Abstract
The term ‘probiotic’ is derived from the Greek/Latin word “pro” and the Greek word “bios,” meaning “of life”. The concept of probiotics was first described by Metchnikoff in 1907 (1). The World Health Organization (WHO) and the Food and Agriculture Organization of the United Nations have defined probiotics as “live microorganisms, which, when administered in adequate amounts, confer a health benefit on the host” (1, 2). These agents are often administered concurrently with substances that promote bacterial colonization and growth (prebiotics); in this instance, they are referred to as synbiotics. Probiotics are bacteria or yeasts. Most probiotics come from two groups: Lactobacillus and Bifidobacterium. Each group comprises different species and strains. Some probiotics, such as Saccharomyces boulardi, are yeasts (3, 4). In a healthy individual, there is a homeostasis between commensal intestinal microbiota and pathogenic bacteria. The composition of colonic microbiota is fundamental to gut barrier function. Anaerobic bacteria are the predominant microorganisms in the gastrointestinal tract, preventing the overgrowth of pathogenic bacteria in a phenomenon termed “colonization resistance” (2). When this homeostatic mechanism is altered, an ecological imbalance occurs, and gut barrier function is impaired. Gut barrier and immune dysfunction is associated with the onset of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) in critically ill patients (5). Several mechanisms by which probiotics exert their beneficial activity have been proposed, including competitive exclusion of bacterial adherence; release of bacteriocins to inhibit the growth of pathogens; production of butyrate; antioxidative effects; stimulation of mucus and SIgA production; enhancement of macromolecular degradation, which reduces antigen load; suppression of immune cell proliferation; inhibition of epithelial cell nuclear factor kappa B (NFκB) activation; modulation of epithelial apoptosis; maintenance of epithelial barrier; and modulation of immune function (2, 5, 6). There is substantial evidence that during periods of critical illness, significant alterations occur in the gut microflora due to several factors, including changes in circulating stress hormones, gut ischemia, immunosuppression, the use of antibiotics, and a lack of nutrients (6, 7). ICU and surgical patients are now believed to be at high risk of bacterial translocation, resulting in exacerbation of the disease state. Intestinal microbes can have a major role in such patients.
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