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PubMed1997

Reduced bone density in patients with inflammatory bowel disease.

BACKGROUND: Reduced bone mineral density in patients with inflammatory bowel disease is thought to be due to disturbances in calcium homeostasis or the effects of corticosteroid treatment. AIMS: To assess the prevalence and mechanism of reduced bone mineral density in 79 patients with inflammatory bowel disease (44 with Crohn's disease, 35 with ulcerative colitis) who did not have significant risk factors for low bone densities. METHODS: Dual x ray absorptiometry was used to measure bone mineral density and serum and urinary markers of osteoblast (alkaline phosphatase, procollagen 1 carboxy terminal peptide and osteocalcin) and osteoclast (pyridinoline, deoxypyridinoline, and type 1 collagen carboxy terminal peptide) activities to assess bone turnover. RESULTS: There was a high prevalence of low bone mineral density (prevalence of T scores < -1.0 from 51%-77%; T scores < -2.5 (osteoporosis) from 17%-28%) with hips being more often affected than vertebrae (p < 0.001). Reduced bone mineral density did not relate to concurrent or past corticosteroid intake, or type, site, or severity of disease. Whereas calcium homeostasis was normal, bone markers showed increased bone resorption without a compensatory increase in bone formation. CONCLUSIONS: The greater prevalence of reduced hip bone mineral density, as opposed to vertebral, mineral density and the pattern of a selective increase in bone resorption contrasts with that found in other known causes of metabolic bone disease.

Absorptiometry, Photon↗
PubMed1984

Whole body cellular and collagen nitrogen in healthy and wasted man.

The classical literature shows that wasting of body protein takes place mainly from the cellular compartment leaving high proportions of extracellular collagen. Whole body nitrogen ( WBN ) is proportional to whole body protein (cellular + extracellular) while whole body potassium ( WBK ) is almost entirely intracellular. WBK might be an adequate index of cellular wasting. WBN was measured by neutron activation and WBK by counting 40K in 29 healthy males and 131 male and female patients with wide ranges of body composition. Our wasted patients with Crohn's disease or ulcerative colitis, had higher WBN / WBK ratios than matched healthy controls and the difference between the two groups was in the cellular ratio (23.6 mol of N/mol of K, 0.33 g of N/mmol of K, 3 mmol of K/g of N). A multiple regression model for all the subjects represented cellular nitrogen by a term in WBK and extracellular nitrogen by simple anthropometric measurements. The partial regression coefficient of WBN on WBK was 22.6 +/- 1.1 (SE) mol of N/mol of K; this was also similar to the cellular ratio. Our results were compatible with extracellular protein (mainly collagen, which is 35% of normal whole body protein) remaining resistant to wasting even when severe loss of cellular protein occurs. The high ratios of WBN / WBK in wasted patients can be explained by this disproportionate wasting of cellular substances and they do not imply alterations in the cellular N/K ratio. We suggested that the stable ratio of WBK to cellular protein makes it an effective index of cellular wasting. The resistance of collagen to wasting and the preponderance of extracellular mass in the fat-free mass of wasted subjects, make WBN and fat-free mass unreliable guides to the extent of wasting.

Activation Analysis↗
PubMed2001

Transforming growth factor-beta messenger RNA and protein in murine colitis.

Using a CD4+ T-cell-transplanted SCID mouse model of colitis, we have analyzed TGF-beta transcription and translation in advanced disease. By in situ hybridization, the epithelium of both control and inflamed tissues transcribed TGF-beta1 and TGF-beta3 mRNAs, but both were expressed significantly farther along the crypt axis in disease. Control lamina propria cells transcribed little TGF-beta1 or TGF-beta3 mRNA, but in inflamed tissues many cells expressed mRNA for both isoforms. No TGF-beta2 message was detected in either control or inflamed tissues. Immunohistochemistry for latent and active TGF-beta1 showed that all cells produced perinuclear latent TGF-beta1. The epithelial cell basal latent protein resulted in only low levels of subepithelial active protein, which co-localized with collagen IV and laminin in diseased and control tissue. Infiltrating cells expressed very low levels of active TGF-beta. By ELISA, very low levels (0-69 pg/mg) of soluble total or active TGF-beta were detected in hypotonic tissue lysates. TGF-beta1 and TGF-beta3 are produced by SCID mouse colon and transcription is increased in the colitis caused by transplantation of CD4+ T-cells, but this does not result in high levels of soluble active protein. Low levels of active TGF-beta may be a factor contributing to unresolved inflammation.

