Displaying publications 21 - 40 of 42 in total

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  1. Wang Y, Lim YY, He Z, Wong WT, Lai WF
    PMID: 33559482 DOI: 10.1080/10408398.2021.1882381
    The last decide has witnessed a growing research interest in the role of dietary phytochemicals in influencing the gut microbiota. On the other hand, recent evidence reveals that dietary phytochemicals exhibit properties of preventing and tackling symptoms of Alzheimer's disease, which is a neurodegenerative disease that has also been linked with the status of the gut microbiota over the last decade. Till now, little serious discussions, however, have been made to link recent understanding of Alzheimer's disease, dietary phytochemicals and the gut microbiota together and to review the roles played by phytochemicals in gut dysbiosis induced pathologies of Alzheimer's disease. Deciphering these connections can provide insights into the development and future use of dietary phytochemicals as anti-Alzheimer drug candidates. This review aims at presenting latest evidence in the modulating role of phytochemicals in the gut microbiota and its relevance to Alzheimer's disease and summarizing the mechanisms behind the modulative activities. Limitations of current research in this field and potential directions will also be discussed for future research on dietary phytochemicals as anti-Alzheimer agents.
    Matched MeSH terms: Dysbiosis
  2. Osman MA, Neoh HM, Ab Mutalib NS, Chin SF, Mazlan L, Raja Ali RA, et al.
    Sci Rep, 2021 02 03;11(1):2925.
    PMID: 33536501 DOI: 10.1038/s41598-021-82465-0
    Dysbiosis of the gut microbiome has been associated with the pathogenesis of colorectal cancer (CRC). We profiled the microbiome of gut mucosal tissues from 18 CRC patients and 18 non-CRC controls of the UKM Medical Centre (UKMMC), Kuala Lumpur, Malaysia. The results were then validated using a species-specific quantitative PCR in 40 CRC and 20 non-CRC tissues samples from the UMBI-UKMMC Biobank. Parvimonas micra, Fusobacterium nucleatum, Peptostreptococcus stomatis and Akkermansia muciniphila were found to be over-represented in our CRC patients compared to non-CRC controls. These four bacteria markers distinguished CRC from controls (AUROC = 0.925) in our validation cohort. We identified bacteria species significantly associated (cut-off value of > 5 fold abundance) with various CRC demographics such as ethnicity, gender and CRC staging; however, due to small sample size of the discovery cohort, these results could not be further verified in our validation cohort. In summary, Parvimonas micra, Fusobacterium nucleatum, Peptostreptococcus stomatis and Akkermansia muciniphila were enriched in our local CRC patients. Nevertheless, the roles of these bacteria in CRC initiation and progression remains to be investigated.
    Matched MeSH terms: Dysbiosis/complications; Dysbiosis/diagnosis*; Dysbiosis/microbiology
  3. Megat Mohd Azlan PI, Chin SF, Low TY, Neoh HM, Jamal R
    Proteomics, 2019 05;19(10):e1800176.
    PMID: 30557447 DOI: 10.1002/pmic.201800176
    Dysbiosis of gut microbiome can contribute to inflammation, and subsequently initiation and progression of colorectal cancer (CRC). Throughout these stages, various proteins and metabolites are secreted to the external environment by microorganisms or the hosts themselves. Studying these proteins may help enhance our understanding of the host-microorganism relationship or they may even serve as useful biomarkers for CRC. However, secretomic studies of gut microbiome of CRC patients, until now, are scarcely performed. In this review article, the focus is on the roles of gut microbiome in CRC, the current findings on CRC secretome are highlighted, and the emerging challenges and strategies to drive forward this area of research are addressed.
    Matched MeSH terms: Dysbiosis*
  4. Castaño-Rodríguez N, Goh KL, Fock KM, Mitchell HM, Kaakoush NO
    Sci Rep, 2017 11 21;7(1):15957.
