Table 2.
Examples of microbial dysbiosis and/or bacteria associated with disease
| Disease | Dysbiosis and bacterial species | Protective or pathogenic microorganisms, effect on host | Reference |
|---|---|---|---|
| Crohn's disease (CD) | •↑Microbial diversity, ↑mucosal adherent bacteria ↓Bifidobacteria ↑Enteropathogenic bacteria (incl. Eschericia coli), ↓Firmicutes (except colorectal CD ↑Firmicutes increased), ↑Enterobacteriaceae, ↓Lachnospiraceae, ↑Ruminococcus gnavus, ↓Faecalibacterium prausnizii, ↓Roseburia. CD patients have a fivefold increase in risk for developing CRC | F. prausnitzii shows anti-inflammatory effects in colitis mice models, reduction of F. p. is associated with recurrence in postoperative ileal CD. Epsilonproteobacteria and Helicobacteraceae are families that harbour known pathogens, e.g. Campylobacter and H. pylori | 75–79 |
| Ulcerative colitis (UC) | •↓Microbial diversity, ↑mucosal adherent bacteria ↑Enteropathogenic bacteria (incl. Escherichia coli), ↓Clostridium coccoides ↑Epsilon proteobacteria ↓Faecalibacterium prausnizii, ↑Helicobacteraceae, ↓Lachnospiraceae ↑Ruminococcus gnavus. UC patients have a fivefold increase in risk for developing CRC | ||
| Colorectal Cancer (CRC) | •Enterotoxin-producing Bacteroides fragilis (ETBF) increases tumorigenesis in ApcMin/+ mice, stimulates cell proliferation | Enterotoxin increases the ion permeability of epithelial cells | 80,81 |
| •Enterobacteria spp., ↑Citrobacter spp., ↑Shigella spp., ↑Salmonella spp., genera with pathogenic potential have been found at increased levels in normal tissue flanking CRC tumours | Several genera with pathogenic potential, e.g. cell invasive species (Salmonella) | 76 | |
| •Rats colonized with Enterococcus faecalis showed increased DNA damage compared with control rats | Produces reactive oxygen species, which is a possible cause of chromosomal instability (CIN) | 82 | |
| •↑Escherichia coli, pks+, more prevalent in CRC patients than in healthy individuals | Colibactin, causes double-stranded DNA breaks leading to genomic instability | 83–85 | |
| •Three separate studies reported associations of Streptococcus gallolyticus (formerly S. bovis) with CRC (carcinomas or adenomas) | Able to avoid detection by immune system, form biofilms on collagen-rich surfaces | 86,87 | |
| •↑Fusobacterium spp., consistently over-represented in tumour-adherent microbiota | Pathogen causing periodontal infections and Lemierre's syndrome | 88–90 | |
| Obesity | •Ratio of Firmicutes: Bacteroides increase in both obese human subjects and mice Weight loss by diet (1 year) increased ↑Bacteroides and reduced Firmicutes ↑Lactobacillus ↑Faecalibacterium prausnizii (obese children) | Shifts in microbiota composition alter aspects of energy harvest | 91–93 |
| •Numerous studies show that antibiotic treatment leads to weight gain in human subjects (including children) and animals | |||
| •Transplantation of microbiota of obese mice into lean mice led to increased body weight, establishing causality | |||
| Diabetes, type 1 | •Decrease in ratio of Firmicutes: Bacteroides, and ↓microbial diversity was found to correlate with the development of type 1 diabetes-associated autoimmunity (children). ↑Bacteroides ovatus, ↓Clostridiales | 94,95 | |
| •BB-diabetes prone rats (BBDP, diabetes type I model) with a decrease in ↓↓Bacteroides spp., did not develop diabetes. Difference in microbiota composition compared to rats that did develop clinical disease was detectable before clinical onset Treatment with antibiotics decreased incidence and onset | |||
| •BB-diabetes-resistant rats had higher levels of ↑Bifidobacterium and ↑Lactotobacillus compared to BBDP rats | |||
| Immunosenescence | •Decreased microbial diversity, increase in interpersonal variability, ↓Bifidobacterium, ↓Faecalibacterium prausnitzii, ↓Clostridium cluster XIVa, ↑Streptococcus spp., ↑↑Staphylococcus spp. ↓↓Enterococcus spp, ↑Enterobacteria spp. | Increase in genera that often contain pathogenic species | 18,19,22,23 |