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home:diseases:ibd [03.21.2019] – [Patient interviews] sallieqhome:diseases:ibd [09.14.2022] (current) – external edit 127.0.0.1
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 ===== Introduction ===== ===== Introduction =====
  
-[[http://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/basics/definition/con-20034908|Mayo Clinic overview]]+[[https://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/basics/definition/con-20034908|Mayo Clinic overview]]
  
-<blockquote> The metagenomic approach allowed us to detect a reduced complexity of the bacterial phylum Firmicutes as a signature of the faecal microbiota in patients with CD. It also indicated the presence of new bacterial species. (({{pubmed>long:1856500}}))+<blockquote> The metagenomic approach allowed us to detect a reduced complexity of the bacterial phylum Firmicutes as a signature of the faecal microbiota in patients with CD. It also indicated the presence of new bacterial species. (({{pmid>long:1856500}}))
 </blockquote> </blockquote>
  
  
-<blockquote>  Gut microbial induction of host immune maturation exemplifies host-microbe mutualism. We colonized germ-free (GF) mice with mouse microbiota (MMb) or human microbiota (HMb) to determine whether small intestinal immune maturation depends on a coevolved host-specific microbiota. Gut bacterial numbers and phylum abundance were similar in MMb and HMb mice, but bacterial species differed, especially the Firmicutes. HMb mouse intestines had low levels of CD4(+) and CD8(+) T cells, few proliferating T cells, few dendritic cells, and low antimicrobial peptide expression-all characteristics of GF mice. Rat microbiota also failed to fully expand intestinal T cell numbers in mice. Colonizing GF or HMb mice with mouse-segmented filamentous bacteria (SFB) partially restored T cell numbers, suggesting that SFB and other MMb organisms are required for full immune maturation in mice. Importantly, MMb conferred better protection against Salmonella infection than HMb. A host-specific microbiota appears to be critical for a healthy immune system. (({{pubmed>long:22726443}}))+<blockquote>  Gut microbial induction of host immune maturation exemplifies host-microbe mutualism. We colonized germ-free (GF) mice with mouse microbiota (MMb) or human microbiota (HMb) to determine whether small intestinal immune maturation depends on a coevolved host-specific microbiota. Gut bacterial numbers and phylum abundance were similar in MMb and HMb mice, but bacterial species differed, especially the Firmicutes. HMb mouse intestines had low levels of CD4(+) and CD8(+) T cells, few proliferating T cells, few dendritic cells, and low antimicrobial peptide expression-all characteristics of GF mice. Rat microbiota also failed to fully expand intestinal T cell numbers in mice. Colonizing GF or HMb mice with mouse-segmented filamentous bacteria (SFB) partially restored T cell numbers, suggesting that SFB and other MMb organisms are required for full immune maturation in mice. Importantly, MMb conferred better protection against Salmonella infection than HMb. A host-specific microbiota appears to be critical for a healthy immune system. (({{pmid>long:22726443}}))
 </blockquote> </blockquote>
  
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 ===== Evidence of infectious cause ===== ===== Evidence of infectious cause =====
  
-These papers are really helpful.(({{pubmed>long:16849736}})) (({{pubmed>long:17699621}}))+These papers are really helpful.(({{pmid>long:16849736}})) (({{pmid>long:17699621}}))
  
  
  
