Lipocortin-present perforating and lipocortin-absent nonperforating Crohn's disease

Sakanoue, Youichirou; Horai, T; Okamoto, Tomoaki; Hatada, Takuya; Shoji, Yasutsugu; Fujita, Shinsuke; Kusunoki, Masato; Utsunomiya, Joji

doi:10.1016/s0002-9610(05)80901-8

Cited by 13 publications

(6 citation statements)

References 14 publications

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“…Our data thus corroborate epidemiological (2) and lipocortin (20) data subdividing CD into two (5), the identification of these two CD subpopulations provides a powerful paradigm with which to investigate immune regulation.…”

Section: Discussionsupporting

confidence: 84%

Molecular evidence for two forms of Crohn disease.

Gilberts¹,

Greenstein²,

Katsel³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Recent epidemiological evidence suggests that there are two forms of Crohn disease (CD): perforating and nonperforating. We hypothesized that, just as with tuberculoid and lepromatous leprosy, differences in the two forms of CD would be both identified and determined by differences in the host immune response. Resected intestinal tissue from control patients as well as perforating and nonperforating CD patients was evaluated for mRNA levels. We employed 32p PCR amplification with published or custom-designed primers of a housekeeping gene (13-actin); a human T-cell marker (CD3-6); and the cytokines tumor necrosis factor a, transforming growth factor (3, granulocyte/macrophage colony-stimulating factor, interleukin (IL) 1(3, IL-lra, and IL-6. Differences were identified with IL-1,B (control = 162 ± 57 vs. perforating = 464 ± 154 vs. nonperforating = 12,582 ± 4733; P c 0.02) and IL-lra (control = 1337 ± 622 vs. perforating = 2194 ± 775 vs. nonperforating = 9715 ± 2988; P < 0.02). These data corroborate the epidemiological observation that there are two forms of CD. Nonperforating CD, the more benign form, is associated with increased IL-1,B and IL-lra mRNA expression. We conclude that it is the host immune response that determines which form of CD becomes manifest in any given individual and discuss the investigative, diagnostic, and therapeutic implications of these observations.

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Section: Discussionsupporting

confidence: 84%

Molecular evidence for two forms of Crohn disease.

Gilberts¹,

Greenstein²,

Katsel³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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“…They are the aggressive (perforating) and contained (nonperforating) forms (21-24). The total number of patients evaluated, which supports this division, is 891 (20,21,23,24), compared with 349 patients in whom such a separation is not demonstrated (18,19). Accordingly, we now suggest that CD should similarly be stratified into the perforating and nonperforating subdivisions before evaluating any therapeutic intervention in CD (37).…”

Section: Resultsmentioning

confidence: 83%

“…Although controversial (18,19) there is clinical (20,21), epidemiological (22), and molecular (23,24) evidence indicating that there are two distinct clinical manifestations of CD. These CD subclassifications have been designated as "perforating" and "nonperforating" forms (22).…”

mentioning

confidence: 99%

On the etiology of Crohn disease.

Mishina¹,

Katsel²,

Brown³

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

165

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“…An overexpression of annexin 1 or other annexins has been reported in some pathological processes 19, 10, [35][36][37]. Annexin 1 was found to be downregulated in non-perforating Crohn's disease, whereas it was present at control levels in perforating Crohn's disease [38]. Nevertheless, neither the chronology of the appearance of annexin nor the occurrence of a real secretion with respect to inflammation has been well defined.…”

mentioning

confidence: 99%

Annexin 1 is Overexpressed and Specifically Secreted During Experimentally Induced Colitis in Rats

Vergnolle¹,

Coméra²,

Buéno³

1995

Eur J Biochem

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Annexin 1 is a protein induced by glucocorticoids endowed with extracellular anti‐inflammatory properties. In this study, the local expression and secretion of annexins 1–6, in rat proximal colon, were studied at different times after intracolonic administration of 30 mg trinltrobenzenesulfonic acid in 50% ethanol. Secretion was identified by incubating colonic tissues in a culture medium. The expression of annexins was detected by immunoblotting in tissue homogenates and incubation media. Inflammatory stages were evaluated by measuring myeloperoxidase activity. Annexin 1 expression in colons increased after trinitrobenzenesulfonic acid treatment and was maximal between days 1 to 9, during the cellular stage of the inflammation that corresponded to maximal myeloperoxidase activity. From 12 h to 9 days after trinitrobenzenesulfonic acid/ethanol treatment, annexin 1 was specifically secreted. Annexin 3 was also overexpressed during the cellular stage, but the expression of annexins 2, 4, 5, and 6 was unchanged; none of these annexins were secreted. Annexin 1 was shown to be physiologically secreted because its release was specific, abundant, and not correlated with cellular lysis. Annexin 1 may be considered as a putative candidate in the control of the gut inflammatory processes.

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Lipocortin-present perforating and lipocortin-absent nonperforating Crohn's disease

Cited by 13 publications

References 14 publications

Molecular evidence for two forms of Crohn disease.

Molecular evidence for two forms of Crohn disease.

On the etiology of Crohn disease.

Annexin 1 is Overexpressed and Specifically Secreted During Experimentally Induced Colitis in Rats

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