Laboratory of Clinical and Experimental Biochemistry, Reference Centre for Lactobacilli (CERELA-CONICET), Tucuman, Argentina.
BMC Immunol. 2012 Sep 18;13:53. doi: 10.1186/1471-2172-13-53.
Some studies have shown that probiotics, including Lactobacillus rhamnosus CRL1505, had the potential to beneficially modulate the outcome of certain bacterial and viral respiratory infections. However, these studies did not determine the mechanism(s) by which probiotics contribute to host defense against respiratory viruses.
In this work we demonstrated that orally administered Lactobacillus rhamnosus CRL1505 (Lr1505) was able to increase the levels of IFN-γ, IL-10 and IL-6 in the respiratory tract and the number of lung CD3(+)CD4(+)IFN-γ(+) T cells. To mimic the pro-inflammatory and physiopathological consecuences of RNA viral infections in the lung, we used an experimental model of lung inflammation based on the administration of the artificial viral pathogen-associated molecular pattern poly(I:C). Nasal administration of poly(I:C) to mice induced a marked impairment of lung function that was accompanied by the production of pro-inflammatory mediators and inflammatory cell recruitment into the airways. The preventive administration of Lr1505 reduced lung injuries and the production of TNF-α, IL-6, IL-8 and MCP-1 in the respiratory tract after the challenge with poly(I:C). Moreover, Lr1505 induced a significant increase in lung and serum IL-10. We also observed that Lr1505 was able to increase respiratory IFN-γ levels and the number of lung CD3(+)CD4(+)IFN-γ(+) T cells after poly(I:C) challenge. Moreover, higher numbers of both CD103(+) and CD11b(high) dendritic cells and increased expression of MHC-II, IL-12 and IFN-γ in these cell populations were found in lungs of Lr1505-treated mice. Therefore, Lr1505 treatment would beneficially regulate the balance between pro-inflammatory mediators and IL-10, allowing an effective inflammatory response against infection and avoiding tissue damage.
Results showed that Lr1505 would induce a mobilization of cells from intestine and changes in cytokine profile that would be able to beneficially modulate the respiratory mucosal immunity. Although deeper studies are needed using challenges with respiratory viruses, the results in this study suggest that Lr1505, a potent inducer of antiviral cytokines, may be useful as a prophylactic agent to control respiratory virus infection.
一些研究表明，益生菌，包括鼠李糖乳杆菌 CRL1505，具有有益地调节某些细菌和病毒呼吸道感染结果的潜力。然而，这些研究并未确定益生菌有助于宿主抵抗呼吸道病毒的机制。
在这项工作中，我们证明了口服给予鼠李糖乳杆菌 CRL1505（Lr1505）能够增加呼吸道中的 IFN-γ、IL-10 和 IL-6 水平以及肺 CD3+CD4+IFN-γ+T 细胞的数量。为了模拟呼吸道病毒感染的促炎和生理病理后果，我们使用了基于人工病毒病原体相关分子模式聚（I：C）给药的肺部炎症实验模型。聚（I：C）鼻内给药诱导小鼠肺功能明显受损，同时伴有促炎介质的产生和炎性细胞募集到气道。预防性给予 Lr1505 可减轻肺部损伤，并减少呼吸道中 TNF-α、IL-6、IL-8 和 MCP-1 的产生。此外，Lr1505 诱导了肺和血清中 IL-10 的显著增加。我们还观察到，Lr1505 能够增加呼吸道 IFN-γ水平和聚（I：C）后肺 CD3+CD4+IFN-γ+T 细胞的数量。此外，在 Lr1505 治疗的小鼠肺部发现，CD103+和 CD11b（高）树突状细胞数量增加，这些细胞群中 MHC-II、IL-12 和 IFN-γ的表达增加。因此，Lr1505 治疗将有益地调节促炎介质和 IL-10 之间的平衡，从而能够有效抵抗感染并避免组织损伤。
结果表明，Lr1505 将诱导肠道细胞的动员和细胞因子谱的变化，从而能够有益地调节呼吸黏膜免疫。尽管需要使用呼吸道病毒进行更深入的研究，但本研究结果表明，Lr1505 作为一种抗病毒细胞因子的有效诱导剂，可能有助于作为预防剂来控制呼吸道病毒感染。