    PMID: 29162924 DOI: 10.1038/s41598-017-16289-2
    The gastric microbiome has been proposed as an etiological factor in gastric carcinogenesis. We compared the gastric microbiota in subjects presenting with gastric cancer (GC, n = 12) and controls (functional dyspepsia (FD), n = 20) from a high GC risk population in Singapore and Malaysia. cDNA from 16S rRNA transcripts were amplified (515F-806R) and sequenced using Illumina MiSeq 2 × 250 bp chemistry. Increased richness and phylogenetic diversity but not Shannon's diversity was found in GC as compared to controls. nMDS clustered GC and FD subjects separately, with PERMANOVA confirming a significant difference between the groups. H. pylori serological status had a significant impact on gastric microbiome α-diversity and composition. Several bacterial taxa were enriched in GC, including Lactococcus, Veilonella, and Fusobacteriaceae (Fusobacterium and Leptotrichia). Prediction of bacterial metabolic contribution indicated that serological status had a significant impact on metabolic function, while carbohydrate digestion and pathways were enriched in GC. Our findings highlight three mechanisms of interest in GC, including enrichment of pro-inflammatory oral bacterial species, increased abundance of lactic acid producing bacteria, and enrichment of short chain fatty acid production pathways.
    Matched MeSH terms: Dysbiosis/microbiology*
  5. Yusof N, Hamid N, Ma ZF, Lawenko RM, Wan Mohammad WMZ, Collins DA, et al.
    Gut Pathog, 2017;9:75.
    PMID: 29255490 DOI: 10.1186/s13099-017-0224-7
    Background: After an environmental disaster, the affected community is at increased risk for persistent abdominal pain but mechanisms are unclear. Therefore, our study aimed to determine association between abdominal pain and poor water, sanitation and hygiene (WaSH) practices, and if small intestinal bacterial overgrowth (SIBO) and/or gut dysbiosis explain IBS, impaired quality of life (QOL), anxiety and/or depression after a major flood.

    Results: New onset abdominal pain, IBS based on the Rome III criteria, WaSH practices, QOL, anxiety and/or depression, SIBO (hydrogen breath testing) and stools for metagenomic sequencing were assessed in flood victims. Of 211 participants, 37.9% (n = 80) had abdominal pain and 17% (n = 36) with IBS subtyped diarrhea and/or mixed type (n = 27 or 12.8%) being the most common. Poor WaSH practices and impaired quality of life during flood were significantly associated with IBS. Using linear discriminant analysis effect size method, gut dysbiosis was observed in those with anxiety (Bacteroidetes and Proteobacteria, effect size 4.8), abdominal pain (Fusobacteria, Staphylococcus, Megamonas and Plesiomonas, effect size 4.0) and IBS (Plesiomonas and Trabulsiella, effect size 3.0).

    Conclusion: Disturbed gut microbiota because of environmentally-derived organisms may explain persistent abdominal pain and IBS after a major environmental disaster in the presence of poor WaSH practices.

    Matched MeSH terms: Dysbiosis
  6. Mohd Hafiz Arzmi
    MyJurnal
    A balanced oral microbiome is essential in maintaining a healthy oral cavity. Oral microbiome comprises of var-ious microorganisms that belong to different kingdoms, including bacteria (bacteriome) and fungal (mycobiome). Multiple factors have been shown in oral carcinogenesis including alcohol consumption, tobacco smoking, betel nut chewing and microbial infections. Since the oral cavity comprises of various microbial kingdoms, thus, in-ter-kingdom interactions are suggested in promoting oral carcinogenesis. Dysbiosis, which is defined as imbalance inter-kingdom microbiome, alone may not cause oral carcinogenesis; thus, it is suggested that nutritional factor may also play a vital role in this disease development. A recent study has shown that sucrose consumption can induce the production of glucosyltransferases (gtfs) by Streptococcus mutans which lead to the increasing attachment of Candida albicans in polymicrobial biofilms form. The yeast has been reported to be potentially involved in oral carcinogenesis, particularly in the immunocompromised patient. This is due to the inflammation that is caused by candidal infection, which increases pro-inflammatory cytokines such as interleukin-6, interleukin-8 and interleu-kin-10, that have been linked to oral carcinogenesis. However, further study is needed to conform to the claim. In addition, over-consumption of alcoholic beverages has also been related to carcinogenesis which the ethanol has been reported to be converted into acetaldehyde by C. albicans using acetaldehyde dehydrogenases enzymes. In Malaysia, oral cancer has also been related to the consumption of cured and salted fish, which mostly consumed by the Chinese ethnics. However, its relationship to oral microbiome remains unclear. In conclusion, oral microbiome and nutrition may have a role in oral carcinogenesis; however, further study is needed to elucidate the role of both factors in oral cancer development.
