Immune-Mediated Mechanisms of Action of Probiotics and Synbiotics in Treating Pediatric Intestinal Diseases

Abstract

The pediatric population is continually at risk of developing infectious and inflammatory diseases. The treatment for infections, particularly gastrointestinal conditions, focuses on oral or intravenous rehydration, nutritional support and, in certain case, antibiotics. Over the past decade, the probiotics and synbiotics administration for the prevention and treatment of different acute and chronic infectious diseases has dramatically increased. Probiotic microorganisms are primarily used as treatments because they can stimulate changes in the intestinal microbial ecosystem and improve the immunological status of the host. The beneficial impact of probiotics is mediated by different mechanisms. These mechanisms include the probiotics' capacity to increase the intestinal barrier function, to prevent bacterial transferation and to modulate inflammation through immune receptor cascade signaling, as well as their ability to regulate the expression of selected host intestinal genes. Nevertheless, with respect to pediatric intestinal diseases, information pertaining to these key mechanisms of action is scarce, particularly for immune-mediated mechanisms of action. In the present work, we review the biochemical and molecular mechanisms of action of probiotics and synbiotics that affect the immune system.

Keywords: immune system; intestinal microbiota; mechanism of action; pediatric gastrointestinal infection; probiotics.

Figure 1

General probiotic mechanism of action in pediatric gastrointestinal infections. Abbreviations: ASC, apoptosis-associated speck-like protein containing a CARD; ERK, extracellular regulated kinase; IKK, IκB kinase; IL, interleukin; IFN, interferon; IRAK4, IL-1 receptor-associated kinase 4; JNK, Jun N-terminal kinase; NF-κB, nuclear factor κ-B; NEMO, NF-κB essential modulator; TNF-α, tumor factor necrosis alpha; TLR, toll-like receptor, TAB1/2/3, TAK binding proteins; TAK1, ubiquitin-dependent kinase of MKK and IKK; TBK1, serine/threonine-protein kinase 1; TGF, transforming growth factor; TRAF6, Tumor necrosis factor receptor-associated factor 6.