scholarly journals Increased Activated Plasma Cells in Inflammatory Bowel Disease When Compared to Ischemic Acute Colitis

2021 ◽  
Vol 156 (Supplement_1) ◽  
pp. S56-S56
Author(s):  
C Thorburn ◽  
Z Qu ◽  
P Zhang
Keyword(s):  
Inflammatory Bowel Disease ◽  
Ischemic Colitis ◽  
Bowel Disease ◽  
Plasma Cells ◽  
Disease Process ◽  
Staining Intensity ◽  
Active Plasma ◽  
Architectural Distortion ◽  
Active Colitis ◽  
Inflammatory Bowel

Abstract Introduction/Objective Inflammatory bowel disease (IBD) and acute ischemic colitis can both be involved by active colitis. IBD is characterized by crypt architectural distortion, basal lymphoplasmacytosis, and occasional granulomatous changes. However, diagnosis of IBDs is still largely by exclusion of other types of active colitis with similar changes. We previously demonstrated that glucose regulated protein 94 (grp94) is mainly expressed by activated plasma cells. We postulate that increased numbers of grp94-positive plasma cells may support diagnosis of IBDs. Here, we compared IBD and active ischemic colitis for grp94 expression in mucosal plasma cells of colectomy specimens Methods/Case Report Tissue sections from colectomy specimens with active IBD (n = 8) and ischemic colitis (n = 7) were examined for grp94 expression by immunohistochemistry (monoclonal antibody clone 9G10 at dilution of 1:200, Enzo Life Science, Inc Farmindale, NY). The staining intensity and highest number of grp94 in plasma cells per high power field was counted and recorded for each case, and combined scores were calculated as # of plasma cells multiplied by staining intensity (ranging from 0 to 3+). Unpaired student T tests were used to compare these indices between the two groups for statistical significance (p value < 0.05 was considered significantly different) Results (if a Case Study enter NA) Plasma cells in lamina propria identified by grp94 staining showed higher intensity in IBD than ischemic groups. The number of plasma cells and combined scores were also significantly higher in the IBC group than that of ischemic group Conclusion Our data indicates that active plasma cells are much more numerous in IBD than ischemic colitis, supporting the notion that active plasma cells are involved in the development of this disease process. Morphologically, active colitis with increased number of plasma cells appears to be another index favoring the diagnosis of IBD.

scholarly journals Intestinal Protein Characterisation of SARS-CoV-2 Entry Molecules ACE2 and TMPRSS2 in Inflammatory Bowel Disease (IBD) and Fatal COVID-19 Infection

Inflammation ◽  
2021 ◽  
Author(s):  
Milly J. McAllister ◽  
Kathryn Kirkwood ◽  
Shaun C. Chuah ◽  
Emily J. Thompson ◽  
Jennifer A. Cartwright ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Plasma Cells ◽  
Staining Intensity ◽  
Tissue Expression ◽  
Viral Tropism ◽  
Intestinal Protein ◽  
Inflammatory Bowel ◽  
Protein Characterisation

Abstract—The coronavirus SARS-CoV-2 contributes to morbidity and mortality mainly as a result of immune-pathology in the lungs. Recent data has shown multi-system involvement with widespread viral tropism. Here we present a detailed intestinal protein characterisation of SARS-Cov-2 entry molecules ACE2 and TMPRSS2 in patients with inflammatory bowel disease ([IBD]; ulcerative colitis [UC] and Crohn’s disease [CD]) with age- and sex-matched non-IBD controls, and in those with fatal COVID-19 infection. In our dataset, ACE2 and TMPRSS2 displayed a membrane enterocyte staining in the ileum (due to presence of brush border/microvilli) in contrast to a cytoplasmic pattern in the colon. We also showed a high ACE2/low TMPRSS2 expression pattern in the ileum with a reverse trend in the colon. In UC, colonic ACE2 and TMPRSS2 are cytoplasmic in nature, with significantly higher ACE2 staining intensity compared to non-IBD controls. In inflamed and unaffected IBD mucosa, ileal and colonic enterocyte ACE2 and TMPRSS2 expressions are not modified in the histologic presence of inflammation. We observed immune cells within the lamina propria that expressed ACE2 and TMPRSS2, at higher frequencies in IBD when compared to non-IBD controls. These were identified as plasma cells with multiple myeloma oncogene 1/interferon regulatory factor 4 (MUM1/IRF4) expression. We further analysed the gut histology of six fatal COVID-19 cases, with no difference in colonic and ileal ACE2/TMRPSS2 staining (compared to non-IBD controls) and identified ACE2 + lamina propria plasma cells. Of interest, in this COVID-19 cohort, there was no histologic evidence gut inflammation despite known evidence of viral tropism within the enterocytes. Our data provides evidence for tissue expression of entry molecules ACE2 and TMPRSS2 including a close apposition to plasma cells — both pointing towards a role of the gut in the antecedent immune response to SARS-CoV-2 infection.

