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Novel Microbial Compounds as a Boon in Health Management
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Shubha Rani Sharma, Rajani Sharma, Debasish Kar
In 2017, at European Consensus Conference, 28 experts from 10 different countries collaborated to discuss the general issues related to FMT (Cammarota et al., 2017). Selection of donor, preparation of fecal material, its management, and delivery was the main matter of concern. The donor is selected based on both blood and stool inspection. The testing is done at least 4 weeks. Fresh as well as the frozen sample can be used for FMT. A minimum of 30 g fresh samples of stool should be used within 6 h after defecation. During this time, it should be stored between 20 and 30 °C. Special care should be taken to protect anaerobic bacteria during their processing. The collected fecal is quite prone to coagulate. To prevent this, it should be ground and sieved. This process avoids the clogging of infusion syringes and tubes. The processed fecal is mixed with 10% glycerol and stored at –80 °C to be used as a frozen sample. The frozen sample should be thawed before the application. FMT has also been proved effective against ulcerative colitis (UC), a severe IBD. Like CDI, UC has also decreased the prevalence of Bacteroideted and Firmicutes while there is increased prevalences of pathogenic bacteria like Actinobacteria and Proteobacteria (Sartor and Mazmanian, 2012). To treat this, FMT helps to restore the lost microflora from the patient’s gut. Crohn’s disease is also an intestinal inflammatory disease that can be treated by simply re-establishing the healthy microbiomes in the gut, which can be achieved by FMT (Bak et al., 2017).
Gastrointestinal tract and salivary glands
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
Symptoms of persistent or recurrent diarrhoea, abdominal pain, bloating, fever, fatigue can indicate small bowel diseases such as Crohn’s disease (particularly in young people), coeliac disease and bacterial overgrowth syndrome. Serological testing is now the first investigation recommended by NICE for suspected coeliac disease, and endoscopic biopsy can be used to confirm the diagnosis if necessary. Investigation of the small bowel for diagnosis (and assessment of complications) of Crohn’s disease has been revolutionised by MRI, offering high-quality imaging of the small bowel without a radiation risk. Classical fluoroscopic imaging of the small bowel (simple enterography or combined with fluid distension techniques) now has limited application. With an experienced operator ultrasound of the small (and large) bowel has been shown to be useful in assessment of Crohn’s disease, including detection of bowel wall thickening and strictures.
Autologous Hematopoietic Stem Cell Transplantation for Crohn’s Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Robert M. Craig, Richard K. Burt
Crohn’s disease is an immune-mediated disease. An autoimmune etiology remains controversial and unproven. No intestinal self antigen (initiating or spread epitope) has been identified. On the other hand, several animal gene knockout models suggest that inflammatory bowel disease may be a result of immune dsyregulation between Th1 and Th2 cytokines. Deficiency of multiple Th2 cytokines (such as IL-10, IL-2, TGF-β) may cause colitis. Interleukin-10 deficient mice develop acute and chronic colitis.22 IL-2 deficient,23 double mutant IL-2 and IL-4 deficient, and transforming growth factor beta deficient24 mice develop colitis. When raised in a germ free environment, these gene knockout mice remain disease free. Animal models demonstrate the need for both cytokine imbalance and gut bacterial flora as disease triggers. Infusion of the T cell subset CD4+ CD45 RBhigh into SCID mice causes colitis.25 When raised in a germ free environment, CD4+ CD45 RBhigh SCID mice do not develop disease.26 Infusion of the normal broad T cell repertoire or treatment with IL-10 or anti-Th1 antibodies into a CD4+CDRBhigh SCID mouse induces remission of colitis.25
Nanomaterial-induced toxicity in pathophysiological models representative of individuals with pre-existing medical conditions
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Sreejesh Sreedharan, Georgios Zouganelis, Samantha J Drake, Gyanendra Tripathi, Ali Kermanizadeh