    Matched MeSH terms: Dysbiosis
  7. Arulsamy A, Tan QY, Balasubramaniam V, O'Brien TJ, Shaikh MF
    ACS Chem Neurosci, 2020 Nov 04;11(21):3488-3498.
    PMID: 33064448 DOI: 10.1021/acschemneuro.0c00431
    Dysbiosis of gut microbiota may lead to a range of diseases including neurological disorders. Thus, it is hypothesized that regulation of the intestinal microbiota may prevent or treat epilepsy. The purpose of this systematic review is to evaluate the evidence investigating the relationship between gut microbiota and epilepsy and possible interventions. A systematic review of the literature was done on four databases (PubMed, Scopus, EMBASE, and Web of Science). Study selection was restricted to original research articles while following the PRISMA guidelines. Six studies were selected. These studies cohesively support the interaction between gut microbiota and epileptic seizures. Gut microbiota analysis identified increases in Firmicutes, Proteobacteria, Verrucomicrobia, and Fusobacteria with decreases in Bacteroidetes and Actinobacteria in epileptic patients. Ketogenic diet, probiotics, and fecal microbiota transplantation (FMT) improved the dysbiosis of the gut microbiota and seizure activity. However, the studies either had a small sample size, lack of subject variability, or short study or follow-up period, which may question their reliability. Nevertheless, these limited studies conclusively suggest that gut microbiota diversity and dysbiosis may be involved in the pathology of epilepsy. Future studies providing more reliable and in depth insight into the gut microbial community will spark promising alternative therapies to current epilepsy treatment.
    Matched MeSH terms: Dysbiosis
  8. Joseph N, Clayton JB, Hoops SL, Linhardt CA, Mohd Hashim A, Mohd Yusof BN, et al.
    Evol Bioinform Online, 2020;16:1176934320965943.
    PMID: 33281440 DOI: 10.1177/1176934320965943
    Childhood obesity is a serious public health problem worldwide. Perturbations in the gut microbiota composition have been associated with the development of obesity in both children and adults. Probiotics, on the other hand, are proven to restore the composition of the gut microbiome which helps reduce the development of obesity. However, data on the effect of probiotics on gut microbiota and its association with childhood obesity is limited. This study aims to determine the effect of probiotics supplement intervention on gut microbiota profiles in obese and normal-weight children. A total of 37 children, 17 normal weight, and 20 overweight school children from a government school in Selangor were selected to participate in this study. Participants were further divided into intervention and control groups. The intervention groups received daily probiotic drinks while the control groups continued eating their typical diet. Fecal samples were collected from the participants for DNA extraction. The hypervariable V3 and V4 regions of 16S rRNA gene were amplified and sequenced using the Illumina MiSeq platform. No significant differences in alpha diversity were observed between normal weight and obese children in terms of the Shannon Index for evenness or species richness. However, a higher intervention effect on alpha diversity was observed among normal-weight participants compared to obese. The participants' microbiome was found to fluctuate throughout the study. Analysis of the taxa at species level showed an increase in Bacteroides ovatus among the normal weight cohort. Genus-level comparison revealed a rise in genus Lachnospira and Ruminococcus in the overweight participants after intervention, compared to the normal-weight participants. The probiotics intervention causes an alteration in gut microbiota composition in both normal and overweight children. Though the association could not be defined statistically, this study has provided an improved understanding of the intervention effect of probiotics on gut microbiome dysbiosis in an underrepresented population.
