Homeostasis and dysbiosis of the gut microbiome in health and disease

The human gastrointestinal tract (GIT) harbors taxonomically and functionally complex microbial ecosystem. The composition of the microbial species in the GIT ecosystem varies among individuals and throughout development. Bothenvironmental factors as well as host genetics influence the composition and homeostasis of GIT microbiome. Intrinsic GITmicrobiome can be characterized in terms of diversity, richness, dynamics and resilience. In healthy individual, microbialcommunities maintain homeostatic equilibrium and are resistant against perturbations. The resilience and resistance toperturbations of the GIT microbial ecosystem are robust but not absolute. Several factors can affect the homeostaticequilibrium of GIT microbiome and lead to dysbiotic microbiome configuration. Taxonomic and/or functional dysbiosis inthe GIT microbiome is associated with numerous health disorders like inflammatory bowel disease (IBD), malnutrition,metabolic disorders, asthma and neurodegenerative diseases. In this review, we discuss our current understanding ofhomeostasis and dysbiosis of the microbial ecology in the human gut and health disorders that are associated with themicrobiome dysbiosis.

Insights into the gastrointestinal tract microbiomes of Indian population

Trillions of microbes living in the gastrointestinal tract (GIT) of the human body finely tune homeostatic equilibrium in theGIT ecosystem and encode key functionalities that play crucial role in host metabolic functions, synthesis of macro- andmicronutrients, xenobiotics metabolisms, development of innate and adaptive immune systems, tissue and organ developments and resistance against invasion of enteric pathogens. The microbial diversity and richness of GIT ecosystem variesgreatly between individuals and over time. Extent of taxonomic and functional variations in GIT ecosystem is linked withdietary habit, pharmaceuticals usages, age, sex, body mass index, ethnicity, geography, altitude and civilization. Understanding a holistic picture of GIT microbiome of healthy people living across geography and identifying population specific‘keystone’ taxa is of immense importance for identifying microbial species that may provide protection against chronic andmetabolic diseases. Knowledge on geographic or ethnicity specific microbial signatures may also help us to understand thevaried efficacy of different drugs and vaccines in different population. India is the home of more than 1.36 billion peoplebelonging to 2000 human communities residing in well distinct geography. In the present review, we discuss the microbialsignatures in health and diseases of the rural and urban Indians living in sea level and high altitude areas.

Genetic components of stringent response in Vibrio cholerae.

Nutritional stress elicits stringent response in bacteria involving modulation of expression of several genes. This is mainly triggered by the intracellular accumulation of two small molecules, namely, guanosine 3’-diphosphate 5’-triphosphate and guanosine 3’,5’-bis(diphosphate), collectively called (p)ppGpp. Like in other Gram-negative bacteria, the cellular level of (p)ppGpp is maintained in Vibrio cholerae, the causative bacterial pathogen of the disease cholera, by the products of two genes relA and spoT. However, apart from relA and spoT, a novel gene relV has recently been identified in V. cholerae, the product of which has been shown to be involved in (p)ppGpp synthesis under glucose or fatty acid starvation in a ΔrelA ΔspoT mutant background. Furthermore, the GTP binding essential protein CgtA and a non-DNA binding transcription factor DksA also seem to play several important roles in modulating stringent response and regulation of other genes in this pathogen. The present review briefly discusses about the role of all these genes mainly in the management of stringent response in V. cholerae.

Molecular mechanism of acquisition of the cholera toxin genes.

One of the major pathogenic determinants of Vibrio cholerae, the cholera toxin, is encoded in the genome of a filamentous phage, CTX. CTX makes use of the chromosome dimer resolution system of V. cholerae to integrate its single stranded genome into one, the other, or both V. cholerae chromosomes. Here, we review current knowledge about this smart integration process.