Villena Julio, Vizoso-Pinto Maria Guadalupe, Kitazawa Haruki
Immunobiotics Research Group, Tucuman, Argentina; Laboratory of Immunobiotechnology, Reference Centre for Lactobacilli (CERELA-CONICET), Tucuman, Argentina; Food and Feed Immunology Group, Laboratory of Animal Products Chemistry, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
Immunobiotics Research Group, Tucuman, Argentina; Faculty of Medicine, INSIBIO (UNT-CONICET), National University of Tucuman, Tucuman, Argentina.
Front Immunol. 2016 Dec 5;7:563. doi: 10.3389/fimmu.2016.00563. eCollection 2016.
The mucosal tissues of the gastrointestinal tract are the main portal entry of pathogens such as rotavirus (RV), which is a leading cause of death due to diarrhea among young children across the globe and a major cause of severe acute intestinal infection in livestock animals. The interactions between intestinal epithelial cells (IECs) and immune cells with RVs have been studied for several years, and now, it is known that the innate immune responses triggered by this virus can have both beneficial and detrimental effects for the host. It was demonstrated that natural RV infection in infants and experimental challenges in mice result in the intestinal activation of pattern recognition receptors (PRRs) such as toll-like receptor 3 (TLR3) and striking secretion of proinflammatory mediators that can lead to increased local tissue damage and immunopathology. Therefore, modulating desregulated intestinal immune responses triggered by PRRs activation are a significant promise for reducing the burden of RV diseases. The ability of immunoregulatory probiotic microorganisms (immunobiotics) to protect against intestinal infections, such as those caused by RVs, is among the oldest effects studied for these important group of beneficial microbes. In this review, we provide an update of the current status on the modulation of intestinal antiviral innate immunity by immunobiotics and their beneficial impact on RV infection. In addition, we describe the research of our group that demonstrated the capacity of immunobiotic strains to beneficially modulated TLR3-triggered immune response in IECs, reduce the disruption of intestinal homeostasis caused by intraepithelial lymphocytes, and improve the resistance to RV infections.
胃肠道的黏膜组织是轮状病毒(RV)等病原体的主要入侵门户,轮状病毒是全球幼儿腹泻致死的主要原因,也是家畜严重急性肠道感染的主要病因。肠道上皮细胞(IECs)与免疫细胞和轮状病毒之间的相互作用已研究多年,现在已知该病毒引发的先天免疫反应对宿主可能既有有益影响也有有害影响。研究表明,婴儿的自然轮状病毒感染和小鼠的实验性感染会导致模式识别受体(PRRs)如Toll样受体3(TLR3)在肠道被激活,并大量分泌促炎介质,这可能导致局部组织损伤和免疫病理增加。因此,调节由PRRs激活引发的失调肠道免疫反应对于减轻轮状病毒疾病负担具有重大前景。免疫调节益生菌微生物(免疫生物制剂)预防肠道感染(如由轮状病毒引起的感染)的能力是对这些重要有益微生物群体研究最早的效应之一。在本综述中,我们提供了免疫生物制剂对肠道抗病毒先天免疫调节的现状及其对轮状病毒感染有益影响的最新情况。此外,我们描述了我们团队的研究,该研究证明了免疫生物制剂菌株能够有益地调节IECs中由TLR3触发的免疫反应,减少上皮内淋巴细胞引起的肠道稳态破坏,并提高对轮状病毒感染的抵抗力。