Animals↗
PubMed2002

Risk of osteopenia after proctocolectomy and ileal pouch-anal anastomosis for ulcerative colitis.

BACKGROUND: The aim of our study was to evaluate the influence of pouchitis and villous atrophy on bone mineral density and metabolism at least 5 years after ileal pouch-anal anastomosis for ulcerative colitis (UC). METHODS: Eighty-eight subjects with a J-pouch operated on between 1985 and 1994, and 20 ulcerative colitis subjects with a conventional ileostomy were enrolled. Endoscopy was performed and spine and femoral neck bone mineral densities measured. Bone metabolism was assessed by measurement of serum levels of parathyroid hormone, osteocalcin, 25-hydroxyvitamin D3, calcium, alkaline phosphatase and urinary N-telopeptide cross-linked of type I collagen (NTX). RESULTS: In the lumbar spine, 37% of the J-pouch subjects with subtotal to total villous atrophy had osteopenia (Z score <-1), whereas none of the subjects with normal villous structure had reduced bone densities in the spine or femoral neck. The highest prevalence of osteopenia (66.7%) and the lowest spine (mean -0.89+/-0.36; P = 0.006) and femoral neck (mean -0.63+/-0.29; P = 0.07) Z scores were found among the patients (n = 12) with inflammation in the proximal limb of the pouch. No biochemical parameters were found to predict osteopenia and in stepwise regression analysis, the only independent risk factors for osteopenia were low body mass index and villous atrophy. CONCLUSIONS: Patients with a J-pouch showing high inflammatory activity and villous atrophy in the pouch need long-term follow-up and should be ensured adequate intake of calcium and vitamin D.

Bone Density↗
PubMed2002

Increased adhesion molecule expression in serosal fibroblasts isolated from patients with inflammatory bowel disease is secondary to inflammation.

OBJECTIVE: To examine the expression of adhesion molecules by serosal and dermal fibroblasts in patients with inflammatory bowel disease. SUMMARY BACKGROUND DATA: The pathophysiologic process that leads to stricture formation in Crohn's disease (CD) is unknown. Serosal fibroblasts in these patients have an enhanced ability to contract collagen. This property may be reflected in fibroblast adhesion molecule expression, which in turn may be constitutive or secondary to the inflammatory process in patients with CD. METHODS: Fibroblasts were isolated from inflamed and macroscopically normal serosa of patients with CD or ulcerative colitis (UC) and from normal serosa of patients with colon cancer. Dermal fibroblasts were also isolated from the wound edge. Cell surface and whole cell expression of ICAM-1 were evaluated by flow cytometry and Western blot analysis, respectively. NFkappaB was measured by mobility shift assay in parallel experiments. Interleukin 1beta was added to the culture medium. RESULTS: Expression of ICAM-1 and NFkappaB, increased in patients with both CD and UC, was unaltered by interleukin 1beta. The whole cell concentration of ICAM-1 was greater in patients with CD than in patients with UC. Dermal fibroblasts did not display these features. CONCLUSIONS: Patients with inflammatory bowel disease display enhanced ICAM-1 expression in serosal fibroblasts but not dermal fibroblasts, indicating a secondary response to inflammation.

Colitis, Ulcerative↗
PubMedDate not supplied

[Microscopic colitis in patients with chronic diarrhea].

