Human body is a host to a large number of microorganisms. These microorganisms form a very integrated and complex community, and reside in almost every organ of human body and can regulate the overall human physiology. They can influence the immune system, contribute to metabolism, provide resistance against pathogens and can provide essential nutrients (Dekaboruah, Suryavanshi, Chettri, & Verma, 2020). Earlier studies attempted to define the entire set of microbes present in ‘healthy’, disease-free individuals to reach a consensus for determining health status. However, significant variations were observed among individuals, making such a consensus unlikely. Nonetheless, the microbial community in each organ can be defined by its unique core functionalities, which provide resilience to external perturbations and enhance the symbiotic relationship between the microbial community and host tissue (Lloyd-Price, Abu-Ali, & Huttenhower, 2016) referred to as microbiome.

Recently, the definition of microbiome has been revisited and defined “as a characteristic microbial community occupying a reasonable well-defined habitat which has distinct physio-chemical properties” (Berg et al., 2020). The definition takes into account the members, core microbiota, microbial interactions, coevolution and environmental characteristics and phenotypic characterization of species (Berg et al., 2020) providing a more holistic definition of microbiome.

Microbial exposure and colonization begin at birth and continue into adulthood. Over time, a mature microbiome community establishes that is more stable and resilient to external disturbances. However, early-life microbial establishment plays a crucial role in shaping the adult microbiome. This dynamic process of microbiome maturation continues throughout life and is influenced by many factors such as age, geographical location, diet, host genetics and many others (Greenhalgh, Meyer, Aagaard, & Wilmes, 2016).

During the perinatal period, facultative anaerobes such as Enterococcus, Proteobacteria, and Lactobacilli, along with a few anaerobes including Bifidobacteria, form pioneer communities. However, as individuals mature into adulthood, the ecological succession tends to favor more towards a more diverse and anaerobic microbes, a typical representative community of a healthy individual (Kriss, Hazleton, Nusbacher, Martin, & Lozupone, 2018). However, in disease condition this established state is disrupted leading to dysbiosis. Dysbiosis is an imbalanced state of microbiome which can be in any form such as decreased microbial diversity, change in functional characteristics of the microbial community and/or altered local distribution of microbes (Myers & Hawrelak, 2004). These alterations in the microbiome can have profound effects on the metabolic constitution of an individual. While host-derived metabolites remain relatively constant, microbial-derived metabolites depend on the unique microbial profile of each individual, which can vary widely (Van Treuren & Dodd, 2020). Consequently, changes in the microbiome have been linked to numerous diseases, including metabolic disorders (Lippert et al., 2017), hypertension (Li et al., 2017), inflammatory bowel disease (Santana, Rosas, Ribeiro, Marinho, & de Souza, 2022), and cardiovascular disease (Novakovic et al., 2020).

In recent years, many bidirectional communication patterns between the microbiome and other organs in the body have been identified. Of this, gut microbiome crosstalk with other organs particularly brain, is the most widely explored (Appleton, 2018, Liang et al., 2018, Sharma et al., 2023). These crosstalk exploit host endocrine, inflammatory, and neural pathways. Microbes or their metabolites can either directly cause disease or interact with these pathways, leading to changes in the host response to external stimuli. An understanding of these crosstalk can be crucial in deciphering the systemic effects of the microbiome and its role in various diseases (Wang & Wang, 2016). A review by Kalinkovich and Livshits (2019) highlights the significant role of dysbiosis in systemic inflammation and autoimmune disorders. They discussed how certain bacterial species, such as Prevotella, Collinsella aerofaciens, and Citrobacter rodentium, promote a pro-inflammatory immune response through mechanisms like epitope mimicry, self-antigen modification, enhanced apoptosis, and disruption of tight junctions, which compromise intestinal barrier integrity. This breakdown allows microbial products to enter the bloodstream, triggering chronic immune responses (Kalinkovich & Livshits, 2019). Infections may enhance the presentation of self-antigens, which are typically regulated under normal conditions. This self-antigen presentation can lead to the activation of autoreactive CD4 + T cells that drive autoimmune diseases. Dysbiosis exacerbates this cycle by altering intestinal immune cell functionality and promoting bacterial overgrowth, creating a detrimental feedback loop of inflammation and disease progression. Therefore, understanding these crucial links is essential for developing targeted therapies for autoimmune conditions (Campisi et al., 2016).

To describe the microbial dynamics of gut, Firmicutes/Bacteroidetes ratio is often used as a marker of dysbiosis. Studies indicate that a change in Firmicutes/Bacteroidetes ratio could be associated with incidences of type2 diabetes (Kusnadi et al., 2023), childhood obesity (Indiani et al., 2018) prostate enlargement (Takezawa et al., 2021) and others. However, while the Firmicutes/Bacteroidetes ratio provides valuable insights, it is important to recognize that other microbiome diversity metrics, such as alpha and beta diversity, are also widely employed in microbiome studies to assess overall health. These metrics offer a more comprehensive perspective on microbial diversity and its implications for health (Kers & Saccenti, 2022). As no definitive metric has yet been established, further research is necessary to explore the influence of other covariables that may affect these results (Magne et al., 2020).