Commentary - (2023) Volume 14, Issue 1
Received: 23-Dec-2022, Manuscript No. JBP-23-19689; Editor assigned: 26-Dec-2022, Pre QC No. JBP-23-19689 (PQ); Reviewed: 09-Jan-2023, QC No. JBP-23-19689; Revised: 16-Jan-2023, Manuscript No. JBP-23-19689 (R); Published: 23-Jan-2023, DOI: 10.35248/2155-9597.23.14.439
The manipulation of the intestinal microbiota in mouse models has increased consistently with a better understanding of the intestinal microbiota's role in maintaining physiologic homeostasis and in modulating disease processes. While antibiotic treatment models offer a quick, affordable, and widely available alternative to germ-free mouse models, which are typically thought of as the gold standard for research in microbiota. Recent results have shown that the microbiota regulates infectious illnesses and other immunologic difficulties.
The impact of the gut microbiota on human health has drawn increasing attention from the scientific community as well as the general public over the past few decades. The human body's microbiota, which consists of bacteria, viruses, fungi, and archaea that live there, has been linked to the regulation of inflammatory, infectious, and metabolic diseases and is thought to be a major factor in the development, spread, and prevention of human diseases. The necessity and incredibly complicated element in human health has emerged along with the rush of excitement to comprehend it. In particular, the creation of small animal models of the microbiota enables testing of specific microbiota subsets as causative against correlative variables in disease states, as well as providing a method to identify potential therapies.
To investigate how the microbiota affects mouse physiology and disease, two basic approaches have been developed: germ-free models, and antibiotic treatment regimens. Both strategies have advantages and disadvantages. These two different approaches have been used to model the effects of the microbiota on human disease, as well as the commonly used regimens and methods to deplete the microbiota, the effects of these approaches on host physiology, including cellular composition, signalling pathways, and organ function.
Germ-free mice are preserved free from detectable bacteria, viruses, and eukaryotic microbes. They are grown in isolation chambers that completely limit exposure to microorganisms. Germ-free mice allow for the creation of gnotobiotic animals that are solely inhabited by recognized microorganisms or the study of the complete absence of germs. However, due to the specialized facilities needed to produce and care for these mice as well as the associated costs, labour, and expertise, many researchers may not have access to these models.
Using a combination of culture, microscopy, serology, gross morphology, and sequencing-based detection methods, germfree mice must be routinely checked for contamination. Furthermore, the number of distinct genotypes that can be researched is constrained by the requirement that any unique mouse strain be rederived in these facilities in order to be studied under germ-free circumstances. Additionally, keeping mice in isolators may make some research difficult or impractical like behavioural testing or pathogen infections.
The use of antibiotics as treatment has become a substitute strategy to avoid some of these effects. Broad-spectrum antibiotic therapy is frequently used to deplete the intestinal flora of mice, and it is easily adaptable to any genotype or state of the mouse.
Antibiotics have the ability to reduce bacterial populations in mice that were typically infected since birth, in contrast to germfree settings, during which total sterility is maintained throughout life. Germ-free animals are broadly impaired in many aspects of development and early immune education, whereas antibiotics treatment in adult mice specifically allows for study of the role of bacteria in maintaining cell functionality and signalling pathways after development. Alternatively, some studies deliver antibiotics in drinking water to pregnant dams to limit maternal transfer of microbes and then maintain the cage on the regimen during preventing to study the effects of bacterial depletion early in development. Antibiotic-treated mice are not fully free of bacteria, but there are notable decreases in bacterial load that are linked to changes in cell populations, communication pathways, and organ architecture, with outcomes that frequently resemble those of germ-free animals.
The results obtained with these regimens come with the warnings of potential off-target medication effects and insufficient or inconsistent ablation of microorganisms, even though antibiotic treatment offers an affordable and accessible option to germ-free mice. Antibiotic trials are much harder to compare than germ-free mouse studies since so many groups utilize different treatment plans and mouse microbial populations may be institution-specific.
It would be beneficial to standardize antibiotic treatment protocols; for instance, if a standard cocktail were used to demonstrate an initial finding, this could be compared to other research, and further follow-up tests might be done with changed cocktails as needed.
To rule in or out potential off-target drug effects or developmental differences between germ-free and typical pathogen-free mice that may be significant for a phenotype, at least a limited assessment of the replicability of findings in antibiotics-treated mice and germ-free mice would be of high value for most studies. In order to detect any effects of pollutants or antibiotic-resistant microorganisms, it will be crucial for researchers to make sure that microbial loads are routinely evaluated in both antibiotics treatment and germ-free models.
Citation: Ruff W (2023) Comparison of Germ-Free and Antibiotics Treatment Models in Mouse Gut Microbiota. J Bacteriol Parasitol. 14:439.
Copyright: © 2023 Ruff W. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.