   - **[[home:patients:assessing_literature:palliative|Patient response to immunosuppressive medications]]** – Temporary symptomatic remission after taking immunosuppressive medications implies a decrease in the strength of the bacterial die-off reaction known as immunopathology. That none of these medications make patients better over the long-term is also telling. Several immunosuppressants are used to treat Crohn's including glucocorticoids such as prednisone and budesonide, aminosalicylates such as sulfasalazine and mesalamines, immunomodulators such as azathioprine and methotrexate and biologics such as remicade/infliximab and adalimumab.   - **[[home:patients:assessing_literature:palliative|Patient response to immunosuppressive medications]]** – Temporary symptomatic remission after taking immunosuppressive medications implies a decrease in the strength of the bacterial die-off reaction known as immunopathology. That none of these medications make patients better over the long-term is also telling. Several immunosuppressants are used to treat Crohn's including glucocorticoids such as prednisone and budesonide, aminosalicylates such as sulfasalazine and mesalamines, immunomodulators such as azathioprine and methotrexate and biologics such as remicade/infliximab and adalimumab.
-  - **Presence of microbes** – Bacteria have long been suspected to be the cause of Crohn's Disease. Detection rates for bacterial DNA from L-forms (a portion of the metagenomic microbiota that cause disease) in Crohn's tissues is variable due to "the fastidious culture requirements of the cell wall-deficient forms." (({{pubmed>long:15074643}})) The following types and species of bacteria have been found in patients with Crohn's: +  - **Presence of microbes** – Bacteria have long been suspected to be the cause of Crohn's Disease. Detection rates for bacterial DNA from L-forms (a portion of the metagenomic microbiota that cause disease) in Crohn's tissues is variable due to "the fastidious culture requirements of the cell wall-deficient forms." (({{pmid>long:15074643}})) The following types and species of bacteria have been found in patients with Crohn's: 
-    * L-form bacteria (({{pubmed>long:6134652}})) +    * L-form bacteria (({{pmid>long:6134652}})) 
-    * //Bacteroides fragilis// (({{pubmed>long:88760}})) +    * //Bacteroides fragilis// (({{pmid>long:88760}})) 
-    * //Chlamydia trachomatis// (({{pubmed>long:83465}})) +    * //Chlamydia trachomatis// (({{pmid>long:83465}})) 
-    * //Listeria monocytogenes// (({{pubmed>long:7729631}})) +    * //Listeria monocytogenes// (({{pmid>long:7729631}})) 
-    * //Mycobacterium avium//, subspecies paratuberculosis (({{pubmed>long:12843021}})) +    * //Mycobacterium avium//, subspecies paratuberculosis (({{pmid>long:12843021}})) 
-    * //Mycobacterium kansasii// (({{pubmed>long:80630}})) +    * //Mycobacterium kansasii// (({{pmid>long:80630}})) 
-    * //Pseudomonas maltophilia// (({{pubmed>long:780185}}))+    * //Pseudomonas maltophilia// (({{pmid>long:780185}}))
  
 De Hertogh //et al// provide a thorough review of the "unidentified persistent pathogen" theory, stating:  De Hertogh //et al// provide a thorough review of the "unidentified persistent pathogen" theory, stating: 
  
-<blockquote>Various environmental factors may play a role in the development of CD [Crohn's Disease], but microbes are most consistently implied. This theory is based on epidemiological, clinicopathological, genetic and experimental evidence. (({{pubmed>long:18240341}}))</blockquote>+<blockquote>Various environmental factors may play a role in the development of CD [Crohn's Disease], but microbes are most consistently implied. This theory is based on epidemiological, clinicopathological, genetic and experimental evidence. (({{pmid>long:18240341}}))</blockquote>
  
 Other researchers have come to similar conclusions: Other researchers have come to similar conclusions:
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 <blockquote>//M. avium subsp paratuberculosis//, adherent-invasive //E. coli// and //Candida// are good candidates for an infectious aetiology of Crohn's disease on the basis of genetic susceptibility, which relates to impaired function in the defence against intracellular bacteria. <blockquote>//M. avium subsp paratuberculosis//, adherent-invasive //E. coli// and //Candida// are good candidates for an infectious aetiology of Crohn's disease on the basis of genetic susceptibility, which relates to impaired function in the defence against intracellular bacteria.
  
-//**De Chambrunet** et al.// (({{pubmed>long:18622157}}))+//**De Chambrunet** et al.// (({{pmid>long:18622157}}))
 </blockquote>  </blockquote> 
  
 <blockquote>The bacterial community, in whole or in part, resident in the bowel of humans is considered to fuel the chronic immune inflammatory conditions characteristic of Crohn's disease and ulcerative colitis. Chronic or recurrent pouchitis in ulcerative colitis patients is responsive to antibiotic therapy, indicating that bacteria are the etiological agents. <blockquote>The bacterial community, in whole or in part, resident in the bowel of humans is considered to fuel the chronic immune inflammatory conditions characteristic of Crohn's disease and ulcerative colitis. Chronic or recurrent pouchitis in ulcerative colitis patients is responsive to antibiotic therapy, indicating that bacteria are the etiological agents.
  
