Gut Bacteria and Inflammatory Bowel Diseases

Gut Bacteria and Inflammatory Bowel Diseases

Inflammatory bowel disease (IBD) is common in the developed countries of Europe, North America, Australia and New Zealand. Commensal bacteria in the digestive tract  have several roles, including providing the host with essential nutrients. They metabolize indigestible compounds, defend against colonization of opportunistic pathogens and contribute to the development of the intestinal architecture as well as stimulation of the immune system among othersIt has been noted, however, that reciprocal interaction between some commensal gut bacteria and the host may induce allergies and IBD.

There may be several components involved in the genesis of IBD, in which bacteria paly a significant role:

• Overly aggressive Th-1 mediated cytokine response to commensal bacteria may be the pathogen of chronic intestinal inflammation, and therefore Inflammatory Bowel Disease. Here, proinflammatory cytokines cause inflammation in the gut as a result of an immune response. We are probably all aware now of terms like ‘cytokine storm’ (thanks to Covid-19), and how this type of inflammation can cause severe problems.

 

• Disorders in bacterial recognition by macrophages are strongly related to pathogenesis of IBD.

 

• IBD could also result from an abnormal immune response against the commensal microbiota in a genetically susceptible host. Jostins et al.  have identified 163 risk loci associated with IBD, and found that many loci were involved in the sensing and elimination of bacteria (a locus the specific physical location of a gene or other DNA sequence on a chromosome, like a genetic street address). A hypothesis is that the innate immune system in IBD patients could be deficient, which in turn leads to an uncontrolled adaptive response.

 

Ulcerative colitis

Ulcerative colitis (UC) is one of the two major IBDs. In UC patients, the disease is limited to the colon. Numbers of lactobacilli were significantly lower during the active phase of the disease, and analysis suggested that Lactobacillus salivarus was present in remission, but not during active inflammation.

Notably, colonic bacterial communities in UC indicate less diversity of bacterial composition during acute inflammation.

Bacteria of the Clostridiales group were more prominent in samples from the inflamed colon, indicating these bacteria might accumulate during colitis. In a study of an animal colitis model, E. coli may have served as a biomarker for colitis severity. The development of colitis is associated with higher E. coli loads.

UC patients had different gene expression profiles and lower levels of biodiversity than their healthy twins, as well as unusual aerobic bacteria. They also had lower percentages of potentially protective bacterial species than their healthy twins.

The colonic microbiota appeared to interact with the transcriptional profile of the mucosa. This interaction appeared to be lost in the colon of UC patients. Bacterial functions, such as butyrate production, might affect mucosal gene expression. It has been suggested that prebiotic combination (a combination of chicory-derived long-chain inulin and oligofructose) reduced colitis in animal models, associating with alterations to the gut bacteria, decreased proinflammatory cytokines, and increased immunomodulatory molecules. We have also notice in clinic that high doses of Bifidobacteria species neutralise proinflammatory cytokines in the colon.

Crohn’s Disease

Antibiotic use amplified the microbial dysbiosis associated with CD. Furthermore, several studies showed that prebiotic and probiotic use has an effect on the onset of remission in IBD patients. In general, gut bacteria take a critical role in the development of IBD through the regulation of inflammation in the gut.

Crohn’s disease (CD) is another type of IBD. It has been thought to be an autoimmune disease, in which the body’s immune system attacks the gastrointestinal tract and causes inflammation.

Seksik et al. found that the fecal microflora in patients with both inactive and active colonic CD contained significantly more enterobacteria than in healthy subjects. In addition, about 30% of the dominant bacteria did not belong to the usual dominant phylogenetic groups, highlighting the unusual bacterial disturbance of the microbiota in IBD.

Another study found that five bacterial species characterised dysbiosis in CD patients, which were a decrease in Dialister invisus, a species of Clostridium, Faecalibacterium prausnitzii and Bifidobacterium adolescentis, and an increase in Ruminococcus gnavus.

There was a different composition of gut microbiota in unaffected relatives of patients with CD compared with healthy controls. This dysbiosis was not characterized by lack of butyrate producing-bacteria as observed in UC but suggested mucin-degradation capacity of microorganisms.