Microbial Signatures and Innate Immune Gene Expression in Lamina Propria Phagocytes of Inflammatory Bowel Disease PatientsSummary

Autor: Matthew C. Phillips, Irina Fernandez, Maria A. Quintero, David H. Kerman, Judith Pignac-Kobinger, Julie M. Davies, Maria T. Abreu, Amar R. Deshpande, Juan Burgueño, Yuguang Ban, Oriana M. Damas, William Peter Sawyer, Rishu Dheer
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
DNA
Bacterial

Male
Biopsy
Inflammation
Pilot Projects
Biology
Inflammatory bowel disease
digestive system
03 medical and health sciences
0302 clinical medicine
Immune system
Crohn Disease
RNA
Ribosomal
16S

medicine
Humans
Intestinal Mucosa
lcsh:RC799-869
Lamina propria
Crohn's disease
Phagocytes
Innate immune system
Hepatology
Host Microbial Interactions
Immunomagnetic Separation
Gene Expression Profiling
Gastroenterology
medicine.disease
Ulcerative colitis
Immunity
Innate

digestive system diseases
3. Good health
Gastrointestinal Microbiome
Molecular Typing
030104 developmental biology
medicine.anatomical_structure
Editorial
Gene Expression Regulation
Immunology
Dysbiosis
Feasibility Studies
030211 gastroenterology & hepatology
Colitis
Ulcerative

Female
lcsh:Diseases of the digestive system. Gastroenterology
medicine.symptom
Zdroj: Cellular and Molecular Gastroenterology and Hepatology, Vol 9, Iss 3, Pp 387-402 (2020)
Cellular and Molecular Gastroenterology and Hepatology
Popis: Background & Aims: The interaction between intestinal microbiota and the immune system plays a vital role in inflammatory bowel disease (IBD). Although numerous deep-sequencing studies have suggested dysbiosis in IBD, identifying specific bacteria from the stool or mucosa that are responsible for disease susceptibility or severity has remained a challenge. Lamina propria phagocytes ideally are localized to interact with bacteria that are in close proximity to, or have invaded, the tissue. Thus, we examined the microbial populations associated with the lamina propria phagocytes in 20 Crohn’s disease and 12 ulcerative colitis patients. Specifically, we aimed to address whether the phagocyte-associated microbiota differed from the mucosa-associated microbiota and whether this varied based on IBD type or the state of inflammation. Methods: 16S ribosomal RNA gene sequencing and innate immune gene expression profiling was done on CD11b+ lamina propria phagocytes isolated from the biopsies obtained from IBD patients. Results: Phagocyte-associated microbiota was enriched in bacterial species belonging to phylum Proteobacteria, whereas species belonging to phylum Bacteroidetes were enriched in the mucosal microbiota of IBD patients. Disease type was the most influential factor in driving differences in the microbiota of both the mucosa and the lamina propria phagocytes, irrespective of inflammation state o`r anatomic location. Crohn’s disease and ulcerative colitis specimens showed similar patterns of increased inflammatory gene expression in phagocytes isolated from inflamed areas compared with those isolated from uninflamed regions. Conclusions: This pilot study shows the feasibility of using lamina propria phagocytes to characterize the microbiota in IBD patients. The approach used in this study can narrow the spectrum of potentially dysbiotic bacterial populations and clinically relevant gene expression signatures in IBD patients. Keywords: Mucosa, Microbiota, Nanostring, Crohn’s Disease, Ulcerative Colitis
Databáze: OpenAIRE