GASTROINTESTINAL INFECTIONS ARE ASSOCIATED WITH UNIQUE GUT MICROBIOME SIGNATURES IN PATIENTS WITH FLARE OF INFLAMMATORY BOWEL DISEASE
DDW ePoster Library. Axelrad J. 05/23/21; 320980; Su503
Dr. Jordan Axelrad
Dr. Jordan Axelrad
Contributions
Abstract
Engage with the presenter here during ePoster Session: Role of the Gut Microbiome and Pathogens in Immune and Inflammatory Diseases
On Sunday, May 23, 2021 12:15 - 1 p.m. EDT

Number: Su503
GASTROINTESTINAL INFECTIONS ARE ASSOCIATED WITH UNIQUE GUT MICROBIOME SIGNATURES IN PATIENTS WITH FLARE OF INFLAMMATORY BOWEL DISEASE

Society: AGA
Track: Inflammatory Bowel Diseases
Category: Immunology‚ Microbiology & Inflammatory Bowel Diseases

Author(s): Jordan E. Axelrad1, Ze Chen1, Joseph Devlin1, Kyung Ku Jang1, Ken Cadwell11 New York University School of Medicine, New York, New York, United States

Background: Gastrointestinal pathogen PCR (GI PCR) panels have identified enteric infection in nearly 30% of flares of inflammatory bowel disease (IBD), with the most common pathogens comprising Clostridioides difficile, Escherichia coli subtypes, and norovirus. We aimed to characterize the gut microbiome during an episode of diarrhea with C. difficile, any E. coli subtype, or norovirus in patients with and without IBD to evaluate the role of enteric infection in flares.

Methods: We performed a cross-sectional study of patients with a GI PCR panel positive for C. difficile, E. coli subtypes, norovirus, or negative for all pathogens during an episode of diarrhea, and healthy controls, from September 2018 to May 2020. Stool microbiome was analyzed by 16S rRNA sequencing to quantify microbial diversity and identify microbes associated with each pathogen and by IBD status. Multivariate distance matrix regression was performed on the Bray-Curtis dissimilarity matrix to quantify the effect size of IBD, pathogen, and other clinical factors on the observed microbiomes.

Results: We identified 284 patients (100 IBD, 184 non-IBD) with C. difficile (n=53; 14 IBD), an E. coli subtype (n=55, 15 IBD), norovirus (n= 59, 9 IBD), or negative for all pathogens (n=117, 54 IBD, 24 healthy controls). There were no major differences in demographic, clinical, or biomarkers of IBD activity between patients with or without a pathogen. There were no major differences in microbiome diversity by Shannon index between patients with and without a pathogen, however, in patients negative for all pathogens, diversity was reduced in patients with IBD compared to patients without IBD (Figure 1A, p=0.036). Stratifying by IBD and pathogen, there were several differentially abundant microbes denoting a specific gut microbial signature associated with each pathogen and IBD (Figure 1B). Bacteroides and Lachnoclostridium were increased in IBD with C. difficile and Ruminococcus was increased in non-IBD with norovirus. Numerous taxa, including Alistipes, Streptococcus, and Bacteroides, were increased in IBD without a pathogen. Examining the contribution of various clinical covariates to Bray-Curtis dissimilarity-based PCoA analysis (Figure 2A), the presence of a pathogen was a greater relative influence on the gut microbiome compared to IBD, or severity of inflammation as measured by CRP or fecal calprotectin (Figure 2B).

Conclusion: There were major differences in the gut microbiota between patients with and without an enteric pathogen and IBD, demonstrating that gut microbiomes distinguish and differentially respond to pathogens. Patients with IBD and a pathogen produced a distinctive pathogen-specific microbiome, suggesting a unique microbial subset of IBD flare. These findings may have direct implications for the management of IBD flares complicated by an enteric pathogen.
Engage with the presenter here during ePoster Session: Role of the Gut Microbiome and Pathogens in Immune and Inflammatory Diseases
On Sunday, May 23, 2021 12:15 - 1 p.m. EDT

Number: Su503
GASTROINTESTINAL INFECTIONS ARE ASSOCIATED WITH UNIQUE GUT MICROBIOME SIGNATURES IN PATIENTS WITH FLARE OF INFLAMMATORY BOWEL DISEASE

Society: AGA
Track: Inflammatory Bowel Diseases
Category: Immunology‚ Microbiology & Inflammatory Bowel Diseases

Author(s): Jordan E. Axelrad1, Ze Chen1, Joseph Devlin1, Kyung Ku Jang1, Ken Cadwell11 New York University School of Medicine, New York, New York, United States

Background: Gastrointestinal pathogen PCR (GI PCR) panels have identified enteric infection in nearly 30% of flares of inflammatory bowel disease (IBD), with the most common pathogens comprising Clostridioides difficile, Escherichia coli subtypes, and norovirus. We aimed to characterize the gut microbiome during an episode of diarrhea with C. difficile, any E. coli subtype, or norovirus in patients with and without IBD to evaluate the role of enteric infection in flares.

Methods: We performed a cross-sectional study of patients with a GI PCR panel positive for C. difficile, E. coli subtypes, norovirus, or negative for all pathogens during an episode of diarrhea, and healthy controls, from September 2018 to May 2020. Stool microbiome was analyzed by 16S rRNA sequencing to quantify microbial diversity and identify microbes associated with each pathogen and by IBD status. Multivariate distance matrix regression was performed on the Bray-Curtis dissimilarity matrix to quantify the effect size of IBD, pathogen, and other clinical factors on the observed microbiomes.

Results: We identified 284 patients (100 IBD, 184 non-IBD) with C. difficile (n=53; 14 IBD), an E. coli subtype (n=55, 15 IBD), norovirus (n= 59, 9 IBD), or negative for all pathogens (n=117, 54 IBD, 24 healthy controls). There were no major differences in demographic, clinical, or biomarkers of IBD activity between patients with or without a pathogen. There were no major differences in microbiome diversity by Shannon index between patients with and without a pathogen, however, in patients negative for all pathogens, diversity was reduced in patients with IBD compared to patients without IBD (Figure 1A, p=0.036). Stratifying by IBD and pathogen, there were several differentially abundant microbes denoting a specific gut microbial signature associated with each pathogen and IBD (Figure 1B). Bacteroides and Lachnoclostridium were increased in IBD with C. difficile and Ruminococcus was increased in non-IBD with norovirus. Numerous taxa, including Alistipes, Streptococcus, and Bacteroides, were increased in IBD without a pathogen. Examining the contribution of various clinical covariates to Bray-Curtis dissimilarity-based PCoA analysis (Figure 2A), the presence of a pathogen was a greater relative influence on the gut microbiome compared to IBD, or severity of inflammation as measured by CRP or fecal calprotectin (Figure 2B).

Conclusion: There were major differences in the gut microbiota between patients with and without an enteric pathogen and IBD, demonstrating that gut microbiomes distinguish and differentially respond to pathogens. Patients with IBD and a pathogen produced a distinctive pathogen-specific microbiome, suggesting a unique microbial subset of IBD flare. These findings may have direct implications for the management of IBD flares complicated by an enteric pathogen.

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