-//**Sokol** et al.// (({{pubmed>long:18275077}})) </blockquote>+//**Sokol** et al.// (({{pmid>long:18275077}})) </blockquote>
  
  
  
-<blockquote>Bacterial exotoxins downregulate cathelicidin (hCAP-18/LL-37) and human beta-defensin 1 (HBD-1) expression in the intestinal epithelial cells. (({{pubmed>long:18717821}}))  +<blockquote>Bacterial exotoxins downregulate cathelicidin (hCAP-18/LL-37) and human beta-defensin 1 (HBD-1) expression in the intestinal epithelial cells. (({{pmid>long:18717821}}))  
 </blockquote> </blockquote>
  
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 ==== More evidence ==== ==== More evidence ====
  
-[[http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Inflammatory+Bowel+Diseases%2Fmicrobiology%22[Majr]+AND+Review[ptyp]|PubMed reviews on the microbiology of inflammatory bowel diseases]]+[[https://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Inflammatory+Bowel+Diseases%2Fmicrobiology%22[Majr]+AND+Review[ptyp]|PubMed reviews on the microbiology of inflammatory bowel diseases]]
  
 58. El Zaatari FA, Osato MS, Graham DY. Etiology of 58. El Zaatari FA, Osato MS, Graham DY. Etiology of
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-[[http://rheumatology.oxfordjournals.org/cgi/content/abstract/40/1/15|Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis]]+[[https://rheumatology.oxfordjournals.org/cgi/content/abstract/40/1/15|Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis]]
  
  
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 Am J Clin Pathol. 1989 Mar;91(3):259-64.  Am J Clin Pathol. 1989 Mar;91(3):259-64. 
 Johnson LA, Wirostko E, Wirostko WJ.  Johnson LA, Wirostko E, Wirostko WJ. 
-[[http://tinyurl.com/dh8th\Tinyurl|Crohn's disease uveitis]] +[[https://tinyurl.com/dh8th\Tinyurl|Crohn's disease uveitis]] 
  
 "Uveitis is a symptom, and has many identified causes and associations at this point. Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with “autoimmune diseases” like Crohns disease and rheumatic arthritis. I suspect that these other cases are due to CWD bacteria. There are several interesting papers that explore this. The researchers found cell-wall deficient bacteria (sometimes called mollicute-like organisms) in the vitreous fluid of patients with sardoidosis, Crohn’s disease, ulcerative colitis, juvenile rheumatoid arthritis, etc." "Uveitis is a symptom, and has many identified causes and associations at this point. Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with “autoimmune diseases” like Crohns disease and rheumatic arthritis. I suspect that these other cases are due to CWD bacteria. There are several interesting papers that explore this. The researchers found cell-wall deficient bacteria (sometimes called mollicute-like organisms) in the vitreous fluid of patients with sardoidosis, Crohn’s disease, ulcerative colitis, juvenile rheumatoid arthritis, etc."
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 Rifaximin is made by Salix Pharmaceuticals, Inc. Funding for the study was provided by Salix Pharmaceuticals, Inc.  Rifaximin is made by Salix Pharmaceuticals, Inc. Funding for the study was provided by Salix Pharmaceuticals, Inc. 
  
-One of only five hospitals in California whose nurses have been honored with the prestigious Magnet designation, Cedars-Sinai Medical Center is one of the largest nonprofit academic medical centers in the Western United States. Additional information is available at http://www.cedars-sinai.edu+One of only five hospitals in California whose nurses have been honored with the prestigious Magnet designation, Cedars-Sinai Medical Center is one of the largest nonprofit academic medical centers in the Western United States. Additional information is available at https://www.cedars-sinai.edu
  
-[[http://www.newswise.com/articles/view/515982|Targeted Antibiotics Lead to Long-lasting Improvement in IBS Symptoms]] +[[https://www.newswise.com/articles/view/515982|Targeted Antibiotics Lead to Long-lasting Improvement in IBS Symptoms]]  
 + 
 +It is apparently very rare for a patient to actually be allergic to Olmesartan (see Research below). An alternative approach where there is present a confirmed mycobacterial infection was recorded here [[https://www.mattioli1885journals.com/index.php/sarcoidosis/article/view/6769/4736|MAP Abx]] .
  
  
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 This presentation explains how those, and the other Defensins, are important, and I think that those of you who track the science will find it very interesting indeed. This presentation explains how those, and the other Defensins, are important, and I think that those of you who track the science will find it very interesting indeed.
  