It has recently been suggested that there is an association between infectious gastroenteritis and irritable bowel syndrome with chronic diarrhea; and a striking similarity between the microscopic lesion observed in this condition and the lesion described in microscopic colitis (MC). As in developed countries MC is found in only 12.6 to 15% of patients with chronic diarrhea, we thought it worthwhile to investigate in Perú, a developing country with high prevalence of infectious gastroenteritis, the prevalence of MC also in patients with chronic diarrhea. One hundred and ten patients with chronic diarrhea underwent biopsies from the right and left colon, and the biopsies were examined histologically to detect MC of lymphocytic or collagenous type.MC was present in 44 (40%) of the 110 patients with chronic diarrhea, being of lymphocytic type in 42, and of collagenous type in. The prevalence of MC observed in Peruvian patients with chronic diarrhea is high when compared to reports from developed countries. This finding supports the idea that infectious gastroenteritis may, under certain conditions, precipitate the appearance of MC, probably by an autoimmune reaction.

Adult↗
PubMedDate not supplied

Assessment of bone and mineral metabolism in inflammatory bowel disease: case series and review.

OBJECTIVE: To determine the prevalence of low bone mass, fractures, and vitamin D deficiency and the levels of biochemical markers of mineral metabolism in patients with inflammatory bowel disease (IBD). METHODS: Our retrospective study consisted of 30 patients with Crohn's disease (CD) and 18 patients with ulcerative colitis (UC). Dual-energy x-ray absorptiometry was performed to determine bone mineral density at the lumbar spine and hip. Serum calcium, phosphorus, parathyroid hormone, 25-hydroxyvitamin D (25-OHD), and 1,25-dihydroxyvitamin D, urinary N-telopeptide cross-linked collagen type I, and 24-hour urinary calcium levels were evaluated. RESULTS: On the basis of Z-score definitions of low bone mass in the IBD group as a whole, 13 patients (27%) had low bone mass at the lumbar spine. Similarly, at the femoral neck, 13 patients (27%) had low bone mass. There was a higher prevalence of low bone mass in the UC group than in the CD group, consistent with a high prevalence of fractures in that group. Of all patients with IBD, 65% had a history of fractures, of which 23% were atraumatic. Deficiency of 25-OHD was high, with a prevalence of 55% in patients with UC and 83% in patients with CD. Secondary hyperparathyroidism, defined as a parathyroid hormone level >55 pg/mL in conjunction with a low or normal serum calcium and a low 25-OHD level, was present in 50% of patients with CD and only 7% of patients with UC. CONCLUSION: Metabolic bone disease and fractures are common in IBD. The mean bone mineral density of the spine or femoral neck did not differ significantly between patients with CD and those with UC. Patients with UC had a higher prevalence of low bone mass, as defined by a Z-score of less than -2, than did patients with CD, consistent with a high prevalence of fractures in the UC group. In contrast, hyperparathyroidism attributable to vitamin D deficiency was more prevalent in patients with CD than in those with UC. This finding suggests a different etiologic mechanism of low bone mass in patients with CD.

Adolescent↗
PubMed2003

Intestinal goblet cell autoantibody associated enteropathy.

This report describes a case of refractory enteropathy with circulating intestinal goblet cell autoantibodies (IGA). A 19 year old man with hyperthyroidism had suffered from protracted diarrhoea for nearly 10 years. Histological examination showed evidence of collagenous enterocolitis. The diarrhoea did not improve despite fasting under total parenteral nutrition. An immunofluorescence assay demonstrated IGA without anti-enterocyte autoantibodies, the hallmark of autoimmune enteropathy, although other criteria were fulfilled. None of 109 controls, including 55 cases of inflammatory bowel disease and one of lymphocytic colitis, had IGA. This case is considered to be a variant of autoimmune enteropathy, and might be a distinct entity.