Gastrointestinal disease affects the esophagus, stomach, intestines, rectum as well as the liver, gall bladder and pancreas. In that sense, our use of sub-heading “gastrointestinal tract” is not entirely accurate. The focus on the review for the “gastrointestinal tract” was solely the intestines. The most prevalent intestinal disease currently affecting the general population is inflammatory bowel disease (IBD) which is a term used to describe Crohn’s disease and ulcerative colitis. It is believed that the prevalence of IBD in 2016 was 142 out of every 10,000 adults. In addition, the prevalence increased between 2006 and 2016 by 34% (Freeman et al. 2021). Crohn’s disease might initiate transmural inflammation and potentially affect any part of the GIT (most commonly, the terminal ileum or the perianal region). Crohn’s disease is often associated with complications such as abscesses, fistulas and strictures (Maharshak et al. 2008). In contrast, ulcerative colitis is typified by mucosal inflammation and limited to the colon (Lai et al. 2021). Despite the unknown etiology of IBD, it is generally accepted that progressive inflammation is key in initiation and exacerbation of disease conditions. Considering the fact that the intentional or accidental ingestion of NMs is one of the most important routes of exposure for NMs, it is conceivable that the intestines were the primary focus of investigations in nanotoxicological studies. Examination of published literature showed that numerous studies determined NM-induced effects in models representative of healthy individuals in general populations, yet to the best of our knowledge only two measured particle toxicity in models which represent the diseased gut (Busch et al. 2021; Kämpfer et al. 2021). Due to the small number of studies, it is difficult to form any meaningful conclusions on the significance of pre-existing intestinal disease in NM-induced toxicity. However, since a defective mucosal barrier “leaky gut” is a main characteristic of IBD, (Michielan and D’Inca 2015) it seems logical that this might result in increased translocation of particulates into systemic circulation and subsequent adverse effects in humans. Data suggest that assessment of NM-mediated toxicity in models that are representative of diseased intestines in humans should be further explored.
Guided dietary fibre intake as a means of directing short-chain fatty acid production by the gut microbiota
Published in Journal of the Royal Society of New Zealand, 2020
Inflammatory bowel diseases (IBD; Crohn’s disease, CD; ulcerative colitis, UC) are disorders that have genetic predispositions, environmental modifiers, and chronic immune-mediated tissue damage (Xavier and Podolsky 2007). The gut microbiota has been invoked as a major environmental factor in IBD. This is based mainly on evidence obtained from experimental animal models of gut inflammation in which colitis only occurs if genetically predisposed germfree animals are colonised by a gut microbiota (Sartor 2005). Chronic inflammation possibly occurs because bowel barrier function is compromised, permitting continual access of luminal bacterial antigens to sub-epithelial tissue and chronic activation of inflammatory processes because a bacterial invasion appears to be occurring (Macdonald and Monteleone 2005). A single bacterial species has not been identified as the causative agent of IBD. Rather, dysbiosis is associated with CD in particular, where human studies indicate that the diversity of species comprising the microbiota is less than in health (Ott et al. 2004; Frank et al. 2007; Cao et al. 2014; Kostic et al. 2014). In general, there is a depletion of members of clostridial cluster IV (Clostridum leptum cluster) that characteristically produce butyrate. Interest has also been placed on Faecalibacterium prausnitzii and Roseburia species (clostridial cluster XIVa, Clostridium coccoides cluster) because there is an inverse correlation between abundance of these species and disease activity (Laserna-Mendieta et al. 2018). Although a causative effect of dysbiosis has not been established in IBD, butyrate is an energy source for colonocytes and has anti-inflammatory effects. Thus correction of the dysbiosis by guided dietary intervention may be an attractive treatment option. Particular kinds of dietary fibre may be useful in this respect, assuming that bacterial species that can utilise the specific fibre and produce butyrate are still present in, or can gain access to, the diseased gut. IBD patients tend to have low fibre intakes despite recommendations that dietary fibre not be restricted except where there is a presence of bowel strictures (potential for blockage) (http://www.ccfa.org/asets/pdf/diet-nutrition-2013.pdf). This lower intake of dietary fibre may be the actual reason for the reduced capacity of IBD-associated microbiotas to produce butyrate.