to intraepithelial in nasal polyps and the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8) was up regulated in the epithelial cells of nasal polyps compare to normal nasal mucosa. CONCLUSION Our findings showed that mast cells migrate to intraepithelial in nasal polyps and the over expression of chemotaxins (CCL5, CCL11, CX3CL1, IL-8) may be response for mast cells' migration in nasal polyps. Mast cells might be associated with the development of nasal polyps.
Chemokine CCL11 ; metabolism ; Chemokine CCL5 ; metabolism ; Chemokine CX3CL1 ; metabolism ; Epithelial Cells ; metabolism ; Humans ; Immunohistochemistry ; Interleukin-6 ; metabolism ; Interleukin-8 ; metabolism ; Mast Cells ; metabolism ; pathology ; Nasal Mucosa ; cytology ; metabolism ; Nasal Polyps ; metabolism ; pathology ; Up-Regulation

OBJECTIVETo explore the role of eotaxin in the pathogenesis of bronchial asthma and the clinical value in the diagnosis of asthma.

METHODSSerum eotaxin were measured by ELISA in 38 patients with asthma, 28 patients with non-asthma allergy, and 30 healthy controls.

RESULTSThe levels of serum eotaxin in the asthma group were higher than those in the non-asthma allergic and control group (P<0.01). Furthermore, eotaxin levels in patients with acute asthma were significantly higher than those in patients with stable asthma (P<0.001). It was also found that the eotaxin levels of the acute asthma group were positively correlated to the amounts of eosinophils in peripheral blood (r=0.4196, P<0.001), and inversely correlated to the forced expiratory volume in one second (FEV1) (r=-0.3746, P<0.001).

CONCLUSIONIt suggests that eotaxin may play a crucial pathogenic role in the asthmatic process possibly by activating the allergic inflammatory cells and controlling the recruitment of eosinophils from blood to bronchial epithelium of the airway. The concentration of eotaxin is significantly associated with the attack of acute asthma and its severity. Eotaxin may be a potential therapeutic target in patients with asthma.

Adult ; Asthma ; diagnosis ; physiopathology ; Cell Count ; Chemokine CCL11 ; Chemokines, CC ; blood ; physiology ; Eosinophilia ; pathology ; Female ; Forced Expiratory Volume ; Humans ; Male ; Middle Aged

OBJECTIVE: To explore the expression of Eotaxin and the effect of histamine in allergic rhinitis model (AR), and aim to explore the pathogenesis of AR. METHOD: The AR models were established by application of ovum albumin in rats. The expression of Eotaxin in nasal mucosa, serum and nasal cavity lavage fluid, were observed before and after treatment of histamine or its antagonist by immunochemistry, RT-PCR and ELISA technique. RESULT: The expression of Eotaxin in nasal lavage fluid and nasal mucosa increased after treatment of histamine (P < 0.05). Contrarily, the expression of Eotaxin in nasal lavage fluid, nasal mucosa and serum decreased after treatment of the antagonist of histamine. CONCLUSION Both histamine and its receptor can involve in the pathogenesis of AR by affecting the expression of Eotaxin.
Animals ; Chemokine CCL11 ; biosynthesis ; metabolism ; Female ; Histamine ; metabolism ; Male ; Nasal Mucosa ; metabolism ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic, Perennial ; metabolism ; pathology ; Rhinitis, Allergic, Seasonal ; metabolism ; pathology