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Impact of Probiotics on Communication between the Brain-Gut: Implications for the Treatment of the Psychological Effects of Digestive Disease States
Published in Martin Colin R, Derek Larkin, Probiotics in Mental Health, 2018
Melanie G Gareau, Colin Reardon, Kim E Barrett, Philip M Sherman
The advent of molecular based sequencing technologies has identified roughly 1,000 different bacterial species in the gastrointestinal tract, mostly in the bacteroides and firmicutes families (Manson et al., 2008). When looked for, Archaea species also appear to be present in the gut microbiota of a proportion of healthy humans. A delicate balance is thought to exist between symbiont and pathobiont organisms in the microbiome that when altered can result in disease (Round and Mazmanian, 2009). Symbiont organisms are composed of a combination of commensal and probiotic organisms thought to be decreased in disease states at the expense of increased colonization by pathobionts.
Altered microbial biogeography in an innate model of colitis
Published in Gut Microbes, 2022
Antonia Boger-May, Theodore Reed, Diana LaTorre, Katelyn Ruley-Haase, Hunter Hoffman, Lauren English, Connor Roncagli, Anne-Marie Overstreet, David Boone
We observed changes along the proximal to distal axis of the colon in RAG1−/− mice that were absent or significantly altered in TRAG colons. RAG1−/− mice exhibited increase microbial diversity, compared to TRAG mice, in all three regions of the colon (cecum, proximal colon, and distal colon). Differences in microbial populations along the proximal to distal axis of the colon have been described in rodents and humans and alterations in these patterns are found in IBD.11,12,20,46 The spatial structure of the microbiome in the gut likely reflects differences in pH, oxygen, antimicrobials, digesta composition, and transit times along the proximal to distal axis. Galvez et al found that WT and RAG2−/− mice had similar microbial populations along the proximal to distal colon in SPF conditions, but that introduction of pathobionts (Helicobacter, Desulfovibrio) led to expansion of these organisms in the colon of RAG2−/− mice compared to WT mice.47 This suggests that the presence of adaptive immune cells, and possibly IgA, is dispensable for shaping the colon microbiome in the absence of pathobionts, but that IgA may be critical for controlling pathobiont abundance when these organisms are present, as has been reported in models of IgA deficiency.37,38,47,48
Pathobionts: mechanisms of survival, expansion, and interaction with host with a focus on Clostridioides difficile
Published in Gut Microbes, 2021
Harish Chandra, Krishna Kant Sharma, Olli H. Tuovinen, Xingmin Sun, Pratyoosh Shukla
A recent study106 using the mouse model of CDI showed a poor primary antibody response and an inadequate B memory response that does not protect in the recurrent infection model. In addition, there was a poor proliferation of T follicular cells. However, immunization of these mice generated B-memory cells as well as plasma cells.106 In CDI patients, adaptive immunity has been shown to provide protection as evidenced by the clinical data.107 The presence of IgA and IgG antibodies against C. difficile toxins and treatment with toxin-specific humanized monoclonal antibodies show protection from recurrent infections.107 Infants and toddlers are resistant to C. difficile-mediated colitis, although almost half are colonized by C. difficile.101 Thus, C. difficile resides as a normal constituent of the gut microbiome from childhood on and later in life becomes a pathobiont. It has been shown108 with a cohort of healthy infant population that toxigenic C. difficile colonization was accompanied with higher serum antitoxin IgA and IgG titer against TcdA and TcdB. Furthermore, there were significant neutralizing antibody (NAb) titers against TcdB. The protective humoral response associated with C. difficile colonization in infants further confirmed the resistance mechanism in infant population.108
The autoimmune susceptibility gene, PTPN2, restricts expansion of a novel mouse adherent-invasive E. coli
Published in Gut Microbes, 2020
Ali Shawki, Rocio Ramirez, Marianne R. Spalinger, Paul M. Ruegger, Anica Sayoc-Becerra, Alina N. Santos, Pritha Chatterjee, Vinicius Canale, Jonathan D. Mitchell, John C. Macbeth, Casey M. Gries, Michel L. Tremblay, Ansel Hsiao, James Borneman, Declan F. McCole
While a number of studies have investigated potential contributions of commensal bacteria that possess or acquire pathogenic potential, such as the LF82 AIEC in the pathogenesis of IBD, it still remains elusive as to how IBD susceptibility genes modulate the intestinal microbiome to maintain intestinal homeostasis and how disruption of this interaction precipitates changes in the microbiome that promote disease. We show here for the first time how loss of an IBD-associated gene, Ptpn2, in mice (Ptpn2-deficient), independent of an external stressor, alters the intestinal microbiome and favors expansion of a novel mouse AIEC that is capable of both initiating and exacerbating disease. Thus, PTPN2 plays a key role as a “microbial modulator” of the microbiome to protect against pathobiont expansion and colonization. We propose that whole-body Ptpn2-deficiency in mice may serve as a useful model to investigate how host genetics modulate the balance of intestinal microbes, and that this novel mouse AIEC can be utilized to interrogate mechanisms of pathobiont-induced intestinal inflammation.