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首页> 外文期刊>Journal of Agricultural and Food Chemistry >EGCG Induces Pro-inflammatory Response in Macrophages to Prevent Bacterial Infection through the 67LR/p38/JNK Signaling Pathway
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EGCG Induces Pro-inflammatory Response in Macrophages to Prevent Bacterial Infection through the 67LR/p38/JNK Signaling Pathway

机译：EGCG在巨噬细胞中诱导促炎反应，以防止通过67LR / P38 / JNK信号通路的细菌感染

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Extensive studies focused on the therapeutic efficacy of epigallocatechin-3-gallate (EGCG) against bacterial infection. However, little is known about its prophylactic efficacy against bacterial infection. Herein, we found that EGCG showed an effective prophylactic efficacy against bacterial infection with a broad spectrum, including Gram-negative, Gram-positive, and drug-resistant bacteria. Pretreatment with EGCG through intraperitoneal injection, intravenous injection, or intragastric administration significantly reduced the bacterial load, inflammatory response, and mortality in mouse abdominal infection models induced by bacterial inoculation or cecal ligation and puncture. Pretreatment with EGCG by intraperitoneal injection significantly increased the numbers of neutrophils and monocytes/macrophages in the abdominal cavity and peripheral blood of mice, and depletion of neutrophils and monocytes/macrophages by specific antibodies or chemical drugs obviously increased the bacterial load in mice. Of note, EGCG did not directly induce neutrophil and macrophage migration, and it just induced phagocyte migration in the presence of macrophages in a co-cultured system, implying that EGCG-induced phagocyte migration relies on its immunoregulatory effects on macrophages. EGCG markedly induced the production of cytokines and chemokines in macrophages and mouse peritoneal lavage, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, CXC chemokine ligands 1 and 2 (CXCL1 and 2), and monocyte chemotactic protein-1 (MCP-1). EGCG significantly induced the phosphorylation of p38 and JNK mitogen-activated protein kinases (MAPKs) in macrophages, and inhibition of p38 and JNK MAPKs markedly reduced EGCG-induced chemokine and cytokine production. Anti-67-kDa laminin receptor (67LR) antibody treatment significantly reduced EGCG-induced chemokine production and p38 and JNK phosphorylation in macrophages. Together, EGCG showed an obvious prophylactic efficacy against bacterial infection by inducing a pro-inflammatory response in macrophages through the 67LR/p38/JNK signaling pathway, supporting the further development of EGCG as a potent prophylaxis for bacterial infection and providing new clues to understand the healthcare function of green tea.
机译：大量研究集中于表没食子儿茶素没食子酸酯（EGCG）对细菌感染的治疗效果。然而，人们对其预防细菌感染的效果知之甚少。在此，我们发现EGCG对广谱细菌感染具有有效的预防效果，包括革兰氏阴性、革兰氏阳性和耐药细菌。通过腹腔注射、静脉注射或胃内给药进行EGCG预处理可显著降低细菌接种或盲肠结扎和穿刺诱导的小鼠腹腔感染模型的细菌负荷、炎症反应和死亡率。腹腔注射EGCG预处理显著增加小鼠腹腔和外周血中中性粒细胞和单核细胞/巨噬细胞的数量，特异性抗体或化学药物消耗中性粒细胞和单核细胞/巨噬细胞明显增加小鼠的细菌负荷。值得注意的是，EGCG没有直接诱导中性粒细胞和巨噬细胞迁移，它只是在共培养系统中有巨噬细胞存在时诱导吞噬细胞迁移，这意味着EGCG诱导的吞噬细胞迁移依赖于其对巨噬细胞的免疫调节作用。EGCG显著诱导巨噬细胞和小鼠腹腔灌洗液中产生细胞因子和趋化因子，包括肿瘤坏死因子α（TNFα）、白细胞介素-1β（IL-1β）、白细胞介素-6、CXC趋化因子配体1和2（CXCL1和2）以及单核细胞趋化蛋白-1（MCP-1）。EGCG显著诱导巨噬细胞中p38和JNK丝裂原活化蛋白激酶（MAPK）的磷酸化，而抑制p38和JNK MAPK显著降低EGCG诱导的趋化因子和细胞因子的产生。抗67-kDa层粘连蛋白受体（67LR）抗体治疗可显著降低EGCG诱导的巨噬细胞趋化因子产生和p38及JNK磷酸化。总之，EGCG通过67LR/p38/JNK信号通路在巨噬细胞中诱导促炎症反应，显示出明显的预防细菌感染的功效，支持EGCG作为有效预防细菌感染的进一步发展，并为理解绿茶的保健功能提供了新线索。

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