Reduction of gut microbial diversity and short chain fatty acids in BALB/c mice exposure to microcystin-LR

Zhang, Guilin; Zhang, Pengyu; Li, Wei; Hao, Fengqi; Chen, Fangmei; Yang, Yu; Hou, Yue; Yuting, Tao

doi:10.1007/s10646-020-02254-9

Cited by 19 publications

(8 citation statements)

References 53 publications

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“…Furthermore, The relative abundance of those were significantly decreased in IgAN group compared to control group. Especially, Clostridia, Alistipes and Ruminococcaceae were comfirmed as important SCFA-producing bacteria [ 24 , 25 ]. Clostridium was reported to produce acetate by the Wood-Ljungdahl pathway [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy

et al. 2021

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Background IgA nephropathy(IgAN)) is the common pathological type of glomerular diseases. The role of gut microbiota in mediating “gut-IgA nephropathy” has not received sufficient attention in the previous studies. The purpose of this study was to investigate the changes of fecal short-chain fatty acids(SCFAs), a metabolite of the intestinal microbiota, in patients with IgAN and its correlation with intestinal flora and clinical indicators, and to further investigate the role of the gut-renal axis in IgAN. Methods There were 29 patients with IgAN and 29 normal control subjects recruited from January 2018 to May 2018. The fresh feces were collected. The fecal SCFAs were measured by gas chromatography/mass spectrometry and gut microbiota was analysed by16S rDNA sequences, followed by estimation of α- and β-diversity. Correlation analysis was performed using the spearman’s correlation test between SCFAs and gut microbiota. Results The levels of acetic acid, propionic acid, butyric acid, isobutyric acid and caproic acid in the IgAN patients were significantly reduced compared with control group(P < 0.05). Butyric acid(r=-0.336, P = 0.010) and isobutyric acid(r=-0.298, P = 0.022) were negatively correlated with urea acid; butyric acid(r=-0.316, P = 0.016) was negatively correlated with urea nitrogen; caproic acid(r=-0.415,P = 0.025) showed negative correlation with 24-h urine protein level.Exemplified by the results of α-diversity and β-diversity, the intestinal flora of IgAN patients was significantly different from that of the control group. Acetic acid was positively associated with c_Clostridia(r = 0.357, P = 0.008), o_Clostridiales(r = 0.357, P = 0.008) and g_Eubacterium_coprostanoligenes_group(r = 0.283, P = 0.036). Butyric acid was positively associated with g_Alistipes (r = 0.278, P = 0.040). The relative abundance of those were significantly decreased in IgAN group compared to control group. Conclusions The levels of fecal SCFAs in the IgAN patients were reduced, and correlated with clinical parameters and gut microbiota, which may be involved in the pathogenesis of IgAN, and this finding may provide a new therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy

et al. 2021

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“…Previous studies by our research group and several others have reported that exposure to MC significantly altered gut bacteriome in experimental murine models 25,28,29 . Gut dysbiosis affects the host health by exacerbating the pathological outcomes in gastrointestinal disorders, liver diseases, and metabolic conditions like obesity and diabetes and increases the risk of anti-microbial resistance, which has been a global health concern 30,31 .…”

Section: Introductionmentioning

confidence: 64%

Prior exposure to microcystin alters host gut resistome and is associated with dysregulated immune homeostasis in translatable mouse models

Saha

Bose

Stebliankin

et al. 2021

Preprint

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The increased propensity of harmful algal blooms (HABs) and exposure from HABs-cyanotoxin causes human toxicity. It has been associated with the progression of several diseases that encompass the liver, kidneys, and immune system. Recently, a strong association of cyano-HAB toxicity with the altered host gut microbiome has been shown. We tested the hypothesis that prior exposure to cyanotoxin microcystin may alter the microbiome and induce microbiome-host-resistome crosstalk. Using both wild-type and humanized mice, we show that the mice exposed to microcystin had an altered microbiome signature that harbored antimicrobial resistance genes. Host resistome phenotypes such as mefA, msrD, mel, ant6, and tet40 increased in diversity and relative abundance following microcystin exposure. Interestingly, the increased abundance of these genes was traced to resistance to common antibiotics such as tetracycline, macrolides, glycopeptide, and aminoglycosides, crucial for modern-day treatment for several diseases. Increased abundance of these genes was positively associated with increased expression of PD1, a T-cell homeostasis marker, and pleiotropic inflammatory cytokine IL-6 with a concomitant negative association with immunosurveillance markers IL7 and TLR2. Microcystin exposure also caused decreased TLR2, TLR4, and REG3G expressions, increased immunosenescence, and higher systemic levels of IL-6 in both wild-type and humanized mice. In conclusion, the results show a first-ever characterization of the host resistome of microcystin exposure and its connection to host immune status and antibiotic resistance. The results may be crucial for understanding the ability of exposed subjects to fight future bacterial infections and the progression of the debilitating disease in hospital settings.

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“…Statistical analysis found a series of bacterial strains that had significant abundant differences between Ctrl and HBP groups, and Figure 2B shows the genus and species among these strains (including some strains with a trend to be significant). Specifically, the SCFA-generating bacteria Bacteroides fragilis , Bacteroides vulgatus , and Alistipes finegoldii under Bacteroidetes phylum ( Yu et al, 2013 ; Guilin et al, 2020 ; Su et al, 2020 ) were enriched in the HBP group, while B. fragilis and some other members of the Bacteroidetes are also major bacterial producers of glycan ( Coyne et al, 2008 ; Martens et al, 2009 ). Meanwhile, the stains from Enterobacteriales–Enterobacteriaceae branch under Proteobacteria phylum were also overexpressed in the HBP group, including Escherichia ( Escherichia coli ), Klebsiella ( Klebsiella pneumoniae ), and Citrobacter ; and these bacteria are reported to generate TMA ( Kalnins et al, 2015 ; Rath et al, 2017 ; Zeisel and Warrier, 2017 ).…”

Section: Resultsmentioning

confidence: 99%

Glycan Biosynthesis Ability of Gut Microbiota Increased in Primary Hypertension Patients Taking Antihypertension Medications and Potentially Promoted by Macrophage-Adenosine Monophosphate-Activated Protein Kinase

et al. 2021

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Increasing evidences suggest that the gut microbiota have their contributions to the hypertension, but the metagenomic characteristics and potential regulating mechanisms in primary hypertension patients taking antihypertension drugs are not clear yet. We carried out a metagenomic analysis in 30 primary hypertension patients taking antihypertension medications and eight healthy adults without any medication. We found that bacterial strains from species, such as Bacteroides fragilis, Bacteroides vulgatus, Escherichia coli, Klebsiella pneumoniae, and Streptococcus vestibularis, were highly increased in patients; and these strains were reported to generate glycan, short-chain fatty acid (SCFA) and trimethylamine (TMA) or be opportunistic pathogens. Meanwhile, Dorea longicatena, Eubacterium hallii, Clostridium leptum, Faecalibacterium prausnitzii, and some other strains were greatly decreased in the patient group. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis found that ortholog groups and pathways related to glycan biosynthesis and multidrug resistance were significantly increased in the patient group, and some of the hub genes related to N-glycan biosynthesis were increased in the patient group, while those related to TMA precursor metabolism and amino acid metabolism both increased and decreased in the patient group. Metabolites tested by untargeted liquid chromatography–mass spectrometry (LC-MS) proved the decrease of acetic acid, choline, betaine, and several amino acids in patients’ fecal samples. Moreover, meta-analysis of recent studies found that almost all patients were taking at least one kind of drugs that were reported to regulate adenosine monophosphate-activated protein kinase (AMPK) pathway, so we further investigated if AMPK regulated the metagenomic changes by using angiotensin II-induced mouse hypertensive model on wild-type and macrophage-specific AMPK-knockout mice. We found that the changes in E. coli and Dorea and glycan biosynthesis-related orthologs and pathways were similar in our cohort and hypertensive wild-type mice but reversed after AMPK knockout. These results suggest that the gut microbiota-derived glycan, SCFA, TMA, and some other metabolites change in medication-taking primary hypertension patients and that medications might promote gut microbiota glycan biosynthesis through activating macrophage-AMPK.

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Reduction of gut microbial diversity and short chain fatty acids in BALB/c mice exposure to microcystin-LR

Cited by 19 publications

References 53 publications

Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy

Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy

Prior exposure to microcystin alters host gut resistome and is associated with dysregulated immune homeostasis in translatable mouse models

Glycan Biosynthesis Ability of Gut Microbiota Increased in Primary Hypertension Patients Taking Antihypertension Medications and Potentially Promoted by Macrophage-Adenosine Monophosphate-Activated Protein Kinase

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