    Matched MeSH terms: Dysbiosis
  9. Chew SS, Tan LT, Law JW, Pusparajah P, Goh BH, Ab Mutalib NS, et al.
    Cancers (Basel), 2020 Aug 13;12(8).
    PMID: 32823729 DOI: 10.3390/cancers12082272
    Colorectal cancer (CRC) is a global public health issue which poses a substantial humanistic and economic burden on patients, healthcare systems and society. In recent years, intestinal dysbiosis has been suggested to be involved in the pathogenesis of CRC, with specific pathogens exhibiting oncogenic potentials such as Fusobacterium nucleatum, Escherichia coli and enterotoxigenic Bacteroides fragilis having been found to contribute to CRC development. More recently, it has been shown that initiation of CRC development by these microorganisms requires the formation of biofilms. Gut microbial biofilm forms in the inner colonic mucus layer and is composed of polymicrobial communities. Biofilm results in the redistribution of colonic epithelial cell E-cadherin, increases permeability of the gut and causes a loss of function of the intestinal barrier, all of which enhance intestinal dysbiosis. This literature review aims to compile the various strategies that target these pathogenic biofilms and could potentially play a role in the prevention of CRC. We explore the potential use of natural products, silver nanoparticles, upconverting nanoparticles, thiosalicylate complexes, anti-rheumatic agent (Auranofin), probiotics and quorum-sensing inhibitors as strategies to hinder colon carcinogenesis via targeting colon-associated biofilms.
    Matched MeSH terms: Dysbiosis
  10. Yap TW, Leow AH, Azmi AN, Callahan DL, Perez-Perez GI, Loke MF, et al.
    Front Microbiol, 2017;8:536.
    PMID: 28424674 DOI: 10.3389/fmicb.2017.00536
    Background:Helicobacter pylori colonizes the gastric mucosa of more than half of the world's population. There is increasing evidence H. pylori protects against the development of obesity and childhood asthma/allergies in which the development of these diseases coincide with transient dysbiosis. However, the mechanism underlying the association of H. pylori eradication with human metabolic and immunological disorders is not well-established. In this study, we aimed to investigate the local and systemic effects of H. pylori eradication through untargeted fecal lipidomics and plasma metabolomics approaches by liquid chromatography mass spectrometry (LC-MS). Results: Our study revealed that eradication of H. pylori eradication (i.e., loss of H. pylori and/or H. pylori eradication therapy) changed many global metabolite/lipid features, with the majority being down-regulated. Our findings primarily show that H. pylori eradication affects the host energy and lipid metabolism which may eventually lead to the development of metabolic disorders. Conclusion: These predictive metabolic signatures of metabolic and immunological disorders following H. pylori eradication can provide insights into dynamic local and systemic metabolism related to H. pylori eradication in modulating human health.
