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Alzheimer’s Disease, the Microbiome, and 21st Century Medicine
Published in David Perlmutter, The Microbiome and the Brain, 2019
Comparison of the microbiomes of patients with dementia due to Alzheimer’s disease versus age-matched controls showed a marked difference in both the complexity and distribution of microbiota, as shown by Vogt et al. (Vogt et al., 2017) and noted in this book’s chapter by Dr. Zhang. The phyla Firmicutes and Actinobacteria were reduced in patients with Alzheimer’s disease, a finding that parallels results from patients with obesity and type 2 diabetes. Within Firmicutes, the families Ruminococcaceae, Turicibacteraceae, Peptostreptococcaceae, Clostridiaceae, and Mogibacteriaceae were reduced, and within Actinobacteria, the family Bifidobacteriaceae was reduced. In contrast, members of the phylum Bacteroidetes were found to be increased in patients with Alzheimer’s disease, reflected at the family level by an increase in Bacteroidaceae and Rikenellaceae. This reduction led the authors to speculate that the insulin resistance associated with all three conditions (Alzheimer’s, obesity, and type 2 diabetes) may actually be a microbiome-driven mechanism. Furthermore, the degree of abnormality in the cerebrospinal fluid (CSF) samples from Alzheimer’s patients tended to correlate with the microbiome alterations, such that those individuals with more exaggerated microbiome changes tended to also have more severe CSF abnormalities.
Beneficial Lactic Acid Bacteria
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
LAB do not possess a functional respiratory system, so they derive the energy required for their metabolism from the oxidation of chemical compounds, mainly sugars. Sugars are fermented by LAB via homofermentative or heterofermentative pathways. Homofermentative bacteria produce lactic acid as the only product of glucose fermentation through glycolysis or Embden–Meyerhof–Parnas pathway. Heterofermentative bacteria use the pentose phosphate pathway generating carbon dioxide (CO2) and ethanol or acetate, besides lactic acid. Other hexoses are also fermented by LAB after preliminary isomerization or phosphorylation. In addition, LAB with heterofermentative type of fermentation successfully metabolize pentoses. Disaccharides are split enzymatically into monosaccharides entering the appropriate pathways (Von Wright and Axelsson 2011). Genus Bifidobacterium degrades hexose sugars through a particular metabolic pathway or bifid shunt allowing to produce more energy in the form of ATP. Bifidobacterial pathway yields 2.5 mol of ATP, 1.5 mol of acetate, and 1 mol of lactate from 1 mol of fermented glucose, while the homofermentative LAB produce 2 mol of ATP and 2 mol of lactic acid and heterofermentative LAB produce 1 mol each of lactic acid, ethanol, and ATP per 1 mol of fermented glucose. Fructose-6-phosphoketolase enzyme plays a key role in this pathway and is considered to be a taxonomic marker for the family of Bifidobacteriaceae (Pokusaeva 2011). Recently a novel metabolic pathway (galacto-N-biose (GNB)/lacto-N-biose (LNB) I pathway) that utilizes both human milk oligosaccharides and host glycoconjugates and is essential for colonization of the infant gastrointestinal tract was found in genus Bifidobacterium (Fushinobu 2010). This route was suggested to be specific for Bifidobacterium; however, further studies showed ability of some LAB to metabolize LNB and GNB. Nevertheless, metabolic pathways responsible for catabolism of these compounds in LAB are completely different from those described for Bifidobacterium species (Bidart et al. 2014).
Host–Biofilm Interactions at Mucosal Surfaces and Implications in Human Health
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Nityasri Venkiteswaran, Kassapa Ellepola, Chaminda Jayampath Seneviratne, Yuan Kun Lee, Kia Joo Puan, Siew Cheng Wong
The colonic mucosa has certain restricted sites where colonisation and biofilm formation is easier owing to a lower rate of mucosal replication. This accounts for a greater microbial diversity in the colon as compared to the small intestine [51]. Unlike the small intestine, which has a single layer of tightly attached mucosa, the colonic mucus has two organised layers: a dense inner layer and a loose outer layer. The latter forms a favourable habitat for commensals such as Bacteroides acidifaciens, Bacteroides fragilis, Akkermansia muciniphila and those belonging to the family Bifidobacteriaceae. The dense inner mucus adjoining the crypts comprises a more restricted community of Bacteroides spp. and Actinobacter spp. [47]. The presence of the bacterial genera Prevotella, Ruminococcus and Bacteroides are indicative of a healthy microbiota in the intestine [52,53]. Microbiota belonging to the genera Bacteroides and Bifidobacterium are the prominent biofilm formers, which include Bacteroides caccae, Bifidobacterium angulatum, Bifidobacterium adolescentis and Bifidobacterium bifidum. E. coli and Enterococcus faecalis are the facultative anaerobes that frequently caused biofilm infections in the large intestine [54]. Owing to production of mucus in large quantities, the inner colonic mucus is relatively less populated. On the contrary, in conditions such as ulcerative colitis, the inner mucus barrier is defective, less dense and broken. This provides access to opportunistic pathogens such as Bacteroides and also to mucin degraders such as A. muciniphila, leading to inflammation in disease conditions such as Crohn’s disease and ulcerative colitis [55]. Biofilms in the large intestine are associated with food residues, and therefore the microbial species and their biochemical activities are governed mainly by diet [56]. For instance, the infant gut demonstrates differences in microbiome based on the type of food to which it is introduced. Babies who are breast fed postnatally are predominated by organisms belonging to the Bacteroidetes and those fed with formula milk demonstrate higher amount of organisms belonging to the Firmicutes [57,58].
