Snijders F, van Deventer S J, Bartelsman J F, den Otter P, Jansen J, Mevissen M L, van Gool T, Danner S A, Reiss P
Division of Infectious Diseases, Tropical Medicine and AIDS, University of Amsterdam, The Netherlands.
AIDS. 1995 Apr;9(4):367-73.
To determine whether a mucosal cytokine-mediated inflammatory response is involved in cryptosporidial or microsporidial diarrhoea, as well as in diarrhoea of unknown origin in HIV-infected patients.
Prospective study.
Jejunal biopsies were obtained from HIV-infected patients with diarrhoea. Controls were HIV-infected and HIV-seronegative patients without diarrhoea. Two biopsies were homogenized immediately and two other biopsies were first cultured for 20 h. Cytokines [tumour necrosis factor (TNF), interleukin (IL)-1 beta, IL-6, IL-8, IL-10], soluble TNF receptors (sTNFR) p55 and p75, and soluble IL-2 receptor (sIL-2R) were assessed in the homogenates and in the supernatants by sandwich enzyme-linked immunosorbent or enzyme-linked binding assays. The cytokine receptors were also measured in serum.
Six HIV-infected patients with cryptosporidiosis, six with microsporidiosis, seven with diarrhoea of unknown origin, seven without diarrhoea, and seven HIV-seronegative patients were eligible. Four patients were excluded because of the presence of other pathogens. No cytokines were detected in immediately homogenized jejunal tissue. Following culture, IL-6 and IL-8 levels were higher in HIV-infected patients with diarrhoea of unknown origin than in HIV-seronegative controls without diarrhoea, although this was not statistically significant. No differences in serum or post-culture supernatant sTNFR p55 and p75 levels existed between the HIV-infected patients with or without diarrhoea. sTNFR, IL-1 beta, IL-10 and the sIL-2R were only detected in low amounts or not at all, and were equally distributed among all patient groups.
This study indicates that mucosal cytokine-mediated inflammatory responses do not play an important role in the pathogenesis of different types of diarrhoea in HIV-infected patients. These results do not support the use of immunomodulatory therapy in these patients.
确定黏膜细胞因子介导的炎症反应是否参与隐孢子虫或微孢子虫性腹泻，以及HIV感染患者不明原因腹泻的发病过程。
前瞻性研究。
从患有腹泻的HIV感染患者获取空肠活检组织。对照组为未患腹泻的HIV感染患者和HIV血清学阴性患者。将两份活检组织立即匀浆，另两份活检组织先培养20小时。通过夹心酶联免疫吸附或酶联结合测定法评估匀浆和上清液中的细胞因子[肿瘤坏死因子（TNF）、白细胞介素（IL）-1β、IL-6、IL-8、IL-10]、可溶性TNF受体（sTNFR）p55和p75以及可溶性IL-2受体（sIL-2R）。还测定血清中的细胞因子受体。
6例患有隐孢子虫病的HIV感染患者、6例患有微孢子虫病的患者、7例不明原因腹泻患者、7例无腹泻患者以及7例HIV血清学阴性患者符合条件。4例患者因存在其他病原体而被排除。在立即匀浆的空肠组织中未检测到细胞因子。培养后，不明原因腹泻的HIV感染患者的IL-6和IL-8水平高于无腹泻的HIV血清学阴性对照组，尽管差异无统计学意义。患腹泻和未患腹泻的HIV感染患者之间血清或培养后上清液中的sTNFR p55和p75水平无差异。sTNFR、IL-1β、IL-10和sIL-2R仅少量检测到或未检测到，且在所有患者组中分布均匀。
本研究表明，黏膜细胞因子介导的炎症反应在HIV感染患者不同类型腹泻的发病机制中不发挥重要作用。这些结果不支持在这些患者中使用免疫调节疗法。
