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Flow cytometry technique identifies disease and therapy-associated microbial signatures in Crohn\u2019s disease<\/h1>Gastrointestinal Disorders<\/a>, Featured Articles<\/a> <\/span><\/span><\/header>\n<\/div><\/section>
\nBackground<\/strong>
\nRecent research suggests that the incidence of inflammatory bowel disease (IBD) in the UK is 1 in every 123 people, and that previously these numbers have been largely underestimated.<\/h3>\n<\/p>\n
Background<\/h4>\nRecent research suggests that the incidence of inflammatory bowel disease (IBD) in the UK is 1 in every 123 people, and that previously these numbers have been largely underestimated. Crohn\u2019s disease (CD) and ulcerative colitis (UC) are the two main forms of IBD; both are chronic inflammatory conditions of the gastrointestinal (GI) tract, characterized by recurrent episodes of intestinal inflammation with primary symptoms of abdominal pain, diarrhea, blood in the stool, fatigue and weight loss. The main difference between the two is that in CD inflammation can occur anywhere in the GI tract (most frequently the ileum and the colon), whereas in UC inflammation is confined to the colon and rectum. The disease involves thinning of the mucosal lining and involves all layers of the intestinal wall. The main non-modifiable risk factors genetic, environmental and immunologic, but smoking and reduced microbiota diversity (as influenced by diet) are major modifiable factors.<\/p>\n<\/div><\/section>
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\n![\"\"](\"https:\/\/clinlabint.com\/wp-content\/uploads\/sites\/2\/2025\/01\/AdobeStock_554402509.jpeg\" "\\"3D")
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\nIllustration of intestines affected by Crohn\u2019s disease (Adobe Stock.com)<\/em><\/p>\n<\/div><\/section>
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\nDiagnosis and treatment<\/h4>\n
Diagnosis is challenging as the symptoms are often non-specific and progress gradually. If there is a suspicion of CD, blood and stool samples are tested for inflammatory markers (such as C-reactive protein and calprotectin) and signs of infection, among others. Diagnosis is usually confirmed by procedures including colonoscopy, biopsy, and MRI\/CT scan. There is no cure for CD and treatment depends severity, involving steroids, dietary modification, immunosuppressants and biological medications (such as anti-TNF monoclonal antibodies).<\/p>\n
Gut microbiota and CD<\/h4>\n
We have known about the microbiota for over 100 years: this co-existence of a vast number of microorganisms in various sites of the body has even been referred to as a hidden organ and is thought to contribute 150 times more genetic information then the human genome. The gut microbiota is thought to be particularly important for health, being involved in fermentation of food, protection against pathogens, stimulating immune response, and vitamin production. Although there is high taxonomic diversity between individuals, functions of the microbial community seem to be conserved and the link between dysbiosis (an alteration of the gut microbiota) and disease is well known. Patients with CD are linked with lower microbial diversity and much work has been done to define a microbial signature for CD, to differentiate people with CD from healthy controls and people with UC.<\/p>\n
Flow cytometry for microbiota phenotyping in CD<\/h4>\n
Intestinal immunity is mediated through pathogen-specific IgA antibodies that bind to and \u2018coat\u2019 the pathogen; thus, IgA coating is thought to be indicative of disease-driving bacteria. Similarly, it is thought that bacterial surface sugar moieties also affect gut health through interaction with host lectins (such as intelectin 1) that are part of the core colonic mucus proteome, resulting in thinning of the inner colonic mucus layer and closer bacterial access to the epithelial surface. A recent study by Budzinski et al. [1] has used multi-parameter microbiota flow cytometry (mMFC) to characterize the intestinal microbiota of CD patients versus healthy controls for immunoglobulin coating and surface sugar presence. In this proof-of-concept study, the authors were able to use this methodology to perform microbial phenotyping that enabled the classification of CD patients from healthy controls, as well as revealing a signature that stratified patients achieving remission in response to anti-TNF therapy, not only during but also before beginning therapy. As the authors state in their paper, their work demonstrates that:<\/p>\n
\nmMFC presents a viable alternative and supplementation to \u201cconventional\u201d microbiota profiling with the potential to be applied for point-of-care diagnostics and therapy monitoring, but also to investigate the role of defined bacteria in disease pathogenesis.<\/span><\/p>\n<\/blockquote>\n
