Pathology of Regional Ileitis and Ulcerative Colitis

Warren, Shields

doi:10.1001/jama.1954.02940370001001

Cited by 163 publications

(45 citation statements)

References 11 publications

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“…Active episodes of UC share many of the same histopathological characteristics observed in CD; however, the inflammation is confined to the mucosa. The broad pathological process of both diseases involves inflammation, ulceration, and subsequent regeneration of intestinal mucosa (49,164). These episodes are often cyclical in nature, thereby resulting in periods of increased disease activity (flares) followed by days or weeks of quiescence.…”

Section: Ibd Pathogenesismentioning

confidence: 99%

“…This review provides an overview of the biology and pathophysiology of angiogenesis and presents evidence to suggest that "pathological" angiogenesis may act to perpetuate chronic gut inflammation. Vascular changes in IBD were noted as early as 1954 and throughout the late 1950s and 1960s; however, descriptions of these vascular changes and the interpretations of what they meant varied widely (8,78,125,164). In 1970, Brahme and Lindstrom (21) reported increases in vascularity in active Crohn's disease which they showed by radiography of vascular castings.…”

Section: Ibd Pathogenesismentioning

confidence: 99%

“…There are four major isoforms of VEGF-A: VEGF 121 , VEGF 165 , VEGF 189 , and VEGF 206 , which correspond to VEGF 120 , VEGF 164 , VEGF 188 , and VEGF 205 in mice. These isoforms have differing binding properties and the exact roles of each during angiogenesis are not fully understood (46).…”

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

“…Initial reports examining the relationship between inflammation and angio-genesis showed that VEGF-A can facilitate monocyte chemotaxis and increase leukocyte adhesion (35,42). A study by Detmar et al (42) reported that transgenic overexpression of VEGF 164 in the skin of mice led to large increases in leukocyte rolling and firm adhesion and that these mice showed increased vascular density composed of immature vessels, indicating a molecular link between leukocyte recruitment and angiogenesis. Recent reports also demonstrate that VEGF-A is a potent immune modulator under several conditions such as ischemiareperfusion and alloimmunity (126,156).…”

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

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Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

143

114

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Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

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Section: Ibd Pathogenesismentioning

confidence: 99%

Section: Ibd Pathogenesismentioning

confidence: 99%

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

See 2 more Smart Citations

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

143

114

View full text Add to dashboard Cite

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“…Histological examination shows cryptitis, crypt abcess, chronic mucosal damage in the form of architectural distortion, atrophy, and metaplasia and non caseating granulomas. The intestinal wall is thickened as a consequence of transmural edema, inflammation, submucosal fibrosis, and hypertrophy of the muscularis propria, all of which contribute to stricture formation as in Figure 3 [39,40].…”

Section: Hpementioning

confidence: 99%

A Review on Clinicopathological Correlation between Classical Inflammatory Bowel Disease and Immunotherapy Related Inflammatory Bowel Disease

Allen¹

2014

Immunome Res

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Blockade of various immune targets such as cytotoxic T-lymphocyte antigen-4 and Programmed cell death leads to immune-mediated tumor regression and immune-related adverse events, predominantly gastrointestinal events including diarrhea and colitis. The current review is done to understand the underlying mechanism of action and to identify potential biomarkers that could help in the prediction and management of gastrointestinal immune-related adverse events. Histological assessment of bowel biopsies and assessment of serologic markers of inflammatory bowel disease and colitis secondary to immune mediated antibodies are reviewed. Ipilimumab causes dysregulation of gastrointestinal mucosal immunity, which can be evidenced by altered antibody levels to enteric flora and inflammatory cell infiltration into gastrointestinal mucosa associated with diarrhea and clinical evidence of colitis. The pattern of drug induced antibody titers to microbial flora and the histological features and location of the inflammation were distinct from classic inflammatory bowel disease. Although classic inflammatory bowel disease and immune mediated antibodies related gastrointestinal toxicity are both immune mediated, the pattern of biomarkers and histological features suggests that the later may be a distinct clinicopathologic entity.

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Nonspecific Granulomatous Disease of the Stomach

Goldgraber¹

1958

AMA Arch Intern Med

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Pathology of Regional Ileitis and Ulcerative Colitis

Cited by 163 publications

References 11 publications

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

A Review on Clinicopathological Correlation between Classical Inflammatory Bowel Disease and Immunotherapy Related Inflammatory Bowel Disease

Nonspecific Granulomatous Disease of the Stomach

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