Abstract
The adult human intestine is home to an almost inconceivable number of microorganisms. Their population is up to 100 trillion, nearly 10 times larger than the total number of our somatic and germ cells. All three domains, including bacteria, archaea, and eukarya, are contained in the adult human gastrointestinal (GI) tract and the bacteria achieve the highest cell densities and phylogenetic diversities (Whitman et al., 1998). Such gut microbiome can be viewed as a microbial organ placed within a host organ and the genomes of our affiliated microbial partners (the microbiome) may contain more than 100 times the number of genes in our genome. Once established, the indigenous microbiota provides many crucial functions to the host endows us with functional features that we have not had to evolve ourselves (MacDonald and Monteleone, 2005). These have been reviewed elsewhere (Ley et al., 2009; Neish, 2009) and include the contribution to digestion (such as the ability of microbes to break down host non-digestible polysaccharides) and its secondary benefits (the generation of SCFA), the metabolism of xenobiotics, the development of human immune system, and the colonization resistance. Generally, a healthy human state is a homeostasis between the microbiota and the host. Maladies such as Crohn's disease, chronic periodontitis, and bacterial vaginosis are characterized by a disruption of this homeostasis, a state known as dysbiosis (Tamboli et al., 2004). Meanwhile, the composition of the intestinal microbiota can undergo dynamic changes as a result of its interactions with diet, genotype/epigenetic composition, and immune-metabolic function (Kau et al., 2011). We envision a future in which new therapeutics and diagnostics enable the management of our microbiota to treat and prevent disease. Here, the relationship between gut microbiome and diseases and the effort in adjusting the gut microbiome will be discussed briefly.
Highlights
The most frequently reported disease that has been proved to associate with dramatic changes in the gut microbiota is Inflammatory Bowel Disease (IBD; Dicksved et al, 2008)
Recent studies demonstrated the use of probiotics, prebiotics, and synbiotics suggested the potential for controlling these diseases through manipulation of the composition of the gut microbiota, and direct interactions with the gut immune system (MacFarlane et al, 2009)
The hypothesis is that the microbiota in obese individuals can harvest the more energy from food than the one in lean individuals. Another hypothesis is that gut microbiota can modulate plasma LPS levels which triggers chronic low-grade inflammation leading to obesity and diabetes (Cani et al, 2007)
Summary
The most frequently reported disease that has been proved to associate with dramatic changes in the gut microbiota is Inflammatory Bowel Disease (IBD; Dicksved et al, 2008). MacFarlane et al (2009) revealed significant reductions in Bifidobacterium populations in rectal biopsies from IBD patients. Zhang et al (2007) have shown that bacterial diversity of Lactobacilli varied greatly between ulcerated tissue and non-ulcerated tissue in the same UC individuals. The most frequently reported disease that has been proved to associate with dramatic changes in the gut microbiota is Inflammatory Bowel Disease (IBD; Dicksved et al, 2008). Recent studies demonstrated the use of probiotics, prebiotics, and synbiotics suggested the potential for controlling these diseases through manipulation of the composition of the gut microbiota, and direct interactions with the gut immune system (MacFarlane et al, 2009).
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