Reference:<\/strong>
\n1. Budzinski L, Kang GU, Riedel R et al. Single-cell microbiota phenotyping reveals distinct disease and therapy-associated signatures in Crohn’s disease. Gut Microbes 2025;17(1):2452250 ( https:\/\/shorturl.at\/fLbvf<\/a> ).<\/em><\/p>\n<\/div><\/section>
\n
Background<\/strong>
\nRecent research suggests that the incidence of inflammatory bowel disease (IBD) in the UK is 1 in every 123 people, and that previously these numbers have been largely underestimated.<\/h3>\n<\/p>\n
Background<\/h4>\nRecent research suggests that the incidence of inflammatory bowel disease (IBD) in the UK is 1 in every 123 people, and that previously these numbers have been largely underestimated. Crohn\u2019s disease (CD) and ulcerative colitis (UC) are the two main forms of IBD; both are chronic inflammatory conditions of the gastrointestinal (GI) tract, characterized by recurrent episodes of intestinal inflammation with primary symptoms of abdominal pain, diarrhea, blood in the stool, fatigue and weight loss. The main difference between the two is that in CD inflammation can occur anywhere in the GI tract (most frequently the ileum and the colon), whereas in UC inflammation is confined to the colon and rectum. The disease involves thinning of the mucosal lining and involves all layers of the intestinal wall. The main non-modifiable risk factors genetic, environmental and immunologic, but smoking and reduced microbiota diversity (as influenced by diet) are major modifiable factors.<\/p>\n<\/div><\/section>
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\nIllustration of intestines affected by Crohn\u2019s disease (Adobe Stock.com)<\/em><\/p>\n<\/div><\/section>
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<\/span><\/span><\/div>
\nDiagnosis and treatment<\/h4>\n
Diagnosis is challenging as the symptoms are often non-specific and progress gradually. If there is a suspicion of CD, blood and stool samples are tested for inflammatory markers (such as C-reactive protein and calprotectin) and signs of infection, among others. Diagnosis is usually confirmed by procedures including colonoscopy, biopsy, and MRI\/CT scan. There is no cure for CD and treatment depends severity, involving steroids, dietary modification, immunosuppressants and biological medications (such as anti-TNF monoclonal antibodies).<\/p>\n
Gut microbiota and CD<\/h4>\n
We have known about the microbiota for over 100 years: this co-existence of a vast number of microorganisms in various sites of the body has even been referred to as a hidden organ and is thought to contribute 150 times more genetic information then the human genome. The gut microbiota is thought to be particularly important for health, being involved in fermentation of food, protection against pathogens, stimulating immune response, and vitamin production. Although there is high taxonomic diversity between individuals, functions of the microbial community seem to be conserved and the link between dysbiosis (an alteration of the gut microbiota) and disease is well known. Patients with CD are linked with lower microbial diversity and much work has been done to define a microbial signature for CD, to differentiate people with CD from healthy controls and people with UC.<\/p>\n
Flow cytometry for microbiota phenotyping in CD<\/h4>\n
Intestinal immunity is mediated through pathogen-specific IgA antibodies that bind to and \u2018coat\u2019 the pathogen; thus, IgA coating is thought to be indicative of disease-driving bacteria. Similarly, it is thought that bacterial surface sugar moieties also affect gut health through interaction with host lectins (such as intelectin 1) that are part of the core colonic mucus proteome, resulting in thinning of the inner colonic mucus layer and closer bacterial access to the epithelial surface. A recent study by Budzinski et al. [1] has used multi-parameter microbiota flow cytometry (mMFC) to characterize the intestinal microbiota of CD patients versus healthy controls for immunoglobulin coating and surface sugar presence. In this proof-of-concept study, the authors were able to use this methodology to perform microbial phenotyping that enabled the classification of CD patients from healthy controls, as well as revealing a signature that stratified patients achieving remission in response to anti-TNF therapy, not only during but also before beginning therapy. As the authors state in their paper, their work demonstrates that:<\/p>\n
\nmMFC presents a viable alternative and supplementation to \u201cconventional\u201d microbiota profiling with the potential to be applied for point-of-care diagnostics and therapy monitoring, but also to investigate the role of defined bacteria in disease pathogenesis.<\/span><\/p>\n<\/blockquote>\n
