Antibodies to Mycobacterium paratuberculosis and nine species of environmental mycobacteria in Crohn's disease and control subjects.

Stainsby, Karen; Lowes, J.R.; Allan, R N; Ibbotson, J. P.

doi:10.1136/gut.34.3.371

Cited by 62 publications

(24 citation statements)

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“…. [T]here were no statistical differences between these values and those of the control population" (n = 38 vs. 45 controls) (56). "The lnjlunrmuto~ Bowel Disease,@.…”

Section: Serology and Cell-mediated Immunitymentioning

confidence: 90%

Lack of support for a common etiology in Johne's disease of animals and Crohn's disease in humans

Kruiningen

2007

Inflamm Bowel Dis

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Summary:The superficial similarity of Johne's disease to Crohn's disease led to the hypothesis that, like the former, Crohn's disease was caused by Mycobacterium paratuberculosis. Detailed pathologic comparisons, however, reveal little similarity between these two entities, including the lack of important extraintestinal manifestations. Attempts to recover M. paratuberculosis by culture have only rarely succeeded and the significance of spheroplasts that appear more frequently on culture is seriously in question. Five immunocytochemistry studies have failed to find mycobacterial antigens in diseased tissues and the five most recent polymerase chain reaction (PCR) attempts to find genomic evidence of M. paratuberculosis were uniformly negative. Numerous serologic studies failed to demonstrate antibody to M. paratuberculosis and attempts to show cell-mediated immunity were also unrewarding. Inoculation of numerous experimental animals with Crohn's disease tissue has failed to induce Johne's disease, and inoculation of various animal species with M. paratuberculosis has equally failed to result in Crohn's disease. Controlled studies of the treatment of Crohn's disease with antimycobacterial agents have generally resulted in no improvement, and most studies that have shown a positive response are either uncontrolled or include broad-spectrum antibiotics that may be acting on pathogens other than mycobacteria. Finally, although Johne's disease is common in farm animals, and infected animals shed M. paratuberculosis in large numbers, no record of zoonotic transmission has been recorded. Key Words: Crohn's diseaseMycobacteria-Johne's disease-Zoonoses-Spheroplasts.Among research scientists, public health veterinarians, and the milk-consuming public there continues to be concern about the possibility that Mycobacterium paratuberculosis, the causative agent of Johne's disease (JD) of ruminants, is transmissible to humans and that it causes Crohn's disease (CD). Since the hypothesis that M. paratuberculosis causes CD was first mooted, much evidence that argues against it has accumulated. The purpose of this article is to summarize this evidence and to review the relationship between JD of animals and CD. PATHOLOGYA statement that is reiterated often is that which claims that CD is remarkably similar to JD. This author contends that the morphologic similarities are superficial, and in light of current histopathologic interpretation, more suggestive of differing etiopathogenesis.Address correspondence and reprint requests Lo Dr. H. J. Van Kruiningen, Department of Pathobiology, University of Connecticut, 61 N. Eagleville Rd., U-89, Storrs, CT 06269-3089, U.S.A.Manuscript received November 19, 1998; accepted March 24, 1999. Crohn's disease is a chronic, segmental disease of the intestine; it is submucosal and transmural, fibrosing, sclerosing, and stenosing (1-6). Affected most frequently are the distal ileum and proximal colon; however, CD sometimes occurs in other portions of the gastrointestinal tract. Segmental disea...

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“…. [T]here were no statistical differences between these values and those of the control population" (n = 38 vs. 45 controls) (56). "The lnjlunrmuto~ Bowel Disease,@.…”

Section: Serology and Cell-mediated Immunitymentioning

confidence: 90%

Lack of support for a common etiology in Johne's disease of animals and Crohn's disease in humans

Kruiningen

2007

Inflamm Bowel Dis

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“…In contrast to culture results, M. paratuberculosis DNA in intestinal biopsies could not be detected in all studies (5 out of 9). Also, con icting data concerning the presence of antibodies against M. paratuberculosis have been published (72)(73)(74). Furthermore, the frequency of detection ranged from 13% to 72% (75).…”

Section: Mycobacterium Paratuberculosismentioning

confidence: 98%

The Bacterial Flora in Inflammatory Bowel Disease: Current Insights in Pathogenesis and the Influence of Antibiotics and Probiotics