Adult↗
PubMed2005

TGF-beta1 gene transfer to the mouse colon leads to intestinal fibrosis.

Crohn's disease (CD) is a chronic, relapsing inflammatory bowel disease, characterized by transmural inflammation. In CD, the recurrent inflammatory injury and tissue repair that occurs in the intestine can progress uncontrollably, leading to the proliferation of mesenchymal cells as well as fibrosis, characterized by excessive extracellular matrix deposition. These processes thicken the bowel wall, reducing flexibility, and often culminate in obstructive strictures. Because no effective measures are currently available to specifically treat or prevent intestinal stricturing, we sought to gain a better understanding of its pathogenesis by developing a mouse model of intestinal fibrosis. Because transforming growth factor (TGF)-beta1 can mediate both fibrosis and mesenchymal cell proliferation; we studied the effects of delivering adenoviral vectors encoding spontaneously active TGF-beta1 into the colons of mice. We first demonstrated that enema delivery of marker adenoviral vectors led to the transfection of the colonic epithelium and transient transgene expression. Histologically, control vectors caused an acute inflammatory response, involving the recruitment of neutrophils and mononuclear cells into the colonic lamina propria; however, infection caused little if any fibrosis. In contrast, the TGF-beta1 vector caused a more severe and prolonged inflammatory response as well as localized collagen deposition, leading to severe and progressive fibrosis. This was accompanied by the emergence of cells with a myofibroblast phenotype. Ultimately the fibrosis resulted in many of the TGF-beta1-transfected mice developing profound colonic obstruction. Through adenoviral gene transfer technology, we describe a novel mouse model of colitis and implicate TGF-beta1 in the pathogenesis of obstructive intestinal fibrosis.

Adenoviridae↗
PubMed1996

Lymphocytapheresis.

Leukocytapheresis has long been performed with the centrifugal method. But in 1989 in Japan, the Asahi Medical Co. developed the extracorporeal leukocyte-removal filter, Cellsorba. This filter consists of non-woven fabric, which can remove leukocytes from whole blood during extracorporeal circulation. In the incipient stage, this filter was applied to collagen diseases, rheumatoid arthritis, and systemic lupus erythematosus. During the following studies, this filter has been found to have an immunosuppressive effect. Now, it is beginning to be applied to various kinds of autoimmune diseases. Moreover, this filter has recently been recognized to be effective in inflammatory bowel diseases, ulcerative colitis, and Crohn's disease. The outline of Cellsorba and the application of this filter is described here.

Centrifugation↗
PubMed1989

[Mast cells in ulcerative colitis].

Authors have studied the changes in number and electronmicroscopic appearances of mast cells in the mucosa of large intestine of patients suffering from colitis ulcerosa either in its active or remission period. Counting of cells was performed in osmium-fixed, semithin, Giemsa-stained sections to avoid variations in staining due to formaldehyde. In the active stage of the disease the increase in number of mast cells was significant. Their pronounced degranulation was evident in both semi- and ultrathin preparations. Two forms of degranulation were distinguished: 1. by the release of granules; 2. by the extrusion of whole cytoplasmic areas. The latter indicated fast degranulation, in accordance with observations in animal experiments. Mast cells became closely related to the capillaries, Schwann-cells and nerve fibres of the lamina propria, with myofibroblasts and collagenous fibres. At some places they were found between the epithelial cells of Lieberkühn's crypts. It is assumed that this close topographical correlation represents also functional connections. The present morphological findings corroborate current hypotheses and suggest that the increase in number of mast cells in the active stage of coliitis ulcerosa mediates an hyperergic reaction.

Colitis, Ulcerative↗
PubMed1995

T cell adherence and mucosal injury in ulcerative colitis: involvement of integrin-fibronectin interaction in situ.

