Zhang Q B, Etolhi G, Dawodu J B, Gemmell C G, Russell R I
Department of Gastroenterology, Royal Infirmary, Glasgow G4 0SF, Scotland, U.K.
Clin Sci (Lond). 1999 Apr;96(4):409-14.
Mucosal IgA is important in local immune defence. Helicobacter pylori induces a specific IgA response in antral mucosa, but its immunopathology is unknown. Interleukin-8 (IL-8) has been suggested to be important in H. pylori-induced inflammation. Current information on the relationship between H. pylori-induced IgA and mucosal inflammation is limited. To investigate possible associations between mucosal-specific IgA, the toxinogenicity of H. pylori, mucosal levels of IL-8 and gastric inflammation, 52 endoscoped patients were studied. These comprised 28 patients with peptic ulcer and 24 with non-ulcer dyspepsia. Of these patients, 38 had H. pylori infection: 28 with peptic ulcer and 10 with non-ulcer dyspepsia. Antral biopsies were taken for histology, H. pylori culture and measurement of mucosal levels of IL-8 (pg/mg) and specific IgA (A450x1000) by ELISA. Mucosal H. pylori IgA was detectable in 35 out of 38 patients with H. pylori infection, with a median (interquartile) level of 220 (147, 531) units. There was no significant difference in mucosal levels of the IgA antibodies between patients infected with cytotoxin-positive or cagA-positive strains of H. pylori and those with toxin-negative or cagA-negative strains. The IgA levels in those patients with severe neutrophil infiltration were lower than in those with mild or moderate infiltration (P<0.05). There was a weak inverse correlation between antral mucosal IgA and IL-8 in infected patients (r=-0.36; P=0.04). H. pylori infection induced a significant local mucosal IgA response in most infected patients. The level of IgA antibodies does not appear to be correlated with the toxinogenicity of H. pylori. However, patients with severe active inflammation appear to have decreased levels of IgA. An inverse correlation between mucosal IL-8 and IgA may suggest that IL-8-induced inflammation compromises the mucosal IgA defence and renders the mucosa susceptible to further damage.
黏膜IgA在局部免疫防御中起重要作用。幽门螺杆菌可诱导胃窦黏膜产生特异性IgA反应，但其免疫病理学尚不清楚。白细胞介素-8（IL-8）被认为在幽门螺杆菌诱导的炎症中起重要作用。目前关于幽门螺杆菌诱导的IgA与黏膜炎症之间关系的信息有限。为了研究黏膜特异性IgA、幽门螺杆菌的产毒性、IL-8的黏膜水平与胃炎之间可能存在的关联，对52例接受内镜检查的患者进行了研究。这些患者包括28例消化性溃疡患者和24例非溃疡性消化不良患者。其中，38例患者感染了幽门螺杆菌：28例消化性溃疡患者和10例非溃疡性消化不良患者。采集胃窦活检组织进行组织学检查、幽门螺杆菌培养，并通过酶联免疫吸附测定法（ELISA）测量IL-8（pg/mg）的黏膜水平和特异性IgA（A450x1000）。在38例幽门螺杆菌感染患者中，35例可检测到黏膜幽门螺杆菌IgA，中位数（四分位间距）水平为220（147，531）单位。感染细胞毒素阳性或cagA阳性幽门螺杆菌菌株的患者与毒素阴性或cagA阴性菌株患者的黏膜IgA抗体水平无显著差异。严重中性粒细胞浸润患者的IgA水平低于轻度或中度浸润患者（P<0.05）。感染患者的胃窦黏膜IgA与IL-8之间存在弱负相关（r=-0.36；P=0.04）。幽门螺杆菌感染在大多数感染患者中诱导了显著的局部黏膜IgA反应。IgA抗体水平似乎与幽门螺杆菌的产毒性无关。然而，严重活动性炎症患者的IgA水平似乎降低。黏膜IL-8与IgA之间的负相关可能表明，IL-8诱导的炎症损害了黏膜IgA防御，使黏膜易受进一步损伤。