Quantitative insights into effects of intrapartum antibiotics and birth mode on infant gut microbiota in relation to well-being during the first year of life
Published in Gut Microbes, 2022
Roosa Jokela, Katri Korpela, Ching Jian, Evgenia Dikareva, Anne Nikkonen, Terhi Saisto, Kirsi Skogberg, Willem M. de Vos, Kaija-Leena Kolho, Anne Salonen
In contrast, in VD infants the IP antibiotic plays a major role. We showed that especially the impact of cephalosporin exposure during VD was largely similar to the effect of CS delivery on the infant gut microbiota. However, we identified several distinct effects of birth mode and antibiotic exposure. Namely, the absolute abundances of Bacteroidaceae, Coriobacteriaceae, and Burkholderiaceae were reduced by CS birth but not by IP antibiotics during first 6 weeks, while Ruminococcaceae, Porphyromonadaceae, Rikenellaceae, and Pasteurellaceae abundances were negatively affected by both CS birth and antibiotics. Bifidobacteriaceae was most strongly affected by antibiotic exposure. Our observations recapitulate and extend the results of recent studies.36,40,41 Using absolute abundance data, we found the effect of IP antibiotics in VD infants to peak at 12 weeks with some differences that persist up to 12 months. Previous studies using relative abundance data have reported that the effect of birth-related antibiotics typically subsides after 3 months;42 however, most of the studies have not investigated the effect beyond this age.12 A recent prospective study of 100 VD infants reported that the effects of IP antibiotics overruled those of postnatal antibiotics on infant microbiota and persisted until the age of 1 y.43
Resistome and microbial profiling of pediatric patient’s gut infected with multidrug-resistant diarrhoeagenic Enterobacteriaceae using next-generation sequencing; the first study from Pakistan
Published in Libyan Journal of Medicine, 2021
Ome Kalsoom Afridi, Johar Ali, Jeong Ho Chang
The predominance of Bifidobacteriaceae associated non-pathogenic bacterial species in healthy controls reflects their intact gut microbiota while the abundance of Enterobacteriacea associated opportunistic pathogens in MDR microbes infected patients indicates the association of AMR with gut microbial dysbiosis. Our results are supported by a previous study indicating that diarrhea and various doses of antibiotics increase the likelihood of children’s gut microbiota enrichment with MDR bacteria in children [29]. The various gram-negative bacteria identified in the gut microbiota of MDR infected patients in the present study have been reported to be the potential causative agents of diarrhea in children [30]. Bacterial species belonging to the genus Yersinia and Klebsiella identified in the gut microbiota of MDR diarrheagenic Enterobacteriaceae infected patients have been associated with severe diarrheal diseases such as yersiniosis [31].
Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection
Published in Gut Microbes, 2021
Britta E. Heiss, Amy M. Ehrlich, Maria X. Maldonado-Gomez, Diana H. Taft, Jules A. Larke, Michael L. Goodson, Carolyn M. Slupsky, Daniel J. Tancredi, Helen E. Raybould, David A. Mills
Although the mouse-associated microbiota has not been naturally selected to catabolize HMOs, we examined the 2ʹFL control group to assess how 2ʹFL may effect change in an established microbiota. β-diversity (Bray Curtis) varied significantly by day (PERMANOVA, p = .021; Figure 2e) and 2ʹFL supplemented days were distinct from non-2ʹFL days (pairwise PERMANOVA, p = .037). Although no Bifidobacterium was provided, increased Bifidobacteriaceae relative abundance is noted (Figure 2a). Absolute abundance of the genus Bifidobacterium increased by 1–2 logs between baseline (day 0) and day 10 of 2ʹFL supplementation (Kruskal Wallis, p = .024; Supplemental Figure S3c). In contrast to untreated control mice, 2ʹFL treatment results in high log ratios of Bacteroidaceae and Bifidobacteriaceae relative to Lachnospiraceae and Ruminococcaceae ASVs (student’s t test, p = .003; Figure 2f).