Chronic Nonspecific Inflammatory Bowel Disease of the Cecum and Proximal Colon in Children With Grossly Normal-Appearing Colonic Mucosa: Diagnosis by Colonoscopic Biopsies

PEDIATRICS ◽  
1987 ◽  
Vol 80 (2) ◽  
pp. 255-261
Author(s):  
Melvin B. Heyman ◽  
Jay A. Perman ◽  
Linda D. Ferrell ◽  
M. Michael Thaler
Keyword(s):  
Inflammatory Bowel Disease ◽  
Abdominal Pain ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Disease Process ◽  
Proximal Colon ◽  
Chronic Abdominal Pain ◽  
Medical Attention ◽  
Inflammatory Bowel ◽  
Inflammatory Changes

The diagnosis of inflammatory bowel disease rests on radiologic, endoscopic, and histologic creteria. Five patients, 2 to 17 years of age, sought medical attention because of chronic abdominal pain, diarrhea, and heme-positive stools. Rectal biopsies, visual inspection of colonic mucosa through the colonoscope, and contrast radiographs of the large and small intestine yielded nonspecific results. Serial endoscopic biopsies demonstrated a gradient of inflammatory changes diminishing in severity distally from the ileocecal valve and cecum. The disease process was most evident in specimens from the cecum, whereas biopsies distal to the transverse colon had a normal histologic appearance in all five patients. Biopsies from the proximal colon may provide evidence of inflammatory bowel disease not detectable using standard techniques. The combination of chronic abdominal pain, diarrhea, and heme-positive stools associated with inflammatory changes in biopsy specimens obtained from the proximal colon, but normal findings on radiologic, colonoscopic, and rectal biopsy examinations, may represent an early stage in the evolution of chronic nonspecific inflammatory bowel disease, including ulcerative colitis or regional enteritis (Crohn disease).

Serum IgG4 Subclass Deficiency Defines a Distinct, Commonly Encountered, Severe Inflammatory Bowel Disease Subtype

2020 ◽  
Author(s):  
Filippos Koutroumpakis ◽  
Anna Evans Phillips ◽  
Dhiraj Yadav ◽  
Jorge D Machicado ◽  
Maaz Ahsan ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Disease Severity ◽  
Bowel Disease ◽  
Disease Process ◽  
Serum Igg4 ◽  
Tertiary Center ◽  
Inflammatory Bowel ◽  
Subclass Deficiency ◽  
Igg4 Deficiency