-The presentation runs for 30 minutes. [[http://autoimmunityresearch.org/crohns.ram|Crohns]]+The presentation runs for 30 minutes. [[https://autoimmunityresearch.org/crohns.ram|Crohns]]
  
 ==== Serum levels of 'vitamin' D  ==== ==== Serum levels of 'vitamin' D  ====
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 BACKGROUND: The active form of vitamin D (1,25(OH)2D3) has been shown to inhibit development of inflammatory bowel disease (IBD) in IL-10 KO mice.  BACKGROUND: The active form of vitamin D (1,25(OH)2D3) has been shown to inhibit development of inflammatory bowel disease (IBD) in IL-10 KO mice. 
  
-<blockquote>Data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. (({{pubmed>long:17397543}}))</blockquote>+<blockquote>Data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. (({{pmid>long:17397543}}))</blockquote>
  
  
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 SUBJECTS. One hundred and fifty randomly selected patients with IBD from the hospital register and 73 healthy controls.  SUBJECTS. One hundred and fifty randomly selected patients with IBD from the hospital register and 73 healthy controls. 
  
- <blockquote>Patients with IBD have lower serum levels of 250HD than healthy controls, but similar serum PTH concentrations and vitamin D intake. Vitamin D intake, and the serum levels of 250HD and PTH are not associated with BMD, and malabsorption is unlikely to be a major factor in the aetiology of bone loss in unselected IBD patients. (({{pubmed>long:8568480}}))</blockquote> + <blockquote>Patients with IBD have lower serum levels of 250HD than healthy controls, but similar serum PTH concentrations and vitamin D intake. Vitamin D intake, and the serum levels of 250HD and PTH are not associated with BMD, and malabsorption is unlikely to be a major factor in the aetiology of bone loss in unselected IBD patients. (({{pmid>long:8568480}}))</blockquote> 
  
  
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 <blockquote> <blockquote>
-The number of E. coli in situ correlated with the severity of ileal disease (rho 0.621, P<0.001) and invasive E. coli was restricted to inflamed mucosa. E. coli strains isolated from the ileum were predominantly novel in phylogeny, displayed pathogen-like behavior in vitro and harbored chromosomal and episomal elements similar to those described in extraintestinal pathogenic E. coli and pathogenic Enterobacteriaceae. These data establish that dysbiosis of the ileal mucosa-associated flora correlates with an ileal Crohn's disease (ICD) phenotype, and raise the possibility that a selective increase in a novel group of invasive E. coli is involved in the etiopathogenesis to Crohn's disease involving the ileum. (({{pubmed>long:18043660}}))</blockquote>+The number of E. coli in situ correlated with the severity of ileal disease (rho 0.621, P<0.001) and invasive E. coli was restricted to inflamed mucosa. E. coli strains isolated from the ileum were predominantly novel in phylogeny, displayed pathogen-like behavior in vitro and harbored chromosomal and episomal elements similar to those described in extraintestinal pathogenic E. coli and pathogenic Enterobacteriaceae. These data establish that dysbiosis of the ileal mucosa-associated flora correlates with an ileal Crohn's disease (ICD) phenotype, and raise the possibility that a selective increase in a novel group of invasive E. coli is involved in the etiopathogenesis to Crohn's disease involving the ileum. (({{pmid>long:18043660}}))</blockquote>
  
