Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colitis, Collagenous”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed1997

[Bactericidal permeability increasing protein (BPI-ANCA marked chronic inflammatory bowel diseases and hepatobiliary diseases].

BACKGROUND: Bactericidal permeability increasing protein (BPI) is an antibacterial product of neutrophilic granulocytes that can serve as target antigen for antineutrophil cytoplasmic antibodies (ANCA). The clinical associations of autoantibodies against BPI (BPI-ANCA) are essentially unclear. PATIENTS AND METHODS: 587 sera from patients with chronic inflammatory bowel diseases, inflammatory hepatobiliary diseases, primary systemic vasculitides and other rheumatological diseases were examined for BPI-ANCA by mono-specific ELISA and a standard indirect immunofluorescence test for ANCA. (ACD-CPR versus S-CPR). The treatment groups were similar with respect to age, sex, time interval from collapse to CPR, defibrillation and first epinephrine medication. There was no difference between the ACD group and the standard CPR group in terms of survival rates and neurologic outcome. No differences occurred concerning complications of CPR. CONCLUSION: In our two-tiered EMS system with physician-staffed ambulances ACD-CPR neither improved nor impaired the survival rates and the neurological prognosis in patients with out-of-hospital cardiac arrest. Our results are in accordance with other studies carried out in EMS systems, with first tier call-response intervals between 4 and 6 min. RESULTS: The prevalence of BPI-ANCA was 43% in ulcerative colitis, 23% in Crohn's disease, 35% in primary sclerosing cholangitis, 25% in primary biliary cirrhosis and 29% in autoimmune hepatitides. In a spectrum of systemic vasculitides, inflammatory joint diseases and collagen vascular diseases the prevalence was only 3 to 11%. In contrast to PR3-ANCA and MPO-ANCA, BPI-ANCA was not associated with a particular pattern of fluorescence in the immuno-fluorescence test on ethanol- and formalin-fixed neutrophils. CONCLUSION: This study shows that BPI-ANCA is the third ANCA specificity, besides PR3-ANCA and MPO-ANCA, with a limited spectrum of clinical associations. The diagnostic and prognostic relevance of BPI-ANCA in the above clinical conditions is being examined prospectively.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2006

Modulation of platelet aggregation responses by leukocytapheresis therapy in patients with active ulcerative colitis.

BACKGROUND: Recent studies suggest that platelet activation plays an important role in the pathophysiology of inflammatory bowel disease. In this study, we evaluated the effects of leukocytapheresis (LCAP) on platelet functions in patients with ulcerative colitis (UC). METHODS: Thirteen patients with active UC (five women and eight men) were treated with LCAP therapy. Platelet-rich plasma (PRP) was prepared, and platelet aggregation in response to agonist solution (epinephrine, collagen, and ADP) was measured with a platelet aggregometer. Platelet-derived microparticle (PDMP) plasma levels were determined by enzyme-linked immunosorbent assay. RESULTS: Nine patients responded to LCAP therapy, but no clinical responses were observed in four patients. The aggregation response to 0.1 microg/ml epinephrine was enhanced in all patients. In all responders, enhanced epinephrine aggregation was normalized after the LCAP session. However, in the four nonresponders, enhanced epinephrine aggregation was maintained after the LCAP session. In responders, the mean maximum aggregation induced by 0.1 microg/ml epinephrine was 76.8 +/- 5.0% before and 15.4 +/- 3.8% after LCAP, respectively (P < 0.05). Increased aggregation responses to both 0.2 microg/ml collagen and 1.0 microM ADP were observed, and LCAP also normalized these enhanced responses. LCAP significantly reduced circulating PDMP levels (56.8 +/- 28.3 U/ml before and 46.3 +/- 30.4 U/ml after LCAP, P < 0.05). CONCLUSIONS: LCAP reduced enhanced platelet aggregation responses in active UC patients. Because platelets play an important role in inflammatory and immune responses, therapeutic effects of LCAP may be partially mediated by reduction of increased platelet aggregation activities.

Adult↗
PubMed2003

Abnormal mucosal extracellular matrix deposition is associated with increased TGF-beta receptor-expressing mesenchymal cells in a mouse model of colitis.

Transforming growth factor-beta (TGF-beta) depresses mucosal inflammation and upregulates extracellular matrix (ECM) deposition. We analyzed TGF-beta receptors RI and RII as well as ECM components using the CD4(+) T-cell-transplanted SCID mouse model of colitis. The principal change in colitis was an increased proportion of TGF-beta RII(+) mucosal mesenchymal cells, predominantly alpha-smooth muscle actin (SMA)(+) myofibroblasts, co-expressing vimentin and basement membrane proteins, but not type I collagen. TGF-beta RII(+) SMA(-) fibroblasts producing type I collagen were also increased, particularly in areas of infiltration and in ulcers. Type IV collagen and laminin were distributed throughout the gut lamina propria in disease but were restricted to the basement membrane in controls. In areas of severe epithelial damage, type IV collagen was lost and increased type I collagen was observed. To examine ECM production by these cells, mucosal mesenchymal cells were isolated. Cultured cells exhibited a similar phenotype and matrix profile to those of in vivo cells. The data suggested that there were at least two populations of mesenchymal cells responsible for ECM synthesis in the mucosa and that ligation of TGF-beta receptors on these cells resulted in the disordered and increased ECM production observed in colitic mucosa.

Activin Receptors, Type I↗
PubMed2005

Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts.

