Abstract
Systemic and local inflammation in relation to the resident microbiota of the human gastro-intestinal (GI) tract and administration of probiotics are the main themes of the present review. The dominating taxa of the human GI tract and their potential for aggravating or suppressing inflammation are described. The review focuses on human trials with probiotics and does not include in vitro studies and animal experimental models. The applications of probiotics considered are systemic immune-modulation, the metabolic syndrome, liver injury, inflammatory bowel disease, colorectal cancer and radiation-induced enteritis. When the major genomic differences between different types of probiotics are taken into account, it is to be expected that the human body can respond differently to the different species and strains of probiotics. This fact is often neglected in discussions of the outcome of clinical trials with probiotics.
Highlights
Systemic and local inflammation in relation to the resident microbiota of the human gastro-intestinal (GI) tract and administration of probiotics are the main themes of the present review
These bacteria are of different types and, traditionally, attempts to identify them have been done by pure-culture technique, i.e., isolates are cultured at the laboratory and both phenotypic and genotypic characteristics are studied in pure cultures
IgA levels tended to be higher in the probiotic groups than in the placebo group, and alpha1-antitrypsin decreased by administration of L. rhamnosus GG, which may indicate that L. rhamnosus GG may alleviate intestinal inflammation in infants with atopic eczema/dermatitis syndrome (AEDS) and cow's milk allergy [112]
Summary
Inflammation is a defence reaction of the body against injury. The word inflammation originates from the Latin word ―inflammatio‖ which means fire, and traditionally inflammation is characterised by redness, swelling, pain, heat and impaired body functions. The process of inflammation is initiated by cells already present in the tissue, e.g., resident macrophages, dendritic cells and mast cells Danger signals trigger these cells into activation, and inflammatory mediators are released, which starts the process responsible for the clinical signs of inflammation. Interaction of TLRs and bacterial molecular patterns results in activation of a complex intracellular signalling cascade, up-regulation of inflammatory genes, production of pro-inflammatory cytokines and interferons, and recruitment of myeloid cells. It stimulates expression of co-stimulatory molecules required to induce an adaptive immune response of antigen presenting cells [22]. The better the barrier effect of the mucosa the smaller the risk of translocation of pro-inflammatory components originating from the gut microbiota
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