Neurobiota Research Center, College of Pharmacy, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, South Korea.
HYUNDAI BIOLAND Co., Ltd., Ansan, 15407, South Korea.
BMC Microbiol. 2021 May 13;21(1):146. doi: 10.1186/s12866-021-02192-4.
BACKGROUND: Gut microbiota closely communicate in the immune system to maintain a balanced immune homeostasis in the gastrointestinal tract of the host. Oral administration of probiotics modulates gut microbiota composition. In the present study, we isolated Lactobacillus rhamnosus HDB1258, which induced tumor necrosis factor (TNF)-α and interleukin (IL)-10 expression in macrophages, from the feces of breastfeeding infants and examined how HDB1258 could regulate the homeostatic immune response in mice with or without lipopolysaccharide (LPS)-induced systemic inflammation. RESULTS: Oral administration of HDB1258 significantly increased splenic NK cell cytotoxicity, peritoneal macrophage phagocytosis, splenic and colonic TNF-α expression, TNF-α to IL-10 expression ratio, and fecal IgA level in control mice, while Th1 and Treg cell differentiation was not affected in the spleen. However, HDB1258 treatment significantly suppressed peritoneal macrophage phagocytosis and blood prostaglandin E2 level in mice with LPS-induced systemic inflammation. Its treatment increased LPS-suppressed ratios of Treg to Th1 cell population, Foxp3 to T-bet expression, and IL-10 to TNF-α expression. Oral administration of HDB1258 significantly decreased LPS-induced colon shortening, myeloperoxidase activity and NF-κB/CD11c cell population in the colon, while the ratio of IL-10 to TNF-α expression increased. Moreover, HDB1258 treatment shifted gut microbiota composition in mice with and without LPS-induced systemic inflammation: it increased the Cyanobacteria and PAC000664_g (belonging to Bacteroidetes) populations and reduced Deferribacteres and EU622763_s group (belonging to Bacteroidetes) populations. In particular, PAC001066_g and PAC001072_s populations were negatively correlated with the ratio of IL-10 to TNF-α expression in the colon, while the PAC001070_s group population was positively correlated. CONCLUSIONS: Oral administered HDB1258 may enhance the immune response by activating innate immunity including to macrophage phagocytosis and NK cell cytotoxicity in the healthy host and suppress systemic inflammation in the host with inflammation by the modulation of gut microbiota and IL-10 to TNF-α expression ratio in immune cells.
背景：肠道微生物群在免疫系统中密切交流，以维持宿主胃肠道的平衡免疫稳态。益生菌的口服给药可调节肠道微生物群的组成。在本研究中，我们从母乳喂养婴儿的粪便中分离出鼠李糖乳杆菌 HDB1258，该菌可诱导巨噬细胞中肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-10 的表达，并研究了 HDB1258 如何调节有或没有脂多糖 (LPS) 诱导的全身炎症的小鼠的稳态免疫反应。
结果：口服 HDB1258 可显著增加对照小鼠脾脏 NK 细胞的细胞毒性、腹腔巨噬细胞的吞噬作用、脾脏和结肠 TNF-α 的表达、TNF-α 与 IL-10 的表达比值以及粪便 IgA 水平，而脾中 Th1 和 Treg 细胞分化不受影响。然而，HDB1258 治疗可显著抑制 LPS 诱导的全身炎症小鼠腹腔巨噬细胞的吞噬作用和血液前列腺素 E2 水平。其治疗增加了 LPS 抑制的 Treg 与 Th1 细胞群、Foxp3 与 T-bet 表达以及 IL-10 与 TNF-α 表达的比值。口服 HDB1258 可显著降低 LPS 诱导的结肠缩短、髓过氧化物酶活性和 NF-κB/CD11c 细胞群在结肠中的作用，同时增加 IL-10 与 TNF-α 的表达比值。此外，HDB1258 治疗改变了有或没有 LPS 诱导的全身炎症的小鼠的肠道微生物群组成：它增加了蓝细菌和 PAC000664_g（属于拟杆菌门）的种群，减少了 Deferribacteres 和 EU622763_s 组（属于拟杆菌门）的种群。特别是，PAC001066_g 和 PAC001072_s 种群与结肠中 IL-10 与 TNF-α 的表达比值呈负相关，而 PAC001070_s 组种群与 IL-10 与 TNF-α 的表达比值呈正相关。
结论：口服 HDB1258 可能通过激活包括巨噬细胞吞噬作用和 NK 细胞细胞毒性在内的固有免疫来增强健康宿主的免疫反应，并通过调节肠道微生物群和免疫细胞中 IL-10 与 TNF-α 的表达比值来抑制炎症宿主的全身炎症。
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