Ileocolonoscopy in Seronegative Spondylarthropathy

Vos, Martine De; Cuvelier, Claude; Mielants, Herman; Veys, Eric; Barbier, F.; Elewaut, André

doi:10.1016/0016-5085(89)91557-6

Cited by 141 publications

(67 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Sections (3 m thick) were deparaffinized, rehydrated, and stained with hematoxylin and eosin. Specimens from patients with AS were divided into 3 subgroups as previously described (14): those with normal gut histology, those with acute inflammation, and those with chronic inflammation. Briefly, acute inflammation was defined by the preservation of normal architecture, with the presence of neutrophils and/or eosinophils in the crypt and villus epithelium.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of interleukin‐23, but not interleukin‐17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

Ciccia

Bombardieri

Principato

et al. 2009

Arthritis & Rheumatism

212

143

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Overexpression of interleukin‐23, but not interleukin‐17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

Ciccia

Bombardieri

Principato

et al. 2009

Arthritis & Rheumatism

212

143

View full text Add to dashboard Cite

“…Ycr.sima cnterocolitica has also been implicated because of similarities between yersiniosis and CD [6]. Histological changes in the intestine very simitar to CD have also been reported in patients with seronegative reactive arthropathy following infection with a number of organisms [7].…”

Section: Introductionmentioning

confidence: 99%

Peripheral cell-mediated immune response to mycobacterial antigens in inflammatory bowel disease

Rowbotham

Howdle

Trejdosiewicz

1995

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYA mycobacterial etiology has been proposed In Crohn's disease (CD). We have sought evidence of increased or modified T lymphocyte immune responses to Mycnhactcrium tuberculosis and Myco. paratubercuhsis in patients with CD (ti = 13), compared with ulcerative colitis (UC; n = 17) and controls (« = 17). Peripheral blood cells were cultured with phytohaemagglutinin (positive mitogen control), mycobacterial purified protein derivative (PPD) preparations, lysates., column fractions and whole, heat-killed bacteria. Responses of T cells and T cell subsets were assessed by expression of activation markers (CD25. CD69). coupled with blast ogenesis assays (^H-thymidine uptake) and estimates of proliferation. Virtually all patients responded to Myco. paratuberculo.\is and Myco. tuberculosis antigens. There were no significant differences between patient groups, although there was a very high overall correlation (r = 095; P<0000\) between responses to the two mycobacterial species. Most of the activation and proliferative responses resided in the CD4'*' (T helper) subset. Although up to 15% of CDS"^ (suppressor/cytotoxic) cells also became activated, the CD8^ cells did not proliferate subsequently. Cells expressing the alternate y/) form of the T cell receptor (TCR 7(S^)did not activate or proliferate in response to mycobacterial antigens. There were no differences in any of these parameters between patient groups. We conclude that there is no specilic increase or alteration in cell-mediated anti-mycobacterial immunity in inflammatory bowel disease (IBD). Thus our data do not suppwrt a mycobacterial etiopathology of Crohn's disease.

show abstract

“…UK. bacteria [9]. In more recent years the clinical and hisiological similarities ofCrohn's disease to Johne's disease of ruminants [10], and the isolation of Mycohacterium paratuherculosis from palients with Crohn's disease, but not controls, produced a candidate organism for involvement in the aetiology ofCrohn's disease [11.12].…”

Section: Introductionmentioning

confidence: 99%

Mucosal cell-mediated immunity to mycobacterial, enterobacterial and other microbial antigens in inflammatory bowel disease

Ibbotson

Lowes

Chahal

et al. 1992

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYCulture studies have suggested that Mycohacterium paratuherculosis m-ay p\ay a role in the aetiology ofCrohn's disease. However, evidence of sensitizalion to mycobacterial antigens amongst patients with Crohn's disease has not yet heen adequately demonstrated. Previous studies of cell-mediated iinmunity ((.'MI) in Crohn's disease were restricted lu responses of peripheral hlood numonuclear cells (PBMC) lomycohacterialanligcns. In this study we have investigated the proliferativc responses of hoth PBMC and mesenteric lymph node mononuclear cells (MLNMC) to a range of myeobaeterial and non-mycobacterial antigens. There was no evidence of speeifie sensitization in the responses of MLNMC and PBMC from patients with inflammatory howel disease (IBD) to the myeobaeterial antigens. However, anergy to A/./«;r(//((/)crcH/o.v(.scould not be excluded. IBD MLNMC responses to most antigens were generally greater than those of PBMC. which were often undetectable. When compared with controls, there was evidenee of increased CMI to a range of non-mycobacterial antigens, especially Yersinia enterocolitica, amongst both MLNMC and PBMC from patients with Crohn's disease and ulccrative colitis (IJC). These results do not provide support to the proposed role of mycobacteria in the ptithogenesis ofCrohn's disease, but indicate that further investigation may determine a role for bacterial-specific T cell-mediated responses in the pathogenesis of IBD.

show abstract

Ileocolonoscopy in Seronegative Spondylarthropathy

Cited by 141 publications

References 8 publications

Overexpression of interleukin‐23, but not interleukin‐17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

Overexpression of interleukin‐23, but not interleukin‐17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

Peripheral cell-mediated immune response to mycobacterial antigens in inflammatory bowel disease

Mucosal cell-mediated immunity to mycobacterial, enterobacterial and other microbial antigens in inflammatory bowel disease

Contact Info

Product

Resources

About