The mechanism whereby mononuclear cells, including T lymphocytes, accumulate in the mucosal lesions of patients with ulcerative colitis (UC) is unknown. Although the role played by vascular adhesion molecules in the abnormal recruitment of leukocytes has been emphasized, it does appear that fibronectin (FN), an extracellular matrix (ECM) protein, can play an important role in the persistence of active inflammation because of its effects on the proliferation, differentiation, and migration of cells. beta 1-integrins (VLA proteins) mediate cell adhesion to ECM proteins such as fibronectin, laminin, and collagen. Peripheral blood T lymphocytes (PBL-T) showed increased expression of VLA proteins after activation, although the expression of VLA proteins by lamina propria lymphocytes (LPL) is not known. In an in-vitro binding assay, PBL-T showed increased adherence to inflamed mucosa from patients with UC after stimulation with CD3 crosslinking. This adherence was partially inhibited by antibodies specific for plasma FN, VLA-4, VLA-5, and VLA-beta 1, and by the synthetic peptide RGDS. These findings suggest that infiltrating T cells derived from blood use FN receptors to anchor at inflammatory sites. It is conceivable that the inhibition of T cell adherence to ECM by antibodies or synthetic peptides could suppress inflammatory activity in UC.

Cell Adhesion Molecules↗
PubMed1999

Bone loss in patients with inflammatory bowel disease is less than expected: a follow-up study.

BACKGROUND: In spite of the accumulating evidence of an increased prevalence of osteopenia and osteoporosis in patients with inflammatory bowel diseases (IBD), the time course of bone loss is not well described, and there is little knowledge about factors indicating an increased risk of rapid bone loss. METHODS: We conducted a follow-up study in 80 IBD patients (45 men and 25 premenopausal and 10 postmenopausal women), 19 with ulcerative colitis and 61 with Crohn disease, with a mean follow-up time of 568 +/- 60 days, to assess bone loss, risk factors of rapid bone loss, and value of bone markers to predict bone loss. Bone mineral density was measured by dual-energy X-ray absorptiometry, bone formation by bone alkaline phosphatase (BAP), and bone resorption by N-terminal telopeptide of type-I collagen (NTX) and free deoxypyridinoline (DPD). RESULTS: Bone density changes per year were 0.46% +/- 3% at the spine, 0.06% +/- 5.1% at the femoral neck, -1.1% +/- 7.7% at the triangle of Ward, and -0.52% +/- 1.86% at total body level. Type and duration of disease, sex, age, and level of NTX, DPD, and BAP at base line did not show significant differences between patients who lost and those who did not lose bone mass. Bone loss was significantly higher in patients with (n = 28) than in those without steroids (n = 52) at the femoral neck and Ward triangle but not at the spine and total body. CONCLUSIONS: Change in bone mass in IBD patients during short-term follow-up is low on average, but there is great heterogeneity within the population, which cannot be explained by the use of steroids alone. Bone loss cannot be predicted by analysis of bone markers.

Adult↗
PubMed1996

Increased degradation of type I collagen in patients with inflammatory bowel disease.

To assess the mechanisms of osteopenia in inflammatory bowel disease (IBD), the serum markers of bone formation (osteocalcin and carboxyterminal propeptide of type I procollagen (PICP)) and bone degradation (carboxyterminal telopeptide of type I collagen (ICTP)), the bone mineral density (BMD) of the lumbar spine and the proximal femur and calcium intake of 150 unselected IBD patients and 73 healthy controls were investigated. The patients had higher ICTP values (3.69 (SD 1.40) microgram/l) than the healthy controls (3.25 (1.00) microgram/l, p = 0.035), but no differences in serum PICP and osteocalcin between these groups were detected. In the patients, the ICTP, PICP, and osteocalcin values did not have any significant correlation with BMD, but the patients with ICTP values above 3.6 microgram/l had significantly lower Z scores than those with lower ICTP. In the controls, however, a positive correlation between serum ICTP and BMD was found. The ulcerative colitis patients with total colitis had higher values of ICTP (3.96 (1.58) microgram/l) than those with a left sided disease (3.04 (0.86) micrograms/l, p = 0.009). The patients with a history of clinically active disease (n = 20) had higher ICTP (4.58 (1.55) microgram/l) and osteocalcin (12.56 (5.64) microgram/l) values than the patients (n = 130) with quiescent disease (ICTP 3.56 (1.33), p = 0.002, and osteocalcin 9.76 (3.62), p = 0.017). Increased serum osteocalcin, PICP, and ICTP concentrations and reduced BMD Z scores were found in a subgroup of Crohn's disease patients with a history of an active disease (n = 11). Raised serum ICTP and normal values of osteocalcin and PICP in IBD patients show increased breakdown of type I collagen without a compensatory increase in its synthesis suggesting an increased rate of bone degradation as a probable mechanism for osteopenia in IBD. Raised ICTP values are related to reduced bone mineral densities.

