Sunaga Hiroshi, Oh Myungmi, Takahashi Noboru, Fujieda Shigeharu
Department of Otorhinolaryngology, Head and Neck surgery, University of Fukui, Fukui, Japan.
Acta Otolaryngol Suppl. 2004 Dec(555):15-9.
We investigated the functions of tonsillar mononuclear cells (TMC) regarding whether a Haemophilus parainfluenzae (HP) outer membranes antigen (HPOM) enhances IgA-related cytokine (IFN-gamma, IL-10. and TGF-beta) production in vitro by TMC in IgA nephropathy (IgAN) patients. In addition, we examined the effect of synthetic oligodeoxynucleotide and HPOM stimulation by TMC on IgA production, whether the constant region antisense to IgA inhibits the production of IgA in vitro by TMC. Eighteen patients with IgAN and 25 patients with chronic tonsillitis (CT) from 6 to 45 years (mean age of 20.9 years) participated in this study. TMC were obtained from resected tonsils, and total and HP-specific IgA levels, along with the concentration of TGF-beta, IL-10 and IFN-gamma in the supernatant of stimulated TMC were measured by ELISA. Isolated TMC were cultured with HPOM in the presence of 23 oligodeoxynucleotides (ODNs), and the induction of total IgA and HP-specific IgA in the supernatant was also measured using ELISA. To investigate the inhibition of IgA production, TMC were cultured with HPOM and antisence to IgA. We found that IgA-related cytokine (IFN-gamma, IL-10, and TGF-beta) production by unstimulated or stimulated TMC was higher in IgAN patients than CT patients. Two types of synthetic oligodeoxynucleotides produced higher HP-specific IgA than with HPOM stimulation alone. HPOM and antisence IgA inhibited the production of total IgA and HP-specific IgA in dose-depend manner. In conclusion, IFN-gamma, TGF-beta, and IL-10 influence each other in the pathogenesis of IgAN, and infection by not only HP but other bacteria or viruses which possess specific DNA sequences such as CpG motifs induce the production of HP-specific IgA by TMC.
我们研究了扁桃体单个核细胞(TMC)的功能,探讨副流感嗜血杆菌(HP)外膜抗原(HPOM)是否能增强IgA肾病(IgAN)患者的TMC在体外产生与IgA相关的细胞因子(干扰素-γ、白细胞介素-10和转化生长因子-β)。此外,我们检测了合成寡脱氧核苷酸以及TMC对HPOM的刺激作用对IgA产生的影响,即IgA恒定区反义寡核苷酸是否能在体外抑制TMC产生IgA。18例年龄在6至45岁(平均年龄20.9岁)的IgAN患者和25例慢性扁桃体炎(CT)患者参与了本研究。TMC取自切除的扁桃体,通过酶联免疫吸附测定法(ELISA)检测总IgA和HP特异性IgA水平,以及刺激后的TMC上清液中转化生长因子-β、白细胞介素-10和干扰素-γ的浓度。将分离出的TMC与HPOM在23种寡脱氧核苷酸(ODN)存在的情况下进行培养,并用ELISA检测上清液中总IgA和HP特异性IgA的诱导情况。为了研究对IgA产生的抑制作用,将TMC与HPOM以及IgA反义寡核苷酸一起培养。我们发现,未刺激或刺激后的TMC产生的与IgA相关的细胞因子(干扰素-γ、白细胞介素-10和转化生长因子-β),IgAN患者高于CT患者。两种合成寡脱氧核苷酸产生的HP特异性IgA比单独用HPOM刺激时更高。HPOM和IgA反义寡核苷酸以剂量依赖方式抑制总IgA和HP特异性IgA的产生。总之,干扰素-γ、转化生长因子-β和白细胞介素-10在IgAN的发病机制中相互影响,不仅HP感染,其他具有特定DNA序列如CpG基序的细菌或病毒感染也会诱导TMC产生HP特异性IgA。