Linskens

Huijsdens

Savelkoul

et al. 2001

Scandinavian Journal of Gastroenterology

194

122

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Linskens RK, Huijsdens XW, Savelkoul PHM, Vandenbroucke-Grauls CMJE, Meuwissen SGM. The bacterial flora in inflammatory bowel disease: current insights in pathogenesis and the influence of antibiotics and probiotics. Scand J Gastroenterol 2001;36 Suppl 234:29-40.The pathogenesis of in ammatory bowel disease (IBD) remains unknown, although in recent years more data have become available. The contribution of genetic and environmental factors is evident, and the luminal bacterial ora plays a major role in the initiation and perpetuation of chronic IBD. Animal models of IBD have shown that colitis does not occur in a germ-free environment. In human IBD, in ammation is present in parts of the gut containing the highest bacterial concentrations. Moreover, the terminal ileum, caecum and rectum are areas of relative stasis, providing prolonged mucosal contact with luminal contents.Enhanced mucosal permeability may play a pivotal role in maintaining a chronic in ammatory state, due to a genetic predisposition or as a result of direct contact with bacteria or their products. A defective epithelial barrier may cause a loss of tolerance to the normal enteric ora. Furthermore, an increased mucosal absorption of viable bacteria and bacterial products is found in IBD. Serum and secreted antibodies are increased and mucosal T-lymphocytes that recognize luminal bacteria are present. However, there is evidence that the immune system reacts over aggressively towards the normal luminal ora rather than the ora being altered in IBD. Several approaches have been used in attempts to discover a speci c microbial agent in the cause of IBD. These include demonstration of the presence of organisms or speci c antigens in affected tissues, culture of microbes from the affected tissues, demonstration of serological responses to several agents, and localization and detection of individual pathogen-speci c nucleic acid sequences in affected tissue by in situ hybridization and polymerase chain reaction. So far, no speci c micro-organism has been directly associated with the pathogenesis of IBD. Analysis of the luminal enteric ora, however, has revealed differences in the composition of this ora compared to healthy controls. In Crohn disease, concentrations of Bacteroides, Eubacteria and Peptostreptococcus are increased, whereas Bi dobacteria numbers are signi cantly reduced. Furthermore, in ulcerative colitis, concentrations of facultative anaerobic bacteria are increased. The arrival of new molecular techniques qualifying and quantifying the complex intestinal ora has induced a revival of interest in this micro ora.Therapeutic approaches geared towards changing the environment at the mucosal border have been attempted by the use of elemental diets, total parenteral nutrition, surgical diversion of the faecal stream and antibiotics. Over the past few years, the use of probiotics in IBD and other intestinal disorders has gained attention. Strengthened by promising experimental data and commercial interests, research in this eld is rapidly expandin...

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“…38 Both groups reported no significant elevation in IgA, IgG or IgM antibody levels, to these antigen preparations in the Crohn's disease patients. Tanaka et al (1991), Brunello et al (1991) and Stainsby et al (1993) concurred, that serologic data did not support a role for MPTB in Crohn's disease. [39][40][41] Naser and El Zaatari, in 2000, tested patients against two newly-defined antigens they identified as P35 and P36.…”

Section: Serology and Cell-mediated Immunitymentioning

confidence: 94%

“…Tanaka et al (1991), Brunello et al (1991) and Stainsby et al (1993) concurred, that serologic data did not support a role for MPTB in Crohn's disease. [39][40][41] Naser and El Zaatari, in 2000, tested patients against two newly-defined antigens they identified as P35 and P36. They reported, for P35 a positive serologic response in 75% of 53 CD patients, 14% of 35 controls and 10% of UC patients.…”

Section: Serology and Cell-mediated Immunitymentioning

confidence: 94%

Where are the weapons of mass destruction — the Mycobacterium paratuberculosis in Crohn's disease?

Kruiningen¹

2011

Journal of Crohn's and Colitis

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Antibodies to Mycobacterium paratuberculosis and nine species of environmental mycobacteria in Crohn's disease and control subjects.

Abstract: Cultural and serological studies have provided limited, often conflicting, evidence of a role for mycobacteria in

Cited by 62 publications

References 18 publications

Lack of support for a common etiology in Johne's disease of animals and Crohn's disease in humans

Lack of support for a common etiology in Johne's disease of animals and Crohn's disease in humans

The Bacterial Flora in Inflammatory Bowel Disease: Current Insights in Pathogenesis and the Influence of Antibiotics and Probiotics

Where are the weapons of mass destruction — the Mycobacterium paratuberculosis in Crohn's disease?

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