Sato K, Saito H, Tomioka H, Yokokura T
Department of Microbiology and Immunology, Shimane Medical University.
Microbiol Immunol. 1988;32(12):1189-200. doi: 10.1111/j.1348-0421.1988.tb01483.x.
Cell wall, cytoplasm, polysaccharide, and peptidoglycan fractions prepared from Lactobacillus casei, L. plantarum, and L. acidophilus were examined for their efficacies to enhance resistance of host mice against Listeria monocytogenes infection. Intraperitoneal injections of those cellular fractions of L. casei led to elicitation of inflammatory cells in the peritoneal cavity and the efficacy was highest in the case of peptidoglycan. Macrophage ratio in the resultant peritoneal exudate cells was also highest in mice given peptidoglycan. Macrophages induced with cell wall fraction of L. casei showed the most potent phorbol myristate acetate (PMA)-triggered respiratory burst (chemiluminescence and O2- production determined on the basis of nitroblue tetrazolium reduction) followed by those elicited with peptidoglycan. All the macrophages induced with cell wall of L. casei (two strains) and L. acidophilus enhanced O2- production in response to PMA but L. plantarum did not enhance O2(-)-producing ability in such a manner. The L. casei-cell wall also enhanced in vitro listericidal activity of mouse peritoneal macrophages, but such an activity was not noted in the case of L. acidophilus-cell wall. When mice were intravenously given the cellular fractions 7 or 13 days before L. monocytogenes infection, cell wall fractions of L. casei caused the most potent protective activity. A weak protective activity was also found in peptidoglycan of L. casei. Therefore, the protective action of L. casei against L. monocytogenes infection in host mice may be attributed to cell wall compounds and partially to the peptidoglycan moiety.
对从干酪乳杆菌、植物乳杆菌和嗜酸乳杆菌制备的细胞壁、细胞质、多糖和肽聚糖组分进行了检测,以评估它们增强宿主小鼠抵抗单核细胞增生李斯特菌感染的能力。腹腔注射干酪乳杆菌的这些细胞组分可导致腹腔内炎性细胞的募集,其中肽聚糖的效果最佳。在给予肽聚糖的小鼠中,所得腹腔渗出细胞中的巨噬细胞比例也最高。用干酪乳杆菌细胞壁组分诱导的巨噬细胞表现出最强烈的佛波酯肉豆蔻酸酯(PMA)触发的呼吸爆发(基于硝基蓝四氮唑还原测定化学发光和O2-产生),其次是由肽聚糖诱导的巨噬细胞。用干酪乳杆菌(两种菌株)和嗜酸乳杆菌细胞壁诱导的所有巨噬细胞对PMA均增强了O2-产生,但植物乳杆菌未以这种方式增强O2-产生能力。干酪乳杆菌细胞壁还增强了小鼠腹腔巨噬细胞的体外杀李斯特菌活性,但嗜酸乳杆菌细胞壁则未观察到这种活性。当在单核细胞增生李斯特菌感染前7天或13天给小鼠静脉注射细胞组分时,干酪乳杆菌细胞壁组分产生了最有效的保护活性。干酪乳杆菌的肽聚糖也发现有较弱的保护活性。因此,干酪乳杆菌对宿主小鼠单核细胞增生李斯特菌感染的保护作用可能归因于细胞壁化合物,部分归因于肽聚糖部分。