Reference:<\/strong>
\n1. Budzinski L, Kang GU, Riedel R et al. Single-cell microbiota phenotyping reveals distinct disease and therapy-associated signatures in Crohn’s disease. Gut Microbes 2025;17(1):2452250 ( https:\/\/shorturl.at\/fLbvf<\/a> ).<\/em><\/p>\n<\/div><\/section>
\n
Recent research suggests that the incidence of inflammatory bowel disease (IBD) in the UK is 1 in every 123 people, and that previously these numbers have been largely underestimated. Crohn\u2019s disease (CD) and ulcerative colitis (UC) are the two main forms of IBD; both are chronic inflammatory conditions of the gastrointestinal (GI) tract, characterized by recurrent episodes of intestinal inflammation with primary symptoms of abdominal pain, diarrhea, blood in the stool, fatigue and weight loss. The main difference between the two is that in CD inflammation can occur anywhere in the GI tract (most frequently the ileum and the colon), whereas in UC inflammation is confined to the colon and rectum. The disease involves thinning of the mucosal lining and involves all layers of the intestinal wall. The main non-modifiable risk factors genetic, environmental and immunologic, but smoking and reduced microbiota diversity (as influenced by diet) are major modifiable factors.<\/p>\n<\/div><\/section>
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\n
<\/div><\/div><\/div>\n
Illustration of intestines affected by Crohn\u2019s disease (Adobe Stock.com)<\/em><\/p>\n<\/div><\/section>
\n
\n
Diagnosis and treatment<\/h4>\n
Diagnosis is challenging as the symptoms are often non-specific and progress gradually. If there is a suspicion of CD, blood and stool samples are tested for inflammatory markers (such as C-reactive protein and calprotectin) and signs of infection, among others. Diagnosis is usually confirmed by procedures including colonoscopy, biopsy, and MRI\/CT scan. There is no cure for CD and treatment depends severity, involving steroids, dietary modification, immunosuppressants and biological medications (such as anti-TNF monoclonal antibodies).<\/p>\n
Gut microbiota and CD<\/h4>\n
We have known about the microbiota for over 100 years: this co-existence of a vast number of microorganisms in various sites of the body has even been referred to as a hidden organ and is thought to contribute 150 times more genetic information then the human genome. The gut microbiota is thought to be particularly important for health, being involved in fermentation of food, protection against pathogens, stimulating immune response, and vitamin production. Although there is high taxonomic diversity between individuals, functions of the microbial community seem to be conserved and the link between dysbiosis (an alteration of the gut microbiota) and disease is well known. Patients with CD are linked with lower microbial diversity and much work has been done to define a microbial signature for CD, to differentiate people with CD from healthy controls and people with UC.<\/p>\n
Flow cytometry for microbiota phenotyping in CD<\/h4>\n
Intestinal immunity is mediated through pathogen-specific IgA antibodies that bind to and \u2018coat\u2019 the pathogen; thus, IgA coating is thought to be indicative of disease-driving bacteria. Similarly, it is thought that bacterial surface sugar moieties also affect gut health through interaction with host lectins (such as intelectin 1) that are part of the core colonic mucus proteome, resulting in thinning of the inner colonic mucus layer and closer bacterial access to the epithelial surface. A recent study by Budzinski et al. [1] has used multi-parameter microbiota flow cytometry (mMFC) to characterize the intestinal microbiota of CD patients versus healthy controls for immunoglobulin coating and surface sugar presence. In this proof-of-concept study, the authors were able to use this methodology to perform microbial phenotyping that enabled the classification of CD patients from healthy controls, as well as revealing a signature that stratified patients achieving remission in response to anti-TNF therapy, not only during but also before beginning therapy. As the authors state in their paper, their work demonstrates that:<\/p>\n
\nmMFC presents a viable alternative and supplementation to \u201cconventional\u201d microbiota profiling with the potential to be applied for point-of-care diagnostics and therapy monitoring, but also to investigate the role of defined bacteria in disease pathogenesis.<\/span><\/p>\n<\/blockquote>\n
Reference:<\/strong>
\n1. Budzinski L, Kang GU, Riedel R et al. Single-cell microbiota phenotyping reveals distinct disease and therapy-associated signatures in Crohn’s disease. Gut Microbes 2025;17(1):2452250 ( https:\/\/shorturl.at\/fLbvf<\/a> ).<\/em><\/p>\n<\/div><\/section>
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