Abstract Background Immunoglobulin G subclass 4 (IgG4) is hypothesized to play an immunomodulatory role, downregulating humoral immune responses. The role of this anti-inflammatory molecule in inflammatory bowel disease (IBD) has not been fully characterized. We sought to define alterations in serum IgG4 in patients with IBD and their association with multiyear disease severity. Methods We analyzed metadata derived from curated electronic health records from consented patients with IBD prospectively followed at a tertiary center over a 10-year time period. Patients with IBD with IgG4 serum levels available formed the study population. Demographics and multiyear clinical data were collected and analyzed. We stratified patients with IBD with low, normal, or high serum IgG4 levels. Results We found IgG4 characterized in 1193 patients with IBD and low IgG4 levels in 233 patients (20%) and elevated IgG4 levels in 61 patients (5%). An IgG4 deficiency did not significantly correlate with other antibody deficiencies. In a multiple Poisson regression analysis, low IgG4 was associated with more years on biologic agents (P = 0.002) and steroids (P = 0.049) and more hospital admissions (P < 0.001), clinic visits (P = 0.010), outpatient antibiotic prescriptions (P < 0.001), and CD-related surgeries (P = 0.011) during the study period after controlling for certain confounders. Elevated IgG4 was only associated with primary sclerosing cholangitis (P = 0.011). A cohort of patients with IgG4-deficient severe IBD received intravenous Ig replacement therapy, which benefited and was continued in 10 out of 11 individuals. Conclusions An IgG4 subclass deficiency, distinct from other antibody deficiencies, occurred commonly in a referral IBD population and was associated with multiple markers of disease severity. This is the first association of IgG4 subclass deficiency with an inflammatory disease process. Further work is needed to define the mechanistic role of IgG4 deficiency in this severe IBD subgroup.

scholarly journals Application of Proteomics to Inflammatory Bowel Disease Research: Current Status and Future Perspectives

2019 ◽  
Vol 2019 ◽  
pp. 1-24 ◽  
Author(s):  
Arash Assadsangabi ◽  
Caroline A. Evans ◽  
Bernard M. Corfe ◽  
Alan Lobo
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cancer Progression ◽  
Bowel Disease ◽  
Biomarker Discovery ◽  
Association Studies ◽  
Disease Process ◽  
Current Status ◽  
Genome Wide Association Studies ◽  
Susceptibility Loci ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic relapsing/remitting inflammatory illness of the gastrointestinal tract of unknown aetiology. Despite recent advances in decoding the pathophysiology of IBD, many questions regarding disease pathogenesis remain. Genome-wide association studies (GWAS) and knockout mouse models have significantly advanced our understanding of genetic susceptibility loci and inflammatory pathways involved in IBD pathogenesis. Despite their important contribution to a better delineation of the disease process in IBD, these genetic findings have had little clinical impact to date. This is because the presence of a given gene mutation does not automatically correspond to changes in its expression or final metabolic or structural effect(s). Furthermore, the existence of these gene susceptibility loci in the normal population suggests other driving prerequisites for the disease manifestation. Proteins can be considered the main functional units as almost all intracellular physiological functions as well as intercellular interactions are dependent on them. Proteomics provides methods for the large-scale study of the proteins encoded by the genome of an organism or a cell, to directly investigate the proteins and pathways involved. Understanding the proteome composition and alterations yields insights into IBD pathogenesis as well as identifying potential biomarkers of disease activity, mucosal healing, and cancer progression. This review describes the state of the art in the field with respect to the study of IBD and the potential for translation from biomarker discovery to clinical application.

scholarly journals Changes in Human Mucosal γδ T Cell Repertoire and Function Associated with the Disease Process in Inflammatory Bowel Disease

1997 ◽  
Vol 3 (3) ◽  
pp. 183-203 ◽  
Author(s):  
Laila D. McVay ◽  
Baiqing Li ◽  
Renée Biancaniello ◽  
Mary Anne Creighton ◽  
Dale Bachwich ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
Bowel Disease ◽  
Disease Process ◽  
T Cell Repertoire ◽  
Γδ T Cell ◽  
Cell Repertoire ◽  
Inflammatory Bowel ◽  
And Function

Mo1338 Is Focal Active Colitis a New Miscellany of Inflammatory Bowel Disease? And Is There a Role for 5 ASA in the Management of FAC?

2013 ◽  
Vol 144 (5) ◽  
pp. S-640
Author(s):  
Mareshah Jaira M. Banaag ◽  
Evelyn E. Daulat ◽  
L. Mediodia ◽  
S. Fernandes ◽  
Asad I. Dajani ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Active Colitis ◽  
Inflammatory Bowel ◽  
Focal Active Colitis

Matrix metalloproteinase-3 production by gut IgG plasma cells in chronic inflammatory bowel disease

2008 ◽  
Vol 14 (2) ◽  
pp. 195-203 ◽  
Author(s):  
John N. Gordon ◽  
Karen M. Pickard ◽  
Antonio Di Sabatino ◽  
Joanna D. Prothero ◽  
Sylvia L.F. Pender ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Matrix Metalloproteinase ◽  
Bowel Disease ◽  
Plasma Cells ◽  
Chronic Inflammatory Bowel Disease ◽  
Matrix Metalloproteinase 3 ◽  
Inflammatory Bowel ◽  
Chronic Inflammatory Bowel

scholarly journals The Role of Citrullination in Inflammatory Bowel Disease: A Neglected Player in Triggering Inflammation and Fibrosis?

2020 ◽  
Vol 27 (1) ◽  
pp. 134-144 ◽  
Author(s):  
Gabriele Dragoni ◽  
Gert De Hertogh ◽  
Séverine Vermeire
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Posttranslational Modification ◽  
Disease Process ◽  
Special Focus ◽  
Extracellular Traps ◽  
Fundamental Process ◽  
Gene Expression Analyses ◽  
Inflammatory Bowel

Abstract Citrullination is a posttranslational modification of proteins mediated by a specific family of enzymes called peptidylarginine deiminases (PAD). Dysregulation of these enzymes is involved in the etiology of various diseases, from cancer to autoimmune disorders. In inflammatory bowel disease (IBD), data for a role of citrullination in the disease process are starting to accumulate at different experimental levels including gene expression analyses, RNA, and protein quantifications. Most data have been generated in ulcerative colitis, but data in Crohn disease are lacking so far. In addition, the citrullination of histones is the fundamental process promoting inflammation through the formation of neutrophil extracellular traps (NETs). Interestingly, NETs have also been shown to activate fibroblasts into myofibroblasts in fibrotic interstitial lung disease. Therefore, citrullination merits more thorough study in the bowel to determine its role in driving disease complications such as fibrosis. In this review we describe the process of citrullination and the different players in this pathway, the role of citrullination in autoimmunity with a special focus on IBD, the emerging role for citrullination and NETs in triggering fibrosis, and, finally, how this process could be therapeutically targeted.

scholarly journals Vasoactive Intestinal Polypeptide (VIP) in the Intestinal Mucosal Nerve Fibers in Dogs with Inflammatory Bowel Disease

Animals ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1759
Author(s):  
Andrzej Rychlik ◽  
Sławomir Gonkowski ◽  
Jarosław Całka ◽  
Krystyna Makowska
Keyword(s):  
Inflammatory Bowel Disease ◽  
Nervous System ◽  
Vasoactive Intestinal Polypeptide ◽  
Bowel Disease ◽  
Disease Process ◽  
Nerve Fibers ◽  
Inflammatory Bowel ◽  
Healthy Dogs ◽  
Adaptive Reactions ◽  
Intestinal Polypeptide

Canine inflammatory bowel disease (IBD) is a group of enteropathies with nonspecific chronic symptoms and poorly understood etiology. Many aspects connected with IBD are not understood. One of them is the participation of the intestinal nervous system in the development of pathological processes. Thus, this study aimed to demonstrate changes in the density of intramucosal nerve fibers containing vasoactive intestinal polypeptide (VIP)—one of the most important intestinal nervous factors caused by the various stages of IBD development. Mucosal biopsy specimens collected from the duodenum, jejunum and descending colon of healthy dogs and dogs with varied severity of IBD were included in the experiment. The density of VIP-like immunoreactive (VIP-LI) nerves was determined by a single immunofluorescence technique and a semi-quantitative method consisting in VIP-LI fiber counts in the field of view (0.1 mm2). The obtained results indicate that IBD induces changes in the density of mucosal VIP-LI nerve fibers in the canine gastrointestinal tract. The initial decrease is followed by an increase in VIP-like immunoreactivity in successive stages of the disease. These observations show that VIP is a neuronal factor that participates in the pathological processes connected with canine IBD. The observed changes probably result from the neuroprotective and/or adaptive properties of VIP. Protective and adaptive reactions induced by inflammation aim to protect the GI tract against damage by proinflammatory factors and ensure the homeostasis in the enteric nervous system (ENS) under the conditions changed by the disease process.

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