    Matched MeSH terms: Dysbiosis
  11. Hasain Z, Mokhtar NM, Kamaruddin NA, Mohamed Ismail NA, Razalli NH, Gnanou JV, et al.
    PMID: 32500037 DOI: 10.3389/fcimb.2020.00188
    Gestational diabetes mellitus (GDM) is defined as impaired glucose tolerance recognized during pregnancy. GDM is associated with metabolic disorder phenotypes, such as obesity, low-grade inflammation, and insulin resistance. Following delivery, nearly half of the women with a history of GDM have persistent postpartum glucose intolerance and an increased risk of developing type 2 diabetes mellitus (T2DM), as much as 7-fold. The alarming upward trend may worsen the socioeconomic burden worldwide. Accumulating evidence strongly associates gut microbiota dysbiosis in women with GDM, similar to the T2DM profile. Several metagenomics studies have shown gut microbiota, such as Ruminococcaceae, Parabacteroides distasonis, and Prevotella, were enriched in women with GDM. These microbiota populations are associated with metabolic pathways for carbohydrate metabolism and insulin signaling, suggesting a potential "gut microbiota signature" in women with GDM. Furthermore, elevated expression of serum zonulin, a marker of gut epithelial permeability, during early pregnancy in women with GDM indicates a possible link between gut microbiota and GDM. Nevertheless, few studies have revealed discrepant results, and the interplay between gut microbiota dysbiosis and host metabolism in women with GDM is yet to be elucidated. Lifestyle modification and pharmacological treatment with metformin showed evidence of modulation of gut microbiota and proved to be beneficial to maintain glucose homeostasis in T2DM. Nonetheless, post-GDM women have poor compliance toward lifestyle modification after delivery, and metformin treatment remains controversial as a T2DM preventive strategy. We hypothesized modulation of the composition of gut microbiota with probiotics supplementation may reverse postpartum glucose intolerance in post-GDM women. In this review, we addressed gut microbiota dysbiosis and the possible mechanistic links between the host and gut microbiota in women with GDM. Furthermore, this review highlights the potential therapeutic use of probiotics in post-GDM women as a T2DM preventive strategy.
    Matched MeSH terms: Dysbiosis
  12. Ahmad Kendong SM, Raja Ali RA, Nawawi KNM, Ahmad HF, Mokhtar NM
    PMID: 34966694 DOI: 10.3389/fcimb.2021.744606
    Colorectal cancer (CRC) is a heterogeneous disease that commonly affects individuals aged more than 50 years old globally. Regular colorectal screening, which is recommended for individuals aged 50 and above, has decreased the number of cancer death toll over the years. However, CRC incidence has increased among younger population (below 50 years old). Environmental factors, such as smoking, dietary factor, urbanization, sedentary lifestyle, and obesity, may contribute to the rising trend of early-onset colorectal cancer (EOCRC) because of the lack of genetic susceptibility. Research has focused on the role of gut microbiota and its interaction with epithelial barrier genes in sporadic CRC. Population with increased consumption of grain and vegetables showed high abundance of Prevotella, which reduces the risk of CRC. Microbes, such as Fusobacterium nucleatum, Bacteroides fragilis and Escherichia coli deteriorate in the intestinal barrier, which leads to the infiltration of inflammatory mediators and chemokines. Gut dysbiosis may also occur following inflammation as clearly observed in animal model. Both gut dysbiosis pre- or post-inflammatory process may cause major alteration in the morphology and functional properties of the gut tissue and explain the pathological outcome of EOCRC. The precise mechanism of disease progression from an early stage until cancer establishment is not fully understood. We hypothesized that gut dysbiosis, which may be influenced by environmental factors, may induce changes in the genome, metabolome, and immunome that could destruct the intestinal barrier function. Also, the possible underlying inflammation may give impact microbial community leading to disruption of physical and functional role of intestinal barrier. This review explains the potential role of the interaction among host factors, gut microenvironment, and gut microbiota, which may provide an answer to EOCRC.
    Matched MeSH terms: Dysbiosis
  13. Lützhøft DO, Sinioja T, Christoffersen BØ, Jakobsen RR, Geng D, Ahmad HFB, et al.
    BMC Microbiol, 2022 Dec 01;22(1):287.
    PMID: 36456963 DOI: 10.1186/s12866-022-02704-w
    BACKGROUND: Gut microbiota dysbiosis is associated with the development of non-alcoholic steatohepatitis (NASH) through modulation of gut barrier, inflammation, lipid metabolism, bile acid signaling and short-chain fatty acid production. The aim of this study was to describe the impact of a choline-deficient amino acid defined high fat diet (CDAHFD) on the gut microbiota in a male Göttingen Minipig model and on selected pathways implicated in the development of NASH.

