Lifestyle alters GUT-bacteria function: Linking immune response and host

Microbiota in human is a mixture society of different species (i.e. bacteria, viruses, funguses) populations with a different way of relationship classification to Human. Human GUT serves as the host of the majority of different bacterial populations (GUT flora, more than 500 species), which are with us (from the beginning) in an innate manner known as the commensal (no harm to each other) and symbiotic (mutual benefit) relationship. A homeostatic balance of host-bacteria relationship is very important and vital for a normal health process. However, this beneficial relationship and delicate homeostatic state can be disrupted by the imbalance of microbiome-composition of gut microbiota, expressing a pathogenic state. A strict homeostatic balance of microbiome-composition strongly depends on several factors; 1- lifestyle, 2- geography, 3- ethnicities, 4- mom as prime of the type of bacterial colonization in infant and 5- the disease. With such diversity in individuals combined with huge number of different bacterial species and their interactions, it is wise to perform an in-depth systems biology (e.g. genomics, proteomics, glycomics, and etcetera) analysis of personalized microbiome. Only in this way, we are able to generate a map of complete GUT microbiota and, in turn, to determine its interaction with host and intra-interaction with pathogenic bacteria. A specific microbiome analysis provides us the knowledge to decipher the nature of interactions between the GUT microbiota and the host and its response to the invading bacteria in a pathogenic state. The GUT-bacteria composition is independent of geography and ethnicity but lifestyle well affects GUT-bacteria composition and function. Microbiome knowledge obtained by systems biology also helps us to change the behavior of GUT microbiota in response to the pathogenic microbes as protection. Functional microbiome changes in response to environmental factors will be discussed in this review. (C) 2017 Elsevier Ltd. All rights reserved.