An Overview of the Therapeutic Aspect of Living Drugs Probiotics

An Overview of the Therapeutic Aspect of Living Drugs Probiotics

Vandana Bharat Patravale (Institute of Chemical Technology, India) and Amita Keertimaan Joshi (B. V. Patel PERD Centre, India)
Copyright: © 2019 |Pages: 34
DOI: 10.4018/978-1-5225-3267-5.ch001
OnDemand PDF Download:
No Current Special Offers


The human body harbors ten times more bacterial cells than human cells. These bacterial cells form the human microbiome that plays a vital role in human health. An imbalance in the gut microbiome (i.e., dysbiosis) can result in various pathological conditions. This dysbiosis can be refurbished with the supplement of “probiotics.” Probiotics have thus been defined as non-pathogenic micro-organisms that, when ingested, exert a positive influence on host health or physiology. The most commonly used probiotic bacteria comes from two genera: Lactobacillus and Bifidobacterium. Various research findings have proposed a correlation between the alteration of microbiota (composition/activity/density) with disorders like infectious diarrhea, inflammatory bowel diseases, obesity, to name a few. The ultimate effect of administration of probiotics on health or physiology is either direct or indirect. This chapter summarizes the concept of probiotics, their therapeutic aspect along with possible mechanism of action.
Chapter Preview

Gut Microbiota

Human gut microbiota is a fascinating, unexplored ecosystem. Gut microbiome is a‘mini-ecosystem’ created by a collection of microbes inhabiting the human gastrointestinal (GI) tract. The intestinal lumen harbors 500 to 1000 different species of living microbes. By an estimate, there are 10 times higher number of microbes than the cells in human body and collectively the genome of these microbes is 50 times larger than the human genome. The predominant bacterial phyla in the human gut, Bacteroides and Firmicutes, are obligate anaerobes. Bacteroides phylum include B. fragilis and B. vulgates. Bacteroides are involved in the digestion of carbohydrate resulting in lowering of intestinal pH that inhibit the growth of harmful bacteria. While, the phylum Firmicutes (strong wall) includes the genera of Lactobacillus, Clostridium, and Bacillus.

The intestinal microbiota is not homogeneous; the density of bacterial cells varies throughout the GI tract depending upon the physiological condition of the GI tract viz., intestinal pH gradient, intestinal oxygen gradient, bile acids etc. The gut microbiota is a continuously evolving ecosystem, depending upon various exogenous and endogenous factors (Flint, Scott, Louis, & Duncan, 2012). The evolution of the microbiota takes in three stages of the human life (Figure 1):

From Birth to Weaning

Interestingly, the newborn human gut is a sterile GI tract, which is quickly inhabited by microbes during birthing process. The type of delivery (vaginal birth versus caesarean section) and the type of diet (breast feeding versus formula feeding) are few of the factors that affect the colonization patterns. The initial colonizing microbes are facultative anaerobes which establish the conditions for the eventual obligate anaerobes. The initial bacteria that colonize gut are Bifidobacterium spp. and Bacteroids spp. Vaginally born babies have predominant population of Bifidobacterium as compared to the babies born via caesarean section, wherein the majority population is from Staphylococcus spp. and Propionibacterium spp. Eventually, delivery process significantly determines the immune system development via gut microbiome. Babies delivered via caesarean section have been found to have lower fecal bacterial cell count as compared to babies born vaginally.

The early microbiome in infants evolves and adapts for the lactose utilization from the milk (breast milk as well as formula milk). However, solely breastfed babies have a highly stable and less variable bacterial microbiome, with Bifidobacterium being the predominant bacteria colonizing the gut, as compared to bottle fed babies (Flint, Scott, Louis, & Duncan, 2012; Duncan, 2013).

Complete Chapter List

Search this Book: