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146 results for “dysbiosis”
Alpha-synuclein overexpression can drive microbiome dysbiosis in mice
<p>Growing evidence indicates that persons living with Parkinson disease (PD), have a unique composition of indigenous gut microbes. Given the long prodromal or pre-diagnosed period, longitudinal studies of the human and rodent gut microbiome prior to symptomatic onset and for the duration of the disease period are currently lacking. PD is characterized in part by accumulation of the protein α-synuclein (α-syn) into insoluble aggregates, in both the central and enteric nervous systems. As such, a number of experimental rodent and non-human primate models of α-syn overexpression recapitulate some of hallmark pathophysiologies of PD. These animal models provide an opportunity to assess how the gut microbiome changes with age under disease relevant conditions. Here, we used a transgenic mouse strain, the Thy1-hSYN “line 61” mice which over express wild-type human α-syn to test how the gut microbiome composition responds in this model of PD pathology during aging. Using shotgun metagenomics, we find significant, age and genotype dependent bacterial taxa that become altered over age. We reveal that α-syn overexpression can drive alterations to the gut microbiome composition and suggest that it limits the expansion of diversity through age. Given emerging data on potential contributions of the gut microbiome to PD pathologies, our data provide an experimental foundation to understand how the PD-associated microbiome may arise as a trigger or co-pathology to disease.</p>
STORMS checklist: Dysbiosis of the enteric microbiota due to Crohn's disease treatment associated with MAIT cell activation
<p>STORMS checklist initiative to standardize reporting of human microbiome research, regarding submission to peer-reviewed journal.</p>
Commensal microbiome dysbiosis in keloid disease
<p>Wound healing is an intensely studied topic involved in many relevant pathophysiological processes, including fibrosis. Despite the large interest in fibrosis, the network that related to commensal microbiota and skin fibrosis remain mysterious. Here, we pay attention to keloid, a classical yet intractable skin fibrotic disease to establish the association between commensal microbiota to scaring tissue. Our histological data reveal the presence of microbiota in the keloids. 16S rRNA sequencing characterize microbial composition and divergence between the pathological and normal skin tissue. Our research provides insights into the pathology of human fibrotic diseases, advocating commensal bacteria and IL-8 signaling as useful targets in future interventions of recurrent keloid disease.</p>
Degenerative Cervical Myelopathy (DCM) induces sex-specific dysbiosis in the mouse gut bacterial microbiome, altering abundance and function
<p><strong>Background:</strong> Degenerative cervical myelopathy (DCM) represents the commonest cause of spinal cord impairment induced by non-traumatic events in the elderly population. It describes a spectrum of disorders that cause progressive spinal cord compression, neurological impairment, loss of bladder and bowel functions, as well as gastrointestinal dysfunction. The gut microbiota has been increasingly recognized as an environmental factor that can modulate both the central nervous system and immune response through the microbiota-gut-brain axis. Changes in gut microbiota composition or in the microbiota producing factors have been linked in the progression and development of several different pathologies such as traumatic spinal cord injury (SCI). Little is known about the molecular mechanisms that trigger DCM manifestation, and the potential role of the gut microbiota.</p> <p><strong>Results: </strong>Herein DCM was induced in female and male C57BL/6 mice by implanting an aromatic polyether material underneath the C5-6 laminae. The extent of DCM-induced changes in microbiota composition, also known as dysbiosis, was assessed by 16S rRNA sequencing from fecal samples at 3 different time points (6, 9 and 12 weeks after DCM induction). Several bacterial members were identified based on BLAST against the largest collection of metagenome-derived genomes from the mouse gut up to date. In both, female and males DCM caused gut dysbiosis compared with the sham group. However, dysbiosis was more pronounced in males than females, where several bacterial members of the families <em>Lachnospiraceae</em> and <em>Muribaculaceae</em> were significantly altered in the DCM group. These changes were also associated with altered immune cell composition in gut-associated lymphoid tissue, blood, and microbe-derived metabolic changes in propionate, butyrate, and lactate-producing bacterial members.</p> <p><strong>Conclusions: </strong>Our results demonstrate for the first time that DCM causes dynamic changes over time in the gut microbiota. Furthermore, we identify specie-specific abundance changes during DCM progression. DCM strongly reduces the abundance of butyrate-producing bacteria, and lactate-producing bacteria in much less extent. Sequence-based pangenomics cores were not resolved between the latter bacteria, but the gap-filling reactions and metabolic modelling successfully identified pyruvate-to-butanoate and pyruvate-to-propionate genes such as Buk and ACH1, respectively. These results aid to better understand markers and the molecular mechanisms that over time trigger DCM manifestation in females and males.</p>
Smoking-induced subgingival dysbiosis precedes clinical signs of periodontal disease
<p>Using 16 rRNA sequencing, a total of 233 subgingival sites from 8 smokers and 9 non-smokers over 6-12 months(804 subgingival samples total) were analyzed to study subgingival microbiome dysbiosis in smokers over time.</p>
Commensal microbiome dysbiosis in keloid disease
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The lower airways microbiota and antimicrobial peptides indicate dysbiosis in sarcoidosis
<p><span><strong>Rationale</strong>: </span><span>The role of the pulmonary microbiome in sarcoidosis is unknown.</span><br><br><span><strong>Objectives</strong>: </span><span>The objectives of the current study was to: 1) </span><span>Examine whether the pulmonary fungal and bacterial microbiota differed in patients with sarcoidosis compared with controls. 2) Examine whether there was an association between the microbiota and levels of the antimicrobial peptides (AMPs) in protected bronchoalveolar lavage (PBAL), indicating an interaction with the innate immune response.</span><br><br><span><strong>Methods</strong>: </span><span>35 sarcoidosis patients and 35 healthy controls underwent bronchoscopy and were sampled with oral wash (OW), protected BAL (PBAL) and left protected sterile brushes (LPSB). The fungal ITS1 region and the V3V4 region of the bacterial 16SrDNA gene were sequenced. Bioinformatic analyses were performed with QIIME 2. The AMPs secretory leucocyte protease inhibitor (SLPI) and human beta defensins 1 and 2 (hBD-1 & hBD-2), were measured in PBAL by enzyme linked immunosorbent assay (ELISA).</span><br><br><span><strong>Measurements and Main Results</strong>: </span><em><span>Aspergillus</span></em><span> dominated the PBAL samples in sarcoidosis. Differences in bacterial taxonomy were minor. There was no significant difference in fungal alpha diversity between sarcoidosis and controls, but the bacterial alpha diversity in sarcoidosis was significantly lower in OW (p=0.047) and PBAL (p=0.03) compared with controls. The beta diversity for sarcoidosis compared with controls differed for both fungi and bacteria. AMP levels were significantly lower in sarcoidosis compared to controls (SLPI & hBD-1: p<0.01). No significant correlations were found between </span><span>a</span><span>-diversity and AMPs.</span><br><br><span><strong>Conclusions</strong>: </span><span>The pulmonary fungal and bacterial microbiota in sarcoidosis differed from controls, with lower antimicrobial peptides levels in sarcoidosis.</span></p>
Neonatal exposure to BPA, BDE-99, and PCB produces persistent changes in hepatic transcriptome associated with gut dysbiosis in adult mouse livers
<p class="western"><span><span><span><b>Background</b>. Recent evidence suggests that multigenic and complex environmentally modulated diseases result from early life exposure to toxicants at least partly via gut microbial influences. Environmental toxicants, polybrominated diphenyl ethers (PBDEs), and polychlorinated biphenyls (PCBs) are breast milk-enriched persistent organic pollutants (POPs) and thus remain a continuing threat to human health despite being banned from production. Recent findings focused on the liver developmental reprogramming capabilities from neonatal BPA exposure; however, little is known on how PBDEs and PCBs regulate the liver transcriptome with respect to the gut microbiome. </span></span></span></p> <p class="western"><span><span><span><b>Objectives</b>. We investigated whether the gut microbiome can be persistently reprogrammed with the liver following neonatal exposure to POPs, and whether microbial biomarkers associated with disease-prone changes in the hepatic epigenetic and transcriptomic landscape in adulthood. </span></span></span></p> <p class="western"><span><span><span><b>Methods. </b>C57BL/6 male and female mouse pups were orally administered vehicle, bisphenol A (BPA), BDE-99 (a breast milk-enriched PBDE congener), or the Fox River PCB mixture (an environmentally relevant PCB mixture), between postnatal day (PND) 2 to 4, once daily for three consecutive days. Tissues were collected at PND5 and PND60 for 16S rDNA sequencing and targeted metabolomics.</span></span></span></p> <p class="western"><span><span><span><b>Results</b>. Neonatal exposure to BDE-99, followed by BPA and PCB, produced the greatest persistent changes in the adult hepatic transcriptome, including an inflammation and cancer-prone transcriptomic signature. BDE-99 exposure resulted in a persistent increase in <i>Akkermansia muciniphila</i> throughout the intestinal sections and feces. We observed persistent increases in acetate and succinate, metabolites <i>A. muciniphila</i><span> is able to produce.</span> Correspondingly, liver H3K4me1 and H3K27 acetylation were enriched around the loci encoding liver cancer-related genes following neonatal BDE-99 exposure. </span></span></span></p> <p class="western"><span><span><span><b>Conclusion. </b><span>Similar to BPA, early life exposure to BDE-99 also produced a cancer-prone hepatic transcriptomic signature corresponding to an increase in permissive epigenetic signatures around cancer-related genes in adulthood. This positively associates with BDE-99 mediated increase in </span><i><span>A. muciniphila</span></i><span> and its metabolites which are established epigenetic modifiers. </span></span></span></span></p>
Data from: Gut microbiome dysbiosis is associated with host genetics in the Norwegian Lundehund
<p class="MsoNormal"><span>A group of diseases have been shown to correlate with a phenomenon called microbiome dysbiosis, where the bacterial species composition of the gut becomes abnormal. The gut microbiome of an animal is influenced by many factors including diet, exposures to bacteria during post-gestational growth, lifestyle, and disease status. Studies also show that host genetics can affect microbiome composition. We sought to test whether host genetic background is associated with gut microbiome composition in the Norwegian Lundehund dog, a highly inbred breed with an effective population size of 13 individuals. The Lundehund has a high rate of a protein-losing enteropathy in the small intestine that is often reported as Lundehund syndrome, which negatively affects longevity and life-quality. An outcrossing project with the Buhund, Norrbottenspets and Icelandic sheepdog was recently established to reintroduce genetic diversity to the Lundehund and improve its health. To assess whether there was an association between host genetic diversity and the microbiome composition, we sampled the fecal microbiomes of 75 dogs of the parental (Lundehund), F1 (Lundehund x Buhund), and F2 (F1 x Lundehund) generations. We found significant variation in microbiome composition from the parental Lundehund generation compared to the outcross progeny. The variation observed in purebred Lundehunds corresponded to dysbiosis as seen by a highly variable microbiome composition with an elevated Firmicutes to Bacteroidetes ratio and an increase in the prevalence of <em>Streptococcus bovis/Streptococcus equinus </em>complex, a known pathobiont that can cause several diseases. We tracked several other environmental factors including diet, the presence of a cat in the household, living on a farm and the use of probiotics, but we did not find evidence of an effect of these on microbiome composition and alpha diversity. In conclusion, we found an association between host genetics and gut microbiome composition, which in turn may be associated with the high incidence of Lundehund syndrome in the purebred parental dogs.</span></p>
Antibiotic "Dysbiosis" in Preterm Infants
ClinicalTrials.gov study NCT02784821. IPD Sharing: NO. Countries: 1. Publications: 3.
Dynamics of Dysbiosis in the Skin and Gut Microbiome of Burn Patients
ClinicalTrials.gov study NCT07209007. IPD Sharing: NO. Countries: 1. Publications: 13.
Proton Pump Inhibitors and Dysbiosis in Cirrhosis
ClinicalTrials.gov study NCT01458990. IPD Sharing: UNDECIDED. Countries: 1. Publications: 4.
Gut dysbiosis and brain microhemorrhages in young vs aged mice with chronic kidney disease
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Neonatal exposure to BPA, BDE-99, and PCB produces persistent changes in hepatic transcriptome associated with gut dysbiosis in adult mouse livers
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Data from: Microbial dysbiosis precedes signs of sea star wasting disease in wild populations of Pycnopodia helianthoides
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The lower airways microbiota and antimicrobial peptides indicate dysbiosis in sarcoidosis
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Data from: Gut microbiome dysbiosis is associated with host genetics in the Norwegian Lundehund
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Thonningianin A ameliorated renal interstitial fibrosis in diabetic nephropathy mice by modulating gut microbiota dysbiosis and repressing inflammation
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Dysbiosis individualizes fitness effect of antibiotic resistance in the mammalian gut
<p>The fitness cost of antibiotic resistance in the absence of antibiotics is crucial to the success of suspending antibiotics as a strategy to lower resistance. Here we show that after antibiotic treatment the cost of resistance within the complex ecosystem of the mammalian gut is personalized. Using mice as an <i>in vivo</i> model, we find that the fitness effect of the same resistant mutation can be deleterious in a host, but neutral or even beneficial in other hosts. Such antagonistic pleiotropy is shaped by the microbiota, as in germ-free mice resistance is consistently costly across all hosts and in hosts with similar microbiotas the host specific effect of resistance is reduced. An eco-evolutionary model of competition for resources identifies a general mechanism underlying between host variation and predicts that the dynamics of compensatory evolution of resistant bacteria should be host specific, a prediction that was supported by experimental evolution<i> in vivo</i>. The microbiome of each human is close to unique and our results suggest that the short-term costs of resistance and its long-term within-host evolution will also be highly personalized, a finding that may contribute to the observed variable outcome of withdrawing antibiotics to reduce resistance levels.</p>
Raw data regarding the analysis published in the paper "Signatures of dysbiosis in fish microbiomes in the context of aquaculture" in Reviews in Aquaculture
<p>This dataset contains supporting material to the paper "Signatures of dysbiosis in fish microbiomes in the context of aquaculture" published in Reviews in Aquaculture</p>
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.