Adult↗
PubMed2000

Differential expression of matrix metalloproteinases and their tissue inhibitors in colon mucosa of patients with inflammatory bowel disease.

BACKGROUND/AIMS: Alterations in synthesis and breakdown of extracellular matrix components are known to play a crucial role in tissue remodelling during inflammation and wound healing. Degradation of collagens is highly regulated by a cascade of matrix metalloproteinases (MMPs). The current study was therefore designed to determine gene expression patterns of MMPs and their tissue inhibitors (TIMPs) in single endoscopic biopsies of patients with inflammatory bowel disease (IBD). PATIENTS/METHODS: mRNA expression was measured by quantitative competitive polymerase chain reaction (PCR) in biopsies from patients with ulcerative colitis (n=21) and Crohn's disease (n=21). Protein expression was analysed by western blotting and immunohistochemistry. RESULTS: MMP-2, MMP-14, and TIMP-1 mRNAs were marginally increased in inflamed, but 9-12-fold increased in ulcerated colonic mucosa in IBD whereas TIMP-2 mRNA expression remained unchanged. MMP-1 and MMP-3 mRNA expression correlated well with the histological degree of acute inflammation, resulting in more than 15-fold increased MMP-1 and MMP-3 mRNA levels in inflamed versus normal colon samples from patients with ulcerative colitis and Crohn's disease. CONCLUSION: Profound overexpression of MMP-1 and MMP-3 mRNA transcripts suggests an important role for these enzymes in the process of tissue remodelling and destruction in inflammatory bowel disease.

Acute Disease↗
PubMed2000

IGF-I and procollagen alpha1(I) are coexpressed in a subset of mesenchymal cells in active Crohn's disease.

This study tested the hypothesis that insulin-like growth factor I (IGF-I) expression is increased at sites of fibrosis in diseased intestine of patients with Crohn's disease (CD). IGF-I mRNA was quantified by RNase protection assay in uninvolved and involved intestine of 13 CD patients (10 ileum, 3 colon) and 7 ulcerative colitis (UC) patients (colon). In situ hybridization histochemistry compared the localization of IGF-I and procollagen alpha1(I) mRNAs. Masson's trichrome staining and immunohistochemistry for IGF-I precursor, alpha-smooth muscle actin (A), vimentin (V), desmin (D), and c-kit were used to examine the mesenchymal cell subtypes that express IGF-I and collagen in uninvolved and involved ileum and colon of CD patients and "normal" ileum and colon from noninflammatory controls. IGF-I mRNA was elevated in involved ileum and colon of patients with CD but not in involved colon of patients with UC. IGF-I and procollagen alpha1(I) mRNA showed overlapping distribution within fibrotic submucosa and muscularis propria of involved CD ileum and colon. In involved CD intestine, increased IGF-I precursor expression localized to mesenchymal cells in regions of tissue disorganization and fibrosis in muscularis mucosa, submucosa, and muscularis propria. In these regions, there were increased numbers of V(+) cells relative to normal or uninvolved intestine. Increased IGF-I expression was localized to cells with a phenotype typical of fibroblasts (V(+)/A(-)/D(-)), myofibroblasts (V(+)/A(+)/D(+)), and, to a lesser extent, cells with normal enteric smooth muscle phenotype (V(-)/A(+)/D(+)). We conclude that increased IGF-I expression in multiple mesenchymal cell subtypes and increased numbers of cells with fibroblast/myofibroblast phenotype are involved in fibrosis associated with CD.

