Department of Veterinary Clinical Pathology, College of Veterinary Medicine & Institute of Veterinary Science, Kangwon National University, Chuncheon 24341; Laboratory Animal Research Center, Samsung Biomedical Research Institute, Samsung Medical Center, Seoul 06351, Korea.
Institute of Research and Development, Chaon Corp., Seongnam 13493, Korea.
BMB Rep. 2019 Apr;52(4):289-294. doi: 10.5483/BMBRep.2019.52.4.310.
The present study evaluated the role of AHNAK in Bartonella henselae infection. Mice were intraperitoneally inoculated with 2 × 10 colony-forming units of B. henselae Houston-1 on day 0 and subsequently on day 10. Blood and tissue samples of the mice were collected 8 days after the final B. henselae injection. B. henselae infection in the liver of Ahnak-knockout and wild-type mice was confirmed by performing polymerase chain reaction, with Bartonella adhesion A as a marker. The proportion of B. henselaeinfected cells increased in the liver of the Ahnak-knockout mice. Granulomatous lesions, inflammatory cytokine levels, and liver enzyme levels were also higher in the liver of the Ahnak-knockout mice than in the liver of the wild-type mice, indicating that Ahnak deletion accelerated B. henselae infection. The proportion of CD4＋interferon-γ (IFN-γ)＋ and CD4＋interleukin (IL)-4＋ cells was significantly lower in the B. henselae-infected Ahnak-knockout mice than in the B. henselae-infected wild-type mice. In vitro stimulation with B. henselae significantly increased IFN-γ and IL-4 secretion in the splenocytes obtained from the B. henselae-infected wild-type mice, but did not increase IFN-γ and IL-4 secretion in the splenocytes obtained from the B. henselae-infected Ahnak-KO mice. In contrast, IL-1α, IL-1β, IL-6, IL-10, RANTES, and tumor necrosis factor-α secretion was significantly elevated in the splenocytes obtained from both B. henselae-infected wild-type and Ahnak-knockout mice. These results indicate that Ahnak deletion promotes B. henselae infection. Impaired IFN-γ and IL-4 secretion in the Ahnak-knockout mice suggests the impairment of Th1 and Th2 immunity in these mice. [BMB Reports 2019; 52(4): 289-294].
本研究评估了 AHNAK 在感染汉赛巴尔通体中的作用。在第 0 天和第 10 天，用 2×10 个集落形成单位的汉赛巴尔通体 Houston-1 经腹腔接种小鼠。在最后一次汉赛巴尔通体注射 8 天后收集小鼠的血液和组织样本。通过聚合酶链反应（以 Bartonella adhesion A 为标记）确认汉赛巴尔通体在 Ahnak 敲除和野生型小鼠肝脏中的感染。在 Ahnak 敲除小鼠的肝脏中，感染细胞的比例增加。与野生型小鼠相比，Ahnak 敲除小鼠的肝脏肉芽肿病变、炎症细胞因子水平和肝酶水平也更高，这表明 Ahnak 缺失加速了汉赛巴尔通体感染。与汉赛巴尔通体感染的野生型小鼠相比，汉赛巴尔通体感染的 Ahnak 敲除小鼠的 CD4+干扰素-γ（IFN-γ）+和 CD4+白细胞介素（IL）-4+细胞的比例显著降低。体外刺激汉赛巴尔通体显著增加了从汉赛巴尔通体感染的野生型小鼠获得的脾细胞中 IFN-γ和 IL-4 的分泌，但未增加从汉赛巴尔通体感染的 Ahnak-KO 小鼠获得的脾细胞中 IFN-γ和 IL-4 的分泌。相比之下，IL-1α、IL-1β、IL-6、IL-10、RANTES 和肿瘤坏死因子-α在从汉赛巴尔通体感染的野生型和 Ahnak 敲除小鼠获得的脾细胞中均显著升高。这些结果表明 Ahnak 缺失促进了汉赛巴尔通体感染。Ahnak 敲除小鼠 IFN-γ和 IL-4 分泌受损表明这些小鼠的 Th1 和 Th2 免疫受损。[BMB 报告 2019;52(4):289-294]。