    RESULTS: Eight weeks of CDAHFD resulted in a significantly altered colon microbiota mainly driven by the bacterial families Lachnospiraceae and Enterobacteriaceae, being decreased and increased in relative abundance, respectively. Metabolomics analysis revealed that CDAHFD decreased colon content of short-chain fatty acid and increased colonic pH. In addition, serum levels of the microbially produced metabolite imidazole propionate were significantly elevated as a consequence of CDAHFD feeding. Hepatic gene expression analysis showed upregulation of mechanistic target of rapamycin (mTOR) and Ras Homolog, MTORC1 binding in addition to downregulation of insulin receptor substrate 1, insulin receptor substrate 2 and the glucagon receptor in CDAHFD fed minipigs. Further, the consequences of CDAHFD feeding were associated with increased levels of circulating cholesterol, bile acids, and glucagon but not total amino acids.

    CONCLUSIONS: Our results indicate imidazole propionate as a new potentially relevant factor in relation to NASH and discuss the possible implication of gut microbiota dysbiosis in the development of NASH. In addition, the study emphasizes the need for considering the gut microbiota and its products when developing translational animal models for NASH.

    Matched MeSH terms: Dysbiosis
  14. Lee JK, Hern Tan LT, Ramadas A, Ab Mutalib NS, Lee LH
    PMID: 32977611 DOI: 10.3390/ijerph17196963
    The mortality rate of very preterm infants with birth weight <1500 g is as high as 15%. The survivors till discharge have a high incidence of significant morbidity, which includes necrotising enterocolitis (NEC), early-onset neonatal sepsis (EONS) and late-onset neonatal sepsis (LONS). More than 25% of preterm births are associated with microbial invasion of amniotic cavity. The preterm gut microbiome subsequently undergoes an early disruption before achieving bacterial maturation. It is postulated that bacterial gut colonisation at birth and postnatal intestinal dysbacteriosis precede the development of NEC and LONS in very preterm infants. In fact, bacterial colonization patterns in preterm infants greatly differ from term infants due to maternal chorioamnionitis, gestational age, delivery method, feeding type, antibiotic exposure and the environment factor in neonatal intensive care unit (NICU). In this regard, this review provides an overview on the gut bacteria in preterm neonates' meconium and stool. More than 50% of preterm meconium contains bacteria and the proportion increases with lower gestational age. Researchers revealed that the gut bacterial diversity is reduced in preterm infants at risk for LONS and NEC. Nevertheless, the association between gut dysbacteriosis and NEC is inconclusive with regards to relative bacteria abundance and between-sample beta diversity indices. With most studies show a disruption of the Proteobacteria and Firmicutes preceding the NEC. Hence, this review sheds light on whether gut bacteria at birth either alone or in combination with postnatal gut dysbacteriosis are associated with mortality and the morbidity of LONS and NEC in very preterm infants.
    Matched MeSH terms: Dysbiosis
  15. Rahman Jamal
    MyJurnal
    Colorectal cancer (CRC) is an important health problem that is on the rise globally, where it is the fourth most com-mon cause of deaths from cancer. CRC is now the 2nd commonest cancer in men and 3rd commonest in women in Malaysia. Diet, lifestyle, genetics and environmental interaction, together with underlying gut conditions such as inflammatory bowel disease have been reported to contribute to the disease. In addition, the gut microbiome has also been increasingly reported to be associated with CRC development, with dysbiosis of the commensal bacteria ob-served in CRC patients. Bacterial genera such as Bacteroides, Fusobacterium and Prevotella are more commonly de-tected in CRC patients compared to healthy individuals. Nevertheless, not much is known about the gut microbiome among Malaysians with different ethnicities. In Malaysia, the Chinese has the highest incidence of CRC, followed by Malays and Indians. The reason behind this difference may be contributed by the differences in the dietary intake that could modulate the gut microbiome and contribute towards the development of CRC. The current knowledge on this field still much depends on reports from individuals of American, European, Chinese, Brazilian and Japanese descendants in origin. The oncogenic potential of bacteria was suggested to include inflammation and the produc-tion of mutagenic toxin. A significant increase in certain intestinal microbiota including the genuses Enteroccus and Streptococcus spp. was detected in the advanced stage of colorectal adenoma. However, there are discrepancies in the previous studies, where some bacteria genera might be over-reported or underestimated. It is likely that the gut microbiome differs between populations. There is also no available data on the gut microbiome of the healthy individuals, colorectal adenoma (pre-cancerous) and colorectal cancer patients in the Malaysian population. Recent advancements in next generation sequencing allow faster and more accurate determination of microbial consortium in various niches of the human body and environment. In particular, sequencing of the 16S rRNA gene with specific primers have been reported to allow accurate determination of bacterial orders commonly found in the human gut as well as for those which are not expected in the digestive system. Recent developments in gut microbiome DNA ex-traction also contributed to the robustness of gut microbiome determination and analysis. All the above will contrib-ute towards an accurate and rapid cataloging process of the Malaysian gut microbiome and also enable comparison between healthy individuals, colorectal adenoma and CRC patients of the Malaysian population.
