Bacterial L-form isolation from inflammatory bowel disease patients

Belsheim, M.R.; Darwish, Rula; Watson, W.C.; Schieven, Berend C.

doi:10.1016/0016-5085(83)90325-6

Cited by 34 publications

(8 citation statements)

References 25 publications

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“…The role of cell wall-deficient forms of bacteria as etiologic agents of disease has been the subject of investigations for many years. They have been frequently isolated from clinical specimens (2,3,11,(17)(18)(19)(20), but experimental challenge studies have generally been negative (8,12,14,24). Disease often results from revertant bacillary forms and not the spheroplasts themselves.…”

Section: Discussionmentioning

confidence: 99%

Spheroplastic phase of mycobacteria isolated from patients with Crohn's disease

Chiodini¹,

Kruiningen²,

Thayer³

et al. 1986

J Clin Microbiol

168

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Two strains of an unclassified Mycobacterium species were isolated after 18 and 30 months of incubation of media inoculated with resected intestinal tissues from patients with Crohn's disease. These strains represented the third and fourth isolates of this organism from Crohn's disease patients. Ultrastructural examination of this strain and two previously isolated strains revealed the presence of spheroplasts which eventually transformed into the bacillary form of a previously unrecognized Mycobacterium species. These cell wall-deficient forms did not stain with conventional dyes and failed to grow on hypertonic media. Restriction polymorphism of the ribosomal DNA genes was used to determine the relationship between the cell wall-deficient and baciliary forms. Identical restriction patterns of the ribosomal DNA genes were found between the spheroplasts and Mycobacterium sp. isolates with EcoRI, BamHI, and XhoI restriction endonucleases, thus providing definitive evidence of their origin. Unidentified spheroplasts were isolated from an additional 12 patients with Crohn's disease, of which 7 of 10 seroagglutinated with antiserum prepared against the Mycobacterium sp. Spheroplasts were isolated from 16 of 26 (61%) patients with Crohn's disease but not from tissues of 13 patients with ulcerative colitis or 13 patients with other diseases of the bowel. These findings support the role of mycobacteria as etiologic agents in some cases of Crohn's disease.

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Section: Discussionmentioning

confidence: 99%

Spheroplastic phase of mycobacteria isolated from patients with Crohn's disease

Chiodini¹,

Kruiningen²,

Thayer³

et al. 1986

J Clin Microbiol

168

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“…This resembles the pathology of a number of other conditions, notably certain infections and autoimmune diseases, and for years these processes were believed to cause Crohn's disease. When it was not possible to consistently culture any specific normal bacteria that fulfilled Koch's postulates from these patients, more elaborate techniques were used to demonstrate the presence of cell wall‐deficient atypical Mycobacteria paratuberculosis 3, L‐form organisms 4, Listeria monocytogenes 5 and measles virus 6. Although an effort was made to demonstrate their pathogenic relevance, the balance of evidence argues against them playing an important aetiological role 7.…”

Section: Introductionmentioning

confidence: 99%

Innate immunity in inflammatory bowel disease: a disease hypothesis

Marks

Segal

2007

The Journal of Pathology

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Crohn's disease arises from a defective interaction between the highly concentrated mass of bacteria in the gastrointestinal tract and the underlying tissues. It has generally been believed to result from an excessively exuberant inflammatory response or from 'autoimmunity'. Recent evidence has emerged that the problem is instead a failure of the way in which the body responds to the penetration of bacteria and other bowel contents through the intestinal mucosal barrier. Rather than Crohn's disease being caused by excessive inflammation, the primary mechanism is actually that of an immunodeficiency. Failure of inflammatory mediator production leads to insufficient recruitment of neutrophils, resulting in inadequate removal of bacteria and other debris. This impairment of acute inflammation can be compensated in some circumstances by signalling through NOD2. If not cleared, the foreign material in the bowel wall is taken up within macrophages, eliciting a granulomatous reaction and the local and systemic sequelae so characteristic of Crohn's disease.

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“…Recently, we and others have reported that several mycoplasmas could induce TNF-ao production by murine macrophages (1,11,30) and by a human monocytic cell line (31), suggesting that pathological findings caused by these microorganisms might be in part attributed to TNF-a released from macrophages. Although L-forms were isolated from chronic and relapsing infectious diseases, these microorganisms have not been proven to be the etiological agents in any specific diseases (3,5,7,12,15,16,19,21,40).…”

mentioning

confidence: 99%

Induction of macrophage-mediated production of tumor necrosis factor alpha by an L-form derived from Staphylococcus aureus

et al. 1993

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We investigated the capability of an L-form derived from Staphylococcus aureus to induce tumor necrosis factor alpha (TNF-ax) production in murine peritoneal macrophages. The activity for TNF-a induction was found in the membrane fraction of the L-form but not in the cytoplasmal fraction purified by the sucrose step gradient centrifugation. TNF-at mRNA was also detected in macrophages stimulated with L-form membranes. L-form induced TNF-a production in macrophages from both lipopolysaccharide-responsive and-unresponsive mouse strains. Regardless of the presence of polymyxin B, the activity of TNF-ai induction of L-form was mostly found in the phenol layer, but not in the aqueous layer, both of which were prepared by phenol extraction method. Fractions of L-form membranes representing molecular masses of approximately between 29 and 36 kDa were primarily responsible for inducing the production of TNF-aI consistently. Moreover, this stimulatory effect was abolished by digestion with Streptomyces griseus protease. In Western blot (immunoblot) analysis with anti-lipoteichoic acid antibody, two bands (65 and 45 kDa) were observed in the sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the phenol layer, whereas one band (14 kDa) was observed in either the aqueous layer or lipoteichoic acid of S. aureus. These results suggest that the component in the membrane of the L-form, distinct from cell wall components such as teichoic acid or lipopolysaccharide, possesses the capability to stimulate TNF-a production by macrophages.

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Bacterial L-form isolation from inflammatory bowel disease patients

Cited by 34 publications

References 25 publications

Spheroplastic phase of mycobacteria isolated from patients with Crohn's disease

Spheroplastic phase of mycobacteria isolated from patients with Crohn's disease

Innate immunity in inflammatory bowel disease: a disease hypothesis

Induction of macrophage-mediated production of tumor necrosis factor alpha by an L-form derived from Staphylococcus aureus

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