Centro de Referencia para Lactobacilos, Chacabuco 145, San Miguel de Tucumán, Argentina.
BMC Microbiol. 2011 Aug 3;11:177. doi: 10.1186/1471-2180-11-177.
Diarrheal infections caused by Salmonella, are one of the major causes of childhood morbidity and mortality in developing countries. Salmonella causes various diseases that range from mild gastroenteritis to enteric fever, depending on the serovar involved, infective dose, species, age and immune status of the host. Probiotics are proposed as an attractive alternative possibility in the prevention against this pathogen infection. Previously we demonstrated that continuous Lactobacillus casei CRL 431 administration to BALB/c mice before and after challenge with Salmonella enterica serovar Typhimurium (S. Typhimurium) decreased the severity of Salmonella infection. The aim of the present work was to deep into the knowledge about how this probiotic bacterium exerts its effect, by assessing its impact on the expression and secretion of pro-inflammatory (TNFα, IFNγ) and anti-inflammatory (IL-10) cytokines in the inductor and effector sites of the gut immune response, and analyzing toll-like receptor (TLR2, TLR4, TLR5 and TLR9) expressions in both healthy and infected mice.
Probiotic administration to healthy mice increased the expression of TLR2, TLR4 and TLR9 and improved the production and secretion of TNFα, IFNγ and IL-10 in the inductor sites of the gut immune response (Peyer's patches). Post infection, the continuous probiotic administration, before and after Salmonella challenge, protected the host by modulating the inflammatory response, mainly in the immune effector site of the gut, decreasing TNFα and increasing IFNγ, IL-6 and IL-10 production in the lamina propria of the small intestine.
The oral administration of L. casei CRL 431 induces variations in the cytokine profile and in the TLRs expression previous and also after the challenge with S. Typhimurium. These changes show some of the immune mechanisms implicated in the protective effect of this probiotic strain against S. Typhimurium, providing an alternative way to reduce the severity of the infection.
由沙门氏菌引起的腹泻感染是发展中国家儿童发病率和死亡率的主要原因之一。沙门氏菌引起的各种疾病范围从轻度肠胃炎到伤寒,这取决于所涉及的血清型、感染剂量、宿主的物种、年龄和免疫状态。益生菌被提议作为预防这种病原体感染的一种有吸引力的替代可能性。以前我们证明,在 BALB/c 小鼠感染鼠伤寒沙门氏菌(S. Typhimurium)前后连续给予干酪乳杆菌 CRL 431 可以降低沙门氏菌感染的严重程度。本研究的目的是深入了解这种益生菌如何发挥作用,评估其对肠道免疫反应诱导和效应部位促炎(TNFα、IFNγ)和抗炎(IL-10)细胞因子表达和分泌的影响,并分析健康和感染小鼠中 Toll 样受体(TLR2、TLR4、TLR5 和 TLR9)的表达。
益生菌给药可增加健康小鼠 TLR2、TLR4 和 TLR9 的表达,并改善肠道免疫反应诱导部位(派尔集合淋巴结)TNFα、IFNγ 和 IL-10 的产生和分泌。感染后,连续给予益生菌,在沙门氏菌攻击前后,通过调节炎症反应来保护宿主,主要在肠道免疫效应部位,减少 TNFα并增加 IFNγ、IL-6 和 IL-10 在小肠固有层的产生。
口服干酪乳杆菌 CRL 431 诱导了细胞因子谱和 TLRs 表达的变化,无论是在 S. Typhimurium 攻击之前还是之后。这些变化显示了该益生菌菌株对 S. Typhimurium 保护作用所涉及的一些免疫机制,为减轻感染的严重程度提供了一种替代方法。