    Matched MeSH terms: Dysbiosis
  16. Loke YL, Chew MT, Ngeow YF, Lim WWD, Peh SC
    PMID: 33364203 DOI: 10.3389/fcimb.2020.603086
    Colorectal cancer (CRC) incidence increases yearly, and is three to four times higher in developed countries compared to developing countries. The well-known risk factors have been attributed to low physical activity, overweight, obesity, dietary consumption including excessive consumption of red processed meats, alcohol, and low dietary fiber content. There is growing evidence of the interplay between diet and gut microbiota in CRC carcinogenesis. Although there appears to be a direct causal role for gut microbes in the development of CRC in some animal models, the link between diet, gut microbes, and colonic carcinogenesis has been established largely as an association rather than as a cause-and-effect relationship. This is especially true for human studies. As essential dietary factors influence CRC risk, the role of proteins, carbohydrates, fat, and their end products are considered as part of the interplay between diet and gut microbiota. The underlying molecular mechanisms of colon carcinogenesis mediated by gut microbiota are also discussed. Human biological responses such as inflammation, oxidative stress, deoxyribonucleic acid (DNA) damage can all influence dysbiosis and consequently CRC carcinogenesis. Dysbiosis could add to CRC risk by shifting the effect of dietary components toward promoting a colonic neoplasm together with interacting with gut microbiota. It follows that dietary intervention and gut microbiota modulation may play a vital role in reducing CRC risk.
    Matched MeSH terms: Dysbiosis
  17. Gopinath D, Kunnath Menon R, Chun Wie C, Banerjee M, Panda S, Mandal D, et al.
    J Oral Microbiol, 2020 Dec 09;13(1):1857998.
    PMID: 33391629 DOI: 10.1080/20002297.2020.1857998
    Objective: While some oral carcinomas appear to arise de novo, others develop within long-standing conditions of the oral cavity that have malignant potential, now known as oral potentially malignant disorders (OPMDs). The oral bacteriome associated with OPMD has been studied to a lesser extent than that associated with oral cancer. To characterize the association in detail we compared the bacteriome in whole mouth fluid (WMF) in patients with oral leukoplakia, oral cancer and healthy controls. Methods: WMF bacteriome from 20 leukoplakia patients, 31 patients with oral cancer and 23 healthy controls were profiled using the Illumina MiSeq platform. Sequencing reads were processed using DADA2, and taxonomical classification was performed using the phylogenetic placement method. Sparse Partial Least Squares Regression Discriminant Analysis model was used to identify bacterial taxa that best discriminate the studied groups. Results: We found considerable overlap between the WMF bacteriome of leukoplakia and oral cancer while a clearer separation between healthy controls and the former two disorders was observed. Specifically, the separation was attributed to 14 taxa belonging to the genera Megaspheara, unclassified enterobacteria, Prevotella, Porphyromonas, Rothia and Salmonella, Streptococcus, and Fusobacterium. The most discriminative bacterial genera between leukoplakia and oral cancer were Megasphaera, unclassified Enterobacteriae, Salmonella and Prevotella.Conclusion: Oral bacteria may play a role in the early stages of oral carcinogenesis as a dysbiotic bacteriome is associated with oral leukoplakia and this resembles that of oral cancer more than healthy controls. Our findings may have implications for developing oral cancer prevention strategies targeting early microbial drivers of oral carcinogenesis.
