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Dysbiosis refers to disturbances in the gut microbiota, leading to altered composition and metabolome of commensal communities, with reduced phylogenetic diversity (1, 2, 3).
As causes, dysbiosis can result from environmental or internal factors, including antibiotics, infections, drugs, medications, aging, lifestyle changes, surgery, and poor nutrition (4, 5, 6). Dysbiosis is influenced by age, particularly in the 7th and 8th decades of life (22). In addition, urbanization and industrialization have significantly altered microbial communities, leading to changes in gut microbial composition, reduced alfa diversity, and the loss of important microbial taxa such as the Prevotellaceae, Spirochaetaceae, and Succinovibrioaceae families. These transformations may be linked to a departure from ancestral environments and lifestyles, which included rural living, diets rich in whole foods, and greater exposure to environmental microbes and antigens. The modern era of industrialization has brought about increased environmental and personal sanitization, the use of pharmaceuticals and antibiotics, exposure to psychological stressors, and the consumption of processed foods. These lifestyle changes have profoundly affected the microbiome and stress physiology, contributing to stress and immune-related diseases. The observed shifts in the environment, microbiome, and disease incidence are likely interconnected. This suggests that an evolutionary mismatch has caused adaptive responses to become maladaptive, leading to negative changes in lifelong health trajectories (25).
In the consequence, dysbiosis is linked to increased intestinal permeability, inflammation, oxidative stress, cancer, and autoimmune disorders. It can also lead to the translocation of bacteria and their products into systemic circulation, affecting host immunity and contributing to diseases (7, 8, 9, 10, 11, 12).
As clinical manifestations dysbiosis can cause conditions like Spontaneous Bacterial Peritonitis (SBP) and is associated with increased susceptibility to infections and metabolic diseases (13, 14, 15).
As microbial changes dysbiosis often involves a decrease in symbionts and commensals, and/or an increase in pathobionts, with an enrichment of Proteobacteria and Enterobacteriaceae (16, 17).
Enterobacteriaceae (phylum: Proteobacteria) and Enterococcaceae (phylum: Firmicutes) expansion may play an important role in the pathogenesis of human diseases and should be considered a microbial signature of intestinal dysbiosis (23, 24).
Impact on Health: Low diversity in gut microbiota is linked to obesity and inflammatory bowel disease. Dysbiosis can stimulate the expression of TLR-4 and Blimp-1, inhibiting NLRP12, which is crucial in ulcerative colitis development (18, 19, 20, 21).
Addressing dysbiosis involves interventions like decontamination with oral antibiotics, primarily effective in the intestine (13).
Emerging evidence suggests that the entire microbial community composition, rather than a few dominant organisms, contributes to a balanced immune response (2).
Dysbiosis disrupts the physiological interaction between epithelial cells and the microbiota (26). That means an increased permeability and inflammation (23).
Due to the loss of microbiome diversity it comes to a bloom of Enterobacteriaceae and Enterococcaceae (23)
Inflammatory type 1 immune cells (Th1 T cells, monocytes, macrophages, and neutrophils) are aberrantly activated to produce cytokines such as Interleukin-1 (IL-1) beta (IL-1F2) and Tumor Necrosis Factor alfa (TNF-alfa). These immune cells increase inflammation in the intestine, and the permeability through the opening of tight junctions (23).
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(22) Collins et al. 1998 Int. Dairy Journal 8: 487-490
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