Individual and co-operative roles of lactic acid and hydrogen peroxide in the killing activity of enteric strain Lactobacillus johnsonii NCC933 and vaginal strain Lactobacillus gasseri KS120.1 against enteric, uropathogenic and vaginosis-associated pathogens
Individual and co-operative roles of lactic acid and hydrogen peroxide in the killing activity of enteric strain Lactobacillus johnsonii NCC933 and vaginal strain Lactobacillus gasseri KS120.1 against enteric, uropathogenic and vaginosis-associated pathogens
复制标题
DOI：
10.1111/j.1574-6968.2009.01887.x
复制
发表时间：
2010-03-01
影响因子：
2.1
通讯作者：
Servin, Alain L.
中科院分区：
文献类型：
--
作者：
Atassi, Fabrice;Servin, Alain L.
乳酸杆菌菌株对细菌病原体的杀灭活性的潜在机制似乎是多因素的。在这里，我们调查各自的贡献过氧化氢和乳酸在杀死细菌病原体与人类阴道，泌尿道或肠道由两个过氧化氢生产菌株。在共培养中，人肠道菌株约氏乳杆菌NCC 933和人阴道菌株加氏乳杆菌KS 120.1菌株杀死肠道沙门氏菌鼠伤寒血清型SL 1344、阴道加德纳菌DSM 4944和尿路大肠杆菌CFT073病原体。无细胞培养物上清液（CFCS）在SL 1344、DSM 4944和CFT073活力方面产生相同的降低，而分离的细菌没有影响。CFCSs的杀伤活性是热稳定的。在存在抑制乳酸依赖性杀伤活性的Dulbecco改良Eagle最小必需培养基的情况下，CFCS对病原体的杀伤效果较差。过氧化氢酶处理的CFCS表现出强烈的活性下降。单独测试，过氧化氢触发了对所有三种病原体的浓度依赖性杀伤活性。只有在浓度高于CFCS中存在的浓度时，单独的乳酸才会产生杀伤活性。在乳酸杆菌CFCS中存在的浓度的乳酸的存在下，过氧化氢显示出增强的杀伤活性。总的来说，这些结果表明，对于产生过氧化氢的乳杆菌属菌株，乳杆菌属的主要代谢物乳酸和过氧化氢协同作用以杀死肠道、阴道病相关和尿路病原体。
The mechanism underlying the killing activity of Lactobacillus strains against bacterial pathogens appears to be multifactorial. Here, we investigate the respective contributions of hydrogen peroxide and lactic acid in killing bacterial pathogens associated with the human vagina, urinary tract or intestine by two hydrogen peroxide-producing strains. In co-culture, the human intestinal strain Lactobacillus johnsonii NCC933 and human vaginal strain Lactobacillus gasseri KS120.1 strains killed enteric Salmonella enterica serovar Typhimurium SL1344, vaginal Gardnerella vaginalis DSM 4944 and urinary tract Escherichia coli CFT073 pathogens. The cell-free culture supernatants (CFCSs) produced the same reduction in SL1344, DSM 4944 and CFT073 viability, whereas isolated bacteria had no effect. The killing activity of CFCSs was heat-stable. In the presence of Dulbecco's modified Eagle's minimum essential medium inhibiting the lactic acid-dependent killing activity, CFCSs were less effective at killing of the pathogens. Catalase-treated CFCSs displayed a strong decreased activity. Tested alone, hydrogen peroxide triggered a concentration-dependent killing activity against all three pathogens. Lactic acid alone developed a killing activity only at concentrations higher than that present in CFCSs. In the presence of lactic acid at a concentration present in Lactobacillus CFCSs, hydrogen peroxide displayed enhanced killing activity. Collectively, these results demonstrate that for hydrogen peroxide-producing Lactobacillus strains, the main metabolites of Lactobacillus, lactic acid and hydrogen peroxide, act co-operatively to kill enteric, vaginosis-associated and uropathogenic pathogens.