    Matched MeSH terms: Dysbiosis
  18. Kho ZY, Lal SK
    Front Microbiol, 2018;9:1835.
    PMID: 30154767 DOI: 10.3389/fmicb.2018.01835
    Interest toward the human microbiome, particularly gut microbiome has flourished in recent decades owing to the rapidly advancing sequence-based screening and humanized gnotobiotic model in interrogating the dynamic operations of commensal microbiota. Although this field is still at a very preliminary stage, whereby the functional properties of the complex gut microbiome remain less understood, several promising findings have been documented and exhibit great potential toward revolutionizing disease etiology and medical treatments. In this review, the interactions between gut microbiota and the host have been focused on, to provide an overview of the role of gut microbiota and their unique metabolites in conferring host protection against invading pathogen, regulation of diverse host physiological functions including metabolism, development and homeostasis of immunity and the nervous system. We elaborate on how gut microbial imbalance (dysbiosis) may lead to dysfunction of host machineries, thereby contributing to pathogenesis and/or progression toward a broad spectrum of diseases. Some of the most notable diseases namely Clostridium difficile infection (infectious disease), inflammatory bowel disease (intestinal immune-mediated disease), celiac disease (multisystemic autoimmune disorder), obesity (metabolic disease), colorectal cancer, and autism spectrum disorder (neuropsychiatric disorder) have been discussed and delineated along with recent findings. Novel therapies derived from microbiome studies such as fecal microbiota transplantation, probiotic and prebiotics to target associated diseases have been reviewed to introduce the idea of how certain disease symptoms can be ameliorated through dysbiosis correction, thus revealing a new scientific approach toward disease treatment. Toward the end of this review, several research gaps and limitations have been described along with suggested future studies to overcome the current research lacunae. Despite the ongoing debate on whether gut microbiome plays a role in the above-mentioned diseases, we have in this review, gathered evidence showing a potentially far more complex link beyond the unidirectional cause-and-effect relationship between them.
    Matched MeSH terms: Dysbiosis
  19. Chong PP, Chin VK, Looi CY, Wong WF, Madhavan P, Yong VC
    Front Microbiol, 2019;10:1136.
    PMID: 31244784 DOI: 10.3389/fmicb.2019.01136
    Irritable bowel syndrome (IBS) is a functional disorder which affects a large proportion of the population globally. The precise etiology of IBS is still unknown, although consensus understanding proposes IBS to be of multifactorial origin with yet undefined subtypes. Genetic and epigenetic factors, stress-related nervous and endocrine systems, immune dysregulation and the brain-gut axis seem to be contributing factors that predispose individuals to IBS. In addition to food hypersensitivity, toxins and adverse life events, chronic infections and dysbiotic gut microbiota have been suggested to trigger IBS symptoms in tandem with the predisposing factors. This review will summarize the pathophysiology of IBS and the role of gut microbiota in relation to IBS. Current methodologies for microbiome studies in IBS such as genome sequencing, metagenomics, culturomics and animal models will be discussed. The myriad of therapy options such as immunoglobulins (immune-based therapy), probiotics and prebiotics, dietary modifications including FODMAP restriction diet and gluten-free diet, as well as fecal transplantation will be reviewed. Finally this review will highlight future directions in IBS therapy research, including identification of new molecular targets, application of 3-D gut model, gut-on-a-chip and personalized therapy.
    Matched MeSH terms: Dysbiosis
  20. Vignesh R, Swathirajan CR, Tun ZH, Rameshkumar MR, Solomon SS, Balakrishnan P
    Front Immunol, 2020;11:607734.
    PMID: 33569053 DOI: 10.3389/fimmu.2020.607734
    Matched MeSH terms: Dysbiosis
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