Antibiotic Treatment Protocols and Germ-Free Mouse Models in Vascular Research

Bayer, Franziska; Ascher, Stefanie; Pontarollo, Giulia; Reinhardt, Carsten

doi:10.3389/fimmu.2019.02174

Cited by 28 publications

(22 citation statements)

References 68 publications

(93 reference statements)

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“…There are controversial opinions on the usage of antibiotics cocktails in comparison to germ-free raised animals. Both methods have their pros and cons as e.g., germ-free conditions might impact gut development (for example [ 25 , 59 , 60 ]) but antibiotics might not deplete bacterial commensals completely and have side effects [ 61 ]. By comparing both attempts in 5xFAD mice, both strategies revealed lowered plaque burden in the hippocampus in mice and ameliorated behavioral deficits, however, microglial activation was selectively found in germ-free raised animals [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

“…All procedures were performed in accordance with the European Communities Council Directive regarding care and use of animals for experimental procedures and were approved by local authorities (Landesuntersuchungsamt Rheinland-Pfalz; approval number G17-1-035, approval date June 2017). Germ-free C57BL/6J that were used for assessing viability of probiotic bacteria after stomach passage were maintained as colonies in sterile flexible film mouse isolator systems at the Translational Animal Research Center (TARC) [ 24 , 25 ]. The germ-free status of the mice was verified every second week by 16S rDNA PCR and by bacterial culture testing.…”

Section: Methodsmentioning

confidence: 99%

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Impact of Gut Microbiome Manipulation in 5xFAD Mice on Alzheimer’s Disease-Like Pathology

et al. 2021

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The gut brain axis seems to modulate various psychiatric and neurological disorders such as Alzheimer’s disease (AD). Growing evidence has led to the assumption that the gut microbiome might contribute to or even present the nucleus of origin for these diseases. In this regard, modifiers of the microbial composition might provide attractive new therapeutics. Aim of our study was to elucidate the effect of a rigorously changed gut microbiome on pathological hallmarks of AD. 5xFAD model mice were treated by antibiotics or probiotics (L. acidophilus and L. rhamnosus) for 14 weeks. Pathogenesis was measured by nest building capability and plaque deposition. The gut microbiome was affected as expected: antibiotics significantly reduced viable commensals, while probiotics transiently increased Lactobacillaceae. Nesting score, however, was only improved in antibiotics-treated mice. These animals additionally displayed reduced plaque load in the hippocampus. While various physiological parameters were not affected, blood sugar was reduced and serum glucagon level significantly elevated in the antibiotics-treated animals together with a reduction in the receptor for advanced glycation end products RAGE—the inward transporter of Aβ peptides of the brain. Assumedly, the beneficial effect of the antibiotics was based on their anti-diabetic potential.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Impact of Gut Microbiome Manipulation in 5xFAD Mice on Alzheimer’s Disease-Like Pathology

et al. 2021

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“…Both these interventions led to a drastic reduction in the expression of the ISRE/IRF‐dependent genes in IEC cells, and the antibiotics already sufficed to protect against TNF, as shown before (Van Hauwermeiren et al , ). Remarkable, though GF mice had no microbes in their gut, they were not basically protected against TNF, maybe because of the immature status of their innate immune defense systems (Bayer et al , ). Taken together with the strongly increased expression of these ISRE/IRF‐dependent genes in GC/GR‐deficient animals, it is reasonable to assume that the protective effect of zinc is based on the reduction in these ISRE/IRF‐dependent genes in a way that involves the microbiota and Paneth cell's cell death.…”

Section: Discussionmentioning

confidence: 99%

Zinc inhibits lethal inflammatory shock by preventing microbe‐induced interferon signature in intestinal epithelium

et al. 2020

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The cytokine TNF drives inflammatory diseases, e.g., Crohn's disease. In a mouse model of TNF ‐induced systemic inflammatory response syndrome ( SIRS ), severe impact on intestinal epithelial cells ( IEC s) is observed. Zinc confers complete protection in this model. We found that zinc no longer protects in animals which lack glucocorticoids ( GC s), or express mutant versions of their receptor GR in IEC s, nor in mice which lack gut microbiota. RNA ‐seq studies in IEC s showed that zinc caused reduction in expression of constitutive ( STAT 1‐induced) interferon‐stimulated response ( ISRE ) genes and interferon regulatory factor ( IRF ) genes. Since some of these genes are involved in TNF ‐induced cell death in intestinal crypt Paneth cells, and since zinc has direct effects on the composition of the gut microbiota (such as several Staphylococcus species) and on TNF ‐induced Paneth cell death, we postulate a new zinc‐related anti‐inflammatory mechanism. Zinc modulates the gut microbiota, causing less induction of ISRE / IRF genes in crypt cells, less TNF ‐induced necroptosis in Paneth cells, and less fatal evasion of gut bacteria into the system.

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“…In conclusion, experiments on GF mouse models can give unique insights into the interplay between the gut microbiota and the host's organ function, platelet reactivity and the immune system [17,48,95]. This technology is indeed one of the most meaningful experimental animal models, as it is complementary and reduces risks linked to the use of antibiotics in animal experiments [33].…”

Section: Figurementioning

confidence: 97%

The Gut Microbiota in Cardiovascular Disease and Arterial Thrombosis

et al. 2019

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The gut microbiota has emerged as a contributing factor in the development of atherosclerosis and arterial thrombosis. Metabolites from the gut microbiota, such as trimethylamine N-oxide and short chain fatty acids, were identified as messengers that induce cell type-specific signaling mechanisms and immune reactions in the host vasculature, impacting the development of cardiovascular diseases. In addition, microbial-associated molecular patterns drive atherogenesis and the microbiota was recently demonstrated to promote arterial thrombosis through Toll-like receptor signaling. Furthermore, by the use of germ-free mouse models, the presence of a gut microbiota was shown to influence the synthesis of endothelial adhesion molecules. Hence, the gut microbiota is increasingly being recognized as an influencing factor of arterial thrombosis and attempts of dietary pre-or probiotic modulation of the commensal microbiota, to reduce cardiovascular risk, are becoming increasingly significant.

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Antibiotic Treatment Protocols and Germ-Free Mouse Models in Vascular Research

Cited by 28 publications

References 68 publications

Impact of Gut Microbiome Manipulation in 5xFAD Mice on Alzheimer’s Disease-Like Pathology

Impact of Gut Microbiome Manipulation in 5xFAD Mice on Alzheimer’s Disease-Like Pathology

Zinc inhibits lethal inflammatory shock by preventing microbe‐induced interferon signature in intestinal epithelium

The Gut Microbiota in Cardiovascular Disease and Arterial Thrombosis

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