Abstract
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.
Highlights
One of the leading causes of children mortality is preventable infectious diseases [1, 2]
We highlight some results of our group, which demonstrate the capacity of immunobiotic strains to beneficially modulate toll-like receptor (TLR)-3-triggered immune response in intestinal epithelial cells (IECs), reduce the disruption of intestinal homeostasis caused by intraepithelial lymphocytes (IELs), and improve the resistance to RVs infection
The IEC senses viral double-strand RNA (dsRNA) through pattern recognition receptors (PRRs), such as toll-like receptor 3 (TLR3), retinoic acid-inducible gene-I (RIG-I), and melanoma differentiation-associated gene-5 (MDA-5), and cellular signaling cascades are activated to react to viral infection [14,15,16] (Figure 1)
Summary
One of the leading causes of children mortality is preventable infectious diseases [1, 2]. Immunobiotics for Rotavirus Infection is reduced in developing areas, and some possible reasons are children infected at an early age, high viral challenge loads, and the lack of transferred maternal antibodies [8, 9]. Some lactic acid bacteria (LAB) strains are able to impact on human and animal health by modulating the mucosal and systemic immune systems. Those immunoregulatory probiotic LAB, known as immunobiotics, provide protection against viral infections by modulating innate and adaptive antiviral immunity. We highlight some results of our group, which demonstrate the capacity of immunobiotic strains to beneficially modulate toll-like receptor (TLR)-3-triggered immune response in intestinal epithelial cells (IECs), reduce the disruption of intestinal homeostasis caused by intraepithelial lymphocytes (IELs), and improve the resistance to RVs infection
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