 <blockquote> A study suggests that the bacteria-immune system 'fight' continues after the instigator bacteria have been cleared by the body, according to Andrew Gewirtz. The fight can result in metabolic syndrome, an important factor in obesity, or inflammatory bowel disease (IBD). <blockquote> A study suggests that the bacteria-immune system 'fight' continues after the instigator bacteria have been cleared by the body, according to Andrew Gewirtz. The fight can result in metabolic syndrome, an important factor in obesity, or inflammatory bowel disease (IBD).
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-"It is increasingly apparent that bacteria are playing a role in healthy development, and need to be properly managed by the mucosal immune system to avoid inflammatory diseases" Gewirtz explained. (({{pubmed>long:22863420}})) </blockquote>+"It is increasingly apparent that bacteria are playing a role in healthy development, and need to be properly managed by the mucosal immune system to avoid inflammatory diseases" Gewirtz explained. (({{pmid>long:22863420}})) </blockquote> 
 + 
 +=====  Patient interviews  ===== 
 + 
 + 
 +<html> 
 +<div class="patientinterviews"> 
 + 
 +<html> 
 +<div class="patientinterviewboxl"> 
 +<div class="patientinterviewimage"></html>{{:home:patients:melinda.gif?nolink|}}<html></div> 
 +<div class="patientinterviewtext"> 
 +<div class="patientinterviewname"></html>Melinda Stiles<html></div></html> 
 + 
 +Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis 
 + 
 +Read the [[https://bacteriality.com/2008/02/17/interview16/|interview]] 
 + 
 +<html></div></div> 
 + 
 + 
 +<br clear="left" /> 
 + 
 +</div> 
 +</html> 
 + 
 + 
 +Interviews of patients with other diseases are [[home:patients:patient_interviews|also available]]. 
 + 
 + 
 +{{tag>disease }}
  
 ===== Research ===== ===== Research =====
  
-Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely.  (({{pubmed>long:25023670}}))+Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely.  (({{pmid>long:25023670}}))
  
-In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity.   (({{pubmed>long:25947920}}))+In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity.   (({{pmid>long:25947920}}))
  
-Development, validation and implementation of an in vitro model for the study of metabolic and immune function in normal and inflamed human colonic epithelium.  (({{pubmed>long:25557335}})) +Development, validation and implementation of an in vitro model for the study of metabolic and immune function in normal and inflamed human colonic epithelium.  (({{pmid>long:25557335}})) 
  
 <blockquote> It is now known that epithelial cells have the capacity to secrete and respond to a range of immunological mediators and this suggests that these cells play a prominent role in the pathogenesis of IBD. Current knowledge about the intestinal epithelium has mainly been obtained using models based on animal cells, transformed human intestinal cell lines and isolated cells from resected colonic bowel segments. Species difference, malignant origin and confounders related to surgery, obviously make these cell models however less applicable for patophysiological studies.  <blockquote> It is now known that epithelial cells have the capacity to secrete and respond to a range of immunological mediators and this suggests that these cells play a prominent role in the pathogenesis of IBD. Current knowledge about the intestinal epithelium has mainly been obtained using models based on animal cells, transformed human intestinal cell lines and isolated cells from resected colonic bowel segments. Species difference, malignant origin and confounders related to surgery, obviously make these cell models however less applicable for patophysiological studies. 
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 </blockquote> </blockquote>
  
-'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens).   (({{pubmed>long:26011307}})) +'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens).   (({{pmid>long:26011307}})) 
  
 Butyric acid-producing anaerobic bacteria as a novel probiotic treatment approach for inflammatory bowel disease.  [[https://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.017541-0#tab2|microbiology research]] Butyric acid-producing anaerobic bacteria as a novel probiotic treatment approach for inflammatory bowel disease.  [[https://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.017541-0#tab2|microbiology research]]
  
-Butyric acid in functional constipation   (({{pubmed>long:24868272}}))+Butyric acid in functional constipation   (({{pmid>long:24868272}}))
  
-Butyric acid in irritable bowel syndrome  (({{pubmed>long:24868283}}))+Butyric acid in irritable bowel syndrome  (({{pmid>long:24868283}}))
      
 [[https://www.sciencemag.org/news/2018/11/do-gut-bacteria-make-second-home-our-brains|Roberts doesn’t know how these gut bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose]] [[https://www.sciencemag.org/news/2018/11/do-gut-bacteria-make-second-home-our-brains|Roberts doesn’t know how these gut bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose]]
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 [[https://www.karger.com/Article/FullText/477386|Resistant Starch Regulates Gut Microbiota: Structure,  [[https://www.karger.com/Article/FullText/477386|Resistant Starch Regulates Gut Microbiota: Structure, 
 Biochemistry and Cell Signalling]] Biochemistry and Cell Signalling]]
 +
 +immune mechanisms and interactions between cells of the immune system and tissue environment (({{pmid>long:28126697}}))   
  
 [{{:home:diseases:file:table_1_yang_et_al.gif|**Table 1  Yang et al **}}] [{{:home:diseases:file:table_1_yang_et_al.gif|**Table 1  Yang et al **}}]
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- +<nodisp>
-{{tag>disease }} +
- +
- +
- +
 ===== Notes and comments ===== ===== Notes and comments =====
  
