ABSTRACT
BACKGROUND AND OBJECTIVES: Nasal polyp is non-neoplastic, chronic inflammatory disease of the nasal mucosa. Oxidative stress may be related to the pathogenesis of nasal polyp. Oxidative stress may be potential inducers of heme oxygenase (HO-1) expression. To illustrate the role of the HO-1 in the nasal polyp, we investigated the expressive pattern of the HO-1 in the nasal polyp and the influence of corticosteroids on its expression. SUBJECTS AND METHOD: The study materials were 28 specimens of nasal polyp (steroid user: 13 cases, steroid non-user: 15 cases) taken from 28 patients during endoscopic sinus surgery and 11 cases of normal nasal mucosa of the inferior turbinate as control. The HO-1 expression was assessed by immunohistochemical staining. RESULTS: The HO-1 was mainly expressed on non-epithelial cells in the lamina propria of nasal polyps in 20/28 (71.4%). The expression of HO-1 was positive in 11 out of 13 (84.6%) and 9 out of 15 (60%) subjects for steroid user and steroid non-user group, respectively. The inflammatory cells were almost identified as macrophage by using a macrophage specific marker (CD68+). The HO-1 was not expressed in normal control at all. There was no significant difference in the expression of HO-1 between the steroid user group and the non-user group. CONCLUSION: HO-1, as an important endogenous antioxidant enzyme, may play a protective role in the pathogenesis of nasal polyp. Steroid may not regulate the HO-1 expression in the nasal polyp.
Subject(s)
Humans , Adrenal Cortex Hormones , Heme Oxygenase (Decyclizing) , Heme , Macrophages , Mucous Membrane , Nasal Mucosa , Nasal Polyps , Oxidative Stress , TurbinatesABSTRACT
BACKGROUND AND OBJECTIVES: A biallelic A/G polymorphism in the Monocyte chemotactic protein (MCP) -1 at position -2518 has been found to affect the level of MCP-1 expression. To investigate if these polymorphisms in chemokine ligand and receptor genes are relevant for the development of allergic rhinitis, we investigated polymorphisms of MCP-1 and CC chemokine receptor 2 (CCR2) known as the receptor of MCP-1. MATERIALS AND METHOD: Blood samples for genetic analysis were obtained from 198 individuals with allergic rhinitis and from 278 healthy subjects without atopic diseases. Polymerase chain reaction-based assay for MCP-1 -2518 A/G (A/G polymorphism in the MCP-1 at position -2518) and CCR2 V64I polymorphisms (replacement of valine by isoleucine in CCR2 64) was used for genotyping. RESULTS: There were no differences in the frequencies of the genotypes in the controls and patients (p>0.05). The frequencies of the MCP-1 G and CCR2 A alleles were not statistically different between controls and allergic rhinitis patients (p>0.05). The odds ratios (95% confidence interval) of MCP-1 G/G and CCR2 A/A genotypes for allergic rhinitis were not statistically significant, whereas, alleles frequencies of MCP-1 -2518G and CCR2 A of controls were various according to the ethnic background. CONCLUSION: Our result suggests MCP-1 -2518 A/G and CCR2 V64I polymorphisms are not part of the factors contributing to genetical susceptibility in the development of allergic rhinitis in Koreans.
Subject(s)
Humans , Alleles , Genetic Predisposition to Disease , Genotype , Isoleucine , Korea , Monocytes , Odds Ratio , Receptors, CCR2 , Rhinitis , ValineABSTRACT
BACKGROUND AND OBJECTIVES: CC chemokine receptor (CCR5) is characteristic of the Th 1 phenotype, the receptor of RANTES, MIP-1alphaand MIP-1beta. The receptor of CCR5 delta32 (a 32 bp deletion in the CCR5 gene, mutant type) results in the production of a non-functional receptor. Given the potential importance of CCR5 in allergic inflammation, we hypothesized that individuals carrying the CCR5 delta32 allele would show a reduced prevalence of allergic rhinitis. SUBJECTS AND METHOD: Blood samples for genetic analysis were obtained from 187 individuals with allergic rhinitis and from 278 healthy subjects without atopic diseases. Polymerase chain reaction-based assay for the CCR5 gene polymorphism was used for genotyping. RESULTS: We could not find the CCR5 delta32 homozygotes and heterozygotes at all in neither of the controls nor allergic rhinitis Korean patients. CONCLUSION: Since the CCR5 delta32 allele frequency did not deviate from that in the healthy control population, it is unlikely that this allele influences predisposition to allergic rhinitis in Koreans.