Uemura Ippei, Takahashi-Suzuki Natsuko, Satoh Takashi
Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Hokkaido University of Science, 7-Jo 15-4-1 Maeda, Teine-ku, Sapporo, Hokkaido 006-8585, Japan.
Immunol Lett. 2025 Oct;275:107024. doi: 10.1016/j.imlet.2025.107024. Epub 2025 Apr 12.
Afatinib, an oral molecular-targeted anticancer agent, is effective but causes significant gastrointestinal side effects. These effects are associated with EGFR inhibition in intestinal cells and changes in the microbiota.
To investigate the effects of afatinib on intestinal mucosal immunity in rats, focusing on IgA levels in the intestine and saliva, and to understand the innate and acquired immune responses to these side effects.
Male Wistar rats received afatinib (5.2 mg/kg) daily for 24 h (Day 1) and for 2 weeks (Day 14). Gene expression in the intestine was analyzed using quantitative polymerase chain reaction. IgA levels in the intestine and saliva were measured using enzyme-linked immunosorbent assay.
Afatinib suppressed α-defensin 5 and pIgR in the jejunum and ileum, indicating reduced innate immunity. It increased IgA levels in the intestine and saliva, suggesting altered acquired immunity. Salivary IgA levels significantly correlated with intestinal IgA levels.
Afatinib affects gastrointestinal mucosal immunity, suppresses innate defense, and alters IgA production. Salivary IgA could serve as a marker for monitoring these effects, aiding cancer therapy management.
阿法替尼是一种口服分子靶向抗癌药物,疗效显著,但会引起严重的胃肠道副作用。这些副作用与肠道细胞中的表皮生长因子受体(EGFR)抑制及微生物群变化有关。
研究阿法替尼对大鼠肠道黏膜免疫的影响,重点关注肠道和唾液中的免疫球蛋白A(IgA)水平,并了解对这些副作用的先天性和获得性免疫反应。
雄性Wistar大鼠每日接受阿法替尼(5.2 mg/kg)治疗,持续24小时(第1天)和2周(第14天)。采用定量聚合酶链反应分析肠道中的基因表达。使用酶联免疫吸附测定法测量肠道和唾液中的IgA水平。
阿法替尼抑制空肠和回肠中的α-防御素5和多聚免疫球蛋白受体(pIgR),表明先天性免疫降低。它增加了肠道和唾液中的IgA水平,提示获得性免疫改变。唾液IgA水平与肠道IgA水平显著相关。
阿法替尼影响胃肠道黏膜免疫,抑制先天性防御,并改变IgA产生。唾液IgA可作为监测这些影响的标志物,有助于癌症治疗管理。