Loading…
Antibiotic-induced gut dysbiosis can lead to several metabolic disturbances:
These changes may result in fat accumulation, insulin resistance, and disrupted immune homeostasis.
While antibiotics are essential for combating bacterial infections, their broad-spectrum activity can also eradicate beneficial gut microbes alongside harmful ones. They potentially lead to dysbiosis, which is associated with health issues.
Antibiotic esp. broad spectrum antibiotics use can have several adverse effects on the gut microbiota, including induction of gut dysbiosis through the diminution of the abundance of critical species or the complete eradication of important commensals (dysbiosis), altered metabolic activity, and the selection of antibiotic-resistant organisms, which can lead to antibiotic-associated diarrhea and recurrent Clostridioides difficile infections.
Antibiotic use doubtless exerts intense pressure on human-microbe interactions.
Although antibiotic therapies are an option to combat dysbiosis, complications include disruption of the homeostatic microbiota and a reduction in “colonization resistance ,” which facilitates entry by invading pathogens
Antibiotic treatment plays a vital role in fighting infections. However, exposure to antibiotics can disrupt the fundamental balance of gut microbiota and host immunity, potentially leading to long-term health issues.
After discontinuing Broad-spectrum antibiotics (ATB) for one to four months, the fecal samples showed a partial recovery in richness, although the overall microbiome profile experienced shifts and did not fully return to its original state.
The nature and doses of antimicrobials encountered today in industrialized societies can contribute to chronic disease
Antibiotic-induced gut dysbiosis can partially be counterbalanced by artificially increasing the levels of Autoinducer-2 (AI-2), a well-known bacterial communication molecule
Antibiotic treatment increases the intestinal inflammatory tone () by down-regulating epithelial PPAR-gamma Signal transduction and decreasing the number of RAR-related Orphan Receptor Gamma/T (ROR-gamma/t) Isoform 2 (NR1F3)t+ Foxp3+ Colonic Treg cells in the colonic mucosa
The resulting upregulation of inflammatory signals caused a shift in the metabolism of differentiated colonocytes toward anaerobic glycolysis, a metabolism characterized by low oxygen consumption
An essential consequence of elevated epithelial oxygenation is increased oxygen emanating from the mucosal surface, which promoted the expansion of Enterobacteriaceae via aerobic respiration in our animal models
There is also evidence that early childhood exposure to antibiotics can lead to several gastrointestinal, immunologic, and neurocognitive conditions.
Exposure to antibiotics both before birth and within the first two years of life can significantly increase the risk of developing atopic conditions, metabolic disorders, asthma, eczema, or allergies.
Infant antibiotic exposure (first year of life) was associated with disruption of gut microbiota and higher risks of childhood obesity and increased adiposity
see also:
Adiposity / Obesity & Childhood / Child
Antibiotics & Early Childhood / Neonates
Antibiotics & Gut microbiota
Antibiotics & Human Microbiota / Human microbiome
Cisplatin & Gut microbiota
Diseases / Disorders & Gut microbiota
Dysbiosis & Industrialisation