Increased serum complement component 3 and mannose-binding lectin levels in adult Chinese patients with chronic rhinosinusitis.

OBJECTIVE: To study the immune function of adult Chinese patients with chronic rhinosinusitis (CRS) to elucidate its potential role in the pathogenesis of CRS. METHODS: A prospective three-arm case-control study. The study population comprised 72 CRS patients without nasal polyps (NPs), 95 CRS patients with NPs, and 110 healthy controls. The concentrations of serum immunoglobulin A (IgA), M (IgM), G (IgG), IgG subclasses (IgG1-4), complement component 3 (C3), and complement component 4 (C4) were measured by nephelometry. Serum mannose-binding lectin (MBL) levels were analyzed by enzyme-linked immunosorbent assay. All CRS patients had a complete blood count with differential, atopic status evaluation, coronal computed tomographic (CT) scan of the sinuses, and nasal endoscopy. RESULTS: Frequency of immunoglobulin, C3, C4, or MBL deficiency showed no difference among groups. The prevalence of coexistence of MBL and immunoglobulin or complement component deficiency did not differ significantly among groups either. However, compared with controls, decreased IgG3 levels were found in CRS patients without NPs, and increased C3 and MBL levels was found in both CRS patients with and without NPs. Moreover, MBL levels were significantly higher in CRS patients with NPs than in CRS patients without NPs, which positively correlated with extent of disease seen on CT scan and endoscopy, and peripheral eosinophil count. CONCLUSIONS: Immunoglobulin, C3, C4, and MBL deficiency is not the main cause of CRS in adult Chinese patients. However, on the contrary, increased C3 and MBL levels in serum might play a modulatory role in CRS development.

Lack of association of Clara cell 10-kDa protein gene variant with chronic rhinosinusitis in a Chinese Han population.

BACKGROUND: Clara cell 10-kDa protein (CC10) is an anti-inflammatory molecule and has been implicated in the involvement of the pathogenesis of asthma and chronic rhinosinusitis (CRS). A single nucleotide polymorphism (SNP) in CC10 gene (A + 38G) was previously shown to be associated with asthma and plasma CC10 levels. The purpose of this study is to examine whether there is an association between the CC10 A + 38G SNP, plasma CC10 levels, and CRS in a central Chinese population of Han nationality. METHODS: The CC10 A + 38G SNP was analyzed by means of polymerase chain reaction with restriction fragment length polymorphism and plasma CC10 levels were measured using enzyme-linked immunosorbent assay in 220 patients with CRS (90 patients with nasal polyps [NPs] and 130 patients without NPs) and 180 healthy control subjects. Among 220 patients with CRS, 108 patients were atopic subjects. Severity of disease was determined by coronal computed tomography (CT) scan in CRS patients, which was graded according to Lund and Mackay. RESULTS: The frequency of the A allele was 0.394, which was not significantly higher than the frequencies of other reported ethnic groups except for German. No association between the CC10 A + 38G SNP and CRS, any subgroup of CRS, or CRS severity could be found. Although subjects carrying the AA genotype had a significantly lower plasma CC10 concentration than those carrying the GG and GA genotypes in both CRS and control groups (p = 0.00 for all), no association was found between the plasma CC10 levels and CRS phenotype. CONCLUSION: The CC10 A + 38G SNP may not exert a substantial influence on the development of CRS in the Chinese Han population.

[Expression difference of toll-like receptors among chronic rhinosinusitis and nasal polyps].

OBJECTIVE: To compare the expression difference of Toll-like receptor-2 (TLR-2) and Toll-like receptor-4 (TLR-4) protein and mRNA among the chronic rhinosinusitis tissues, nasal polyps tissues, and normal mucosa tissues. METHODS: The mRNA expression of TLR-2 and TLR-4 in chronic rhinosinusitis tissues from 10 patients, in nasal polyp tissues from 10 patients, and in inferior turbinate tissues from 10 patients underwent nasal septum operation was detected by means of reverse transcriptase-polymerase chain reaction (RT-PCR). Immunohistochemistry (IHC) was used to detected the expression of TLR-2 and TLR-4 protein in a different set of 20 chronic rhinosinusitis tissues, 20 nasal polyp tissues, and 20 normal inferior turbinate tissues. RESULTS: (1) The mRNA and protein expression of TLR-2 and TLR-4 was detected on epithelial and glandular cells membrane in all chronic rhinosinusitis, nasal polyps and control tissues . (2) The mRNA and protein expression of TLR-2 and the mRNA expression of TLR-4 in chronic rhinosinusitis tissues was significantly increased compared with that in nasal polyps and control tissues (P < 0.05). (3) The expression intensity of TLR-2 and TLR-4 mRNA and protein between nasal polyps and control tissues was found no significant difference (P > 0.05). CONCLUSIONS: Different TLR-2 and TLR-4 protein and mRNA level in chronic rhinosinusitis and nasal polyp tissues might imply that TLR-2 and TLR-4 play different role in the pathogenesis of chronic rhinosinusitis and nasal polyps.

[Relationship between the expression of tenascin C and TGF-beta1 in human nasal polyp tissues].

OBJECTIVE: To explore the mechanism underlying the increased expression of tenascin C (TNC) in human nasal polyp tissues. METHODS: The method of immunohistochemistry was used to detect the protein expression of TNC and transforming growth factor-beta1 (TGF-beta1) and their relationship in nasal polyp tissues. The cell culture, real-time RT-PCR and in situ ELISA techniques were employed to investigate the effect of TGF-beta1 and eosinophils on the TNC mRNA and protein expression in BEAS-2B immortalized human bronchial epithelial cells. RESULTS: (1) TNC and TGF-beta1 protein expression were up-regulated in nasal polyp tissues. TNC expression level was associated with the number of TGF-beta1 positive cells (r = -0.58, P < 0.01) and TGF-beta1 positive eosinophils (r = -0.61, P < 0.01); (2) 1 ng/ml and 10 ng/ml TGF-beta1 induced TNC mRNA expression by 7.20 +/- 3.43-fold and 22.48 +/- 5.35-fold (P < 0.01) in BEAS-2B cells after 4 h stimulation respectively. The fluorescence intensity of TNC protein expression was 129. 50 +/- 47.42 and 151.20 +/- 48.36 after 24 h stimulation respectively. The protein expression was significantly increased compared with that without stimulation (60.60 +/- 38.53, P < 0.05); (3) Coculture BEAS-2B cells and eosinophils at 2:1, 1:1 and 1:2 ratio, TNC mRNA expression was induced by 4.90 +/- 1.40-fold, 5.48 +/- 1.60-fold and 4.78 +/- 1.32-fold (P < 0.01) in BEAS-2B cells after 4 h coculture respectively. The fluorescence intensity of TNC protein expression was 128.75 +/- 44.15, 142.33 +/- 29.06 and 131.33 +/- 20.87 after 24 h coculture respectively. The protein expression was significantly increased compared with that without eosinophils coculture (59.40 +/- 10.14, P < 0.05). Treatment with neutralizing antibody to TGF-beta1 significantly inhibited eosinophil-induced BEAS-2B cells TNC expression in a dose-dependent manner (P < 0.05). CONCLUSION: TGF-beta1 and eosinophils can induce TNC expression in airway epithelial cells. The effect of eosinophils is partially mediated through TGF-beta1. Up-regulated expression of TNC in nasal polyp tissues is related to eosinophil-derived TGF-beta1.