Cells, Cultured↗
PubMed1997

Altered bone metabolism in inflammatory bowel disease.

UNLABELLED: A reduced bone mineral density has been reported in inflammatory bowel disease (IBD). OBJECTIVE: To assess the mechanisms of bone disease in IBD. METHODS: We studied in 90 patients (61 with Crohn's disease, 22 with ulcerative colitis, 7 with indeterminate colitis) biochemical markers of bone metabolism in serum and bone mineral density by peripheral quantitative computed tomography at the forearm. RESULTS: Forty-five percent of the patients had a reduced bone density (Z score < -1). Serum calcium was normal in most patients, vitamin D deficiency was documented in 17%. Osteocalcin, a serum marker of bone formation, was decreased in 26% (1.2 +/- 0.1 ng/ml), whereas the carboxyterminal cross-linked telopeptide of type I collagen (ICTP), a recently described serum parameter of bone breakdown, was stimulated in 38% (10.4 +/- 2.3 microg/L). Of 33 patients with increased ICTP levels, 19 showed a decreased bone density (Z score < -1), and 2 of them never received steroids. An active status of the underlying disease in most patients with increased ICTP levels suggests a direct effect of the underlying IBD. In the whole series of patients with a history of active disease (n = 34), 47% had signs of an increased bone degradation (ICTP > 5 microg/L; mean, 12.9 +/- 4.7 microg/L). Data derived from a retrospective survey of 245 patients with IBD suggest that the prevalence of bone fractures in IBD is unexpectedly high, particularly in patients with a long duration of disease, frequent active phases, and high cumulative doses of corticosteroid intake. CONCLUSIONS: Several mechanisms may be involved in IBD-associated bone disease: (1) a high inflammatory activity directly induces bone degradation via yet unknown pathways, (2) treatment with corticosteroids may exert catabolic effects on the bone, or (3) malabsorption and vitamin D deficiency may activate bone turnover.

Adolescent↗
PubMed2003

Expression of ICAM-1 in colon epithelial cells: an ultrastructural study performed on in vivo and in vitro models.

BACKGROUND: Studies have suggested that in ulcerative colitis (UC), intercellular adhesion molecule-1 (ICAM-1) is involved in migration of leukocytes toward the colonic epithelium. A suitable in vitro model of chronic colonic inflammation does not exist, and the role of the epithelium is based on monolayers of cancer cells. Conflicting results exist on epithelial ICAM-1 expression, and the aim of this study was to compare the expression in various models of colonic epithelium. MATERIALS AND METHODS: Colonic biopsies from four UC patients and four controls were examined by cryoimmuno-electron microscopy using ICAM-1-antibodies. In four other controls, the epithelium was isolated from colonic biopsies, embedded in collagen, and evaluated similarly. Isolated crypts and cultured cancer cells were stimulated with interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha). RESULTS: ICAM-1 was not expressed in the biopsies. In contrast, HT29 cells and the collagen-embedded crypts expressed ICAM-1 on the apical membranes proximal to the junctional complexes when stimulated with IFN-gamma or TNF-alpha in a dose-related manner. CONCLUSIONS: ICAM-1 is not expressed on colonic epithelium in vivo. However, both colonocytes and HT29 cells were capable of expressing ICAM-1 on their apical membranes in response to supraphysiologic cytokine concentrations. These observations question the justification of extrapolating observations from colon cancer cell lines to in vivo inflammatory conditions.

Adult↗