-(({{pubmed>long:000}})) +(({{pmid>long:000}})) 
  
  
-broken link http://mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD007735/frame.html +broken link https://mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD007735/frame.html 
-another, maybe [[http://www.wjgnet.com/1007-9327/14/845.asp|thorough review]] +another, maybe [[https://www.wjgnet.com/1007-9327/14/845.asp|thorough review]] 
  
 <DiseaseHierarchy> <DiseaseHierarchy>
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 <blockquote> <blockquote>
  
-http://www.nejm.org/doi/full/10.1056/NEJMra1102942+https://www.nejm.org/doi/full/10.1056/NEJMra1102942
  
 Ulcerative Colitis Ulcerative Colitis
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 <blockquote> <blockquote>
  
-Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut(({{pubmed>long:14766966}}))+Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut(({{pmid>long:14766966}}))
  
 The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated IgA is partially compensated for by the presence of large amounts of unmutated IgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID–/– mice. Reconstitution of lamina propria IgA production in AID–/– mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of IgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system.  The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated IgA is partially compensated for by the presence of large amounts of unmutated IgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID–/– mice. Reconstitution of lamina propria IgA production in AID–/– mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of IgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system. 
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 <blockquote> <blockquote>
-Eur J Gastroenterol Hepatol. 2006 Jun;18(6):615-21.Heterogeneous expression of human cathelicidin hCAP18/LL-37 in inflammatory bowel diseases.(({{pubmed>long:16702850}}))+Eur J Gastroenterol Hepatol. 2006 Jun;18(6):615-21.Heterogeneous expression of human cathelicidin hCAP18/LL-37 in inflammatory bowel diseases.(({{pmid>long:16702850}}))
 Schauber J, Rieger D, Weiler F, Wehkamp J, Eck M, Fellermann K, Scheppach W, Gallo RL, Stange EF. Schauber J, Rieger D, Weiler F, Wehkamp J, Eck M, Fellermann K, Scheppach W, Gallo RL, Stange EF.
 Department of Medicine II, Division of Gastroenterology cInstitute of Pathology, University of Würzburg, Germany. jschauber@ucsd.edu Department of Medicine II, Division of Gastroenterology cInstitute of Pathology, University of Würzburg, Germany. jschauber@ucsd.edu
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 <blockquote> <blockquote>
-http://www.scientificamerican.com/article.cfm?id=genetics-in-the-gut+https://www.scientificamerican.com/article.cfm?id=genetics-in-the-gut
  
  
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 After looking at various studies of human intestinal bacteria, Scientific American's Katherine Harmon (above) suggests that the microorganisms play a larger part in human health than previously thought, even at times overshadowing genetics. One key study, Harmon says, is a catalog of about 3.3 million human gut microbe genes — research being done by a team of BGI scientists (which our sister publication GenomeWeb Daily News covered here). Harmon also points to work from Emory University's Andrew Gewirtz which has focused on a particular host gene that seems affect intestinal microbes. Those researchers found that a loss of the TLR5 gene in mice leads to a shift in the microbiota communities and an increase in insulin resistance, obesity, and other metabolic disruptions. Gerwitz thinks that inflammation could be driving the cycle of obesity, in conjunction with the changes in gut microbes, in some cases allowing more calories to be extracted from food, though the exact trigger for the cycle is unknown. His group has already started comparing human genes and microbial profiles of healthy people, versus those with metabolic syndrome to see if they can achieve the same results as with the mouse study. After looking at various studies of human intestinal bacteria, Scientific American's Katherine Harmon (above) suggests that the microorganisms play a larger part in human health than previously thought, even at times overshadowing genetics. One key study, Harmon says, is a catalog of about 3.3 million human gut microbe genes — research being done by a team of BGI scientists (which our sister publication GenomeWeb Daily News covered here). Harmon also points to work from Emory University's Andrew Gewirtz which has focused on a particular host gene that seems affect intestinal microbes. Those researchers found that a loss of the TLR5 gene in mice leads to a shift in the microbiota communities and an increase in insulin resistance, obesity, and other metabolic disruptions. Gerwitz thinks that inflammation could be driving the cycle of obesity, in conjunction with the changes in gut microbes, in some cases allowing more calories to be extracted from food, though the exact trigger for the cycle is unknown. His group has already started comparing human genes and microbial profiles of healthy people, versus those with metabolic syndrome to see if they can achieve the same results as with the mouse study.
-http://www.genomeweb.com//node/935506?hq_e=el&hq_m=643944&hq_l=1&hq_v=891326c480+https://www.genomeweb.com//node/935506?hq_e=el&hq_m=643944&hq_l=1&hq_v=891326c480
 </blockquote> </blockquote>
  