BACKGROUND & AIMS: Interleukin (IL)-22, a member of the IL-10 subfamily, is a recently identified T-cell-derived cytokine. We investigated IL-22 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and analyzed its biologic activities in human colonic subepithelial myofibroblasts (SEMFs). METHODS: Mucosal IL-22 expression was evaluated by immunohistochemical procedures. The effects of IL-22 on colonic SEMFs were investigated by cDNA microarrays, Northern blots, enzyme-linked immunosorbent assay, and electrophoretic gel mobility shift assays (EMSAs). RESULTS: IL-22 was not detectable in normal colonic mucosa. In IBD mucosa, IL-22 expression was detectable in CD4-positive T cells. IL-22-positive cells were increased in ulcerative colitis and even more so in Crohn's disease. IL-22 receptor expression colocalized with a marker of SEMFs. IL-22 did not modulate SEMF proliferation and collagen synthesis. cDNA microarray analyses demonstrated that, in colonic SEMFs, IL-22 increased the messenger RNA (mRNA) expression of inflammatory cytokines (IL-6, IL-8, IL-11, and leukemia inhibitory factor [LIF]), chemokines, and matrix metalloproteinases. IL-22 induced an activation of nuclear factor (NF)-kappaB and activating protein (AP)-1 within 1 hour, and a blockade of NF-kappaB and AP-1 activation markedly reduced IL-22 induction of IL-6, IL-8, IL-11, and LIF mRNA. MAP-kinase inhibitors (PD98059, U0216, and SB202190) significantly reduced IL-22 induction of cytokine secretion. The combination of either IL-17 plus IL-22 or IL-19 plus IL-22 additively up-regulated cytokine secretion. CONCLUSIONS: IL-22 derived from activated T cells acts on SEMFs to elicit expression of proinflammatory cytokines and matrix-degrading molecules indicating proinflammatory/remodeling roles in IBD.

Colon↗
PubMed1989

Mortality from ischemic colitis.

Thirty-nine hospital-based cases of ischemic colitis were reviewed. There were 18 males and 21 females. Average age was 68.7 years (range, 18 to 92 years). Associated diseases among 13 patients younger than 65 included renal failure in seven patients and hematologic, vasculitic, or collagen vascular diseases in four. In 26 patients 65 or older, congestive heart failure was seen in 13, vascular disease in eight, and previous aortic surgery in four. Nineteen patients were treated nonsurgically and 8 died (42 percent mortality). Twenty patients (51 percent) underwent surgery: 18 had resection with colostomy or ileostomy and two had resection with reanastomosis; one patient underwent laparotomy followed by second-look exploration without resection. Thirteen of the 20 surgical patients died (65 percent mortality). Both patients who underwent reanastomosis died of sepsis. The data show a close association between ischemic colitis and a number of serious systemic diseases including renal failure, arteriosclerotic heart and vascular disease, and hematologic, vasculitic, and connective-tissue disease. A predilection for the right colon and sigmoid colon and splenic flexure was seen. A formidable mortality rate (53 percent) was found among patients treated both surgically and nonsurgically.

Adolescent↗
PubMed1992

Cellular localization of procollagen gene transcripts in inflammatory bowel diseases.

The cellular localization of procollagen types I, III, IV, and V gene transcripts was determined in tissues from 12 patients with either Crohn's disease (CD) or ulcerative colitis (UC) and nine controls by in situ hybridization with 35S-labeled RNA probes. In CD, the signal intensity and number of labeled cells were significantly increased, particularly in deeper intestinal layers. In contrast, the labeled cells in UC were concentrated in the subepithelial intestinal layers, with an overexpression of procollagen III RNA transcripts. Immunohistological stainings for procollagen types I, III, and IV showed a weaker staining in UC than in CD, indicating that increased transcript levels in UC are unrelated to the enhanced collagen protein deposition, although the increase of procollagen messenger RNA levels correlated with the density of the inflammatory infiltrate. It was concluded that both CD and UC show highly increased procollagen RNA transcript levels but differ in collagen deposition. Thus, different posttranscriptional or posttranslational regulatory mechanisms, such as collagen degradation, may account for the observed differences.

Adult↗
PubMed1998

Reduced bone mineral density and unbalanced bone metabolism in patients with inflammatory bowel disease.

Patients with chronic inflammatory bowel diseases (IBD) are at increased risk to develop osteopenia and osteoporosis. New parameters for the assessment of bone formation and especially bone resorption have significantly improved the diagnostic procedures to characterize bone metabolism. Biochemical characterization of bone turnover in IBD patients may provide important information about the pathogenesis of osteoporosis in this patient population. A cross-sectional study was performed. One hundred forty-nine patients (77 men, 52 premenopausal, and 20 postmenopausal women) with IBD (104 with Crohn's disease [CD] and 45 with ulcerative colitis [UC]) underwent clinical, osteodensitometric, and metabolic bone assessment. Bone mineral density was determined by dual energy X-ray absorptiometry. Bone formation (bone alkaline phosphatase), bone resorption (N-terminal telopeptide of type-I collagen, free desoxypyridinoline, total pyridinoline, and desoxypyridinoline), vitamin D, and parathyroid hormone were assessed. Thirty-six percent of patients with CD and 32% with UC showed osteopenia, 15% with CD and 7% with UC showed osteoporosis. Bone resorption was significantly increased in IBD patients compared to normal controls, whereas bone formation did not show a compensatory increase. Bone formation was even more suppressed in the subset of patients currently treated with corticosteroids. Our data confirm the high prevalence of