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 <blockquote>Nat Rev Gastroenterol Hepatol. 2010 Mar;7(3):126-8. <blockquote>Nat Rev Gastroenterol Hepatol. 2010 Mar;7(3):126-8.
-Crohn's disease: bacterial clearance in Crohn's disease pathogenesis.(({{pubmed>long:20203678}}))+Crohn's disease: bacterial clearance in Crohn's disease pathogenesis.(({{pmid>long:20203678}}))
 Fava F, Danese S. Fava F, Danese S.
    
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-<blockquote>Mucosal flora in Crohn's disease and ulcerative colitis - an overview.(({{pubmed>long:20224153}}))+<blockquote>Mucosal flora in Crohn's disease and ulcerative colitis - an overview.(({{pmid>long:20224153}}))
 by Swidsinski A, Loening-Baucke V, Herber A by Swidsinski A, Loening-Baucke V, Herber A
 Related Articles Related Articles
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 <blockquote>Rheumatology (Oxford). 2001 Jan;40(1):15-23. <blockquote>Rheumatology (Oxford). 2001 Jan;40(1):15-23.
-Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis.(({{pubmed>long:11157137}}))+Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis.(({{pmid>long:11157137}}))
  
 Tiwana H, Natt RS, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M, Ebringer A. Tiwana H, Natt RS, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M, Ebringer A.
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 This presentation was critical in helping me understand GI disease, it is worth reviewing in the light of what we know now: This presentation was critical in helping me understand GI disease, it is worth reviewing in the light of what we know now:
-http://autoimmunityresearch.org/crohns.ram+https://autoimmunityresearch.org/crohns.ram
 It is from the UCSD Host Defenses conferences in 2006. It is from the UCSD Host Defenses conferences in 2006.
  
 Then the gene-disease links are tabulated at: Then the gene-disease links are tabulated at:
-http://www.ncbi.nlm.nih.gov/gene/64127?ordinalpos=1&itool=EntrezSystem2.PEntrez.Gene.Gene_ResultsPanel.Gene_RVDocSum+https://www.ncbi.nlm.nih.gov/gene/64127?ordinalpos=1&itool=EntrezSystem2.PEntrez.Gene.Gene_ResultsPanel.Gene_RVDocSum
  
 ..Trevor.. ..Trevor..
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 </blockquote> </blockquote>
  
-[[http://www.cnn.com/2009/HEALTH/06/11/teen.self.diagnosis/|Teen diagnoses her own disease in science class]]+[[https://www.cnn.com/2009/HEALTH/06/11/teen.self.diagnosis/|Teen diagnoses her own disease in science class]]
 <blockquote>Inflamm Bowel Dis. 2011 Jan 6. [Epub ahead of print]Use of a novel vitamin d bioavailability test demonstrates that vitamin D absorption is decreased in patients with quiescent crohn's disease. <blockquote>Inflamm Bowel Dis. 2011 Jan 6. [Epub ahead of print]Use of a novel vitamin d bioavailability test demonstrates that vitamin D absorption is decreased in patients with quiescent crohn's disease.
 Farraye FA, Nimitphong H, Stucchi A, Dendrinos K, Boulanger AB, Vijjeswarapu A, Tanennbaum A, Biancuzzo R, Chen TC, Holick MF. Farraye FA, Nimitphong H, Stucchi A, Dendrinos K, Boulanger AB, Vijjeswarapu A, Tanennbaum A, Biancuzzo R, Chen TC, Holick MF.
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 </blockquote> </blockquote>
  
-(({{pubmed>long:99999999}})) +(({{pmid>long:99999999}}))  
 + 
 +===== References =====</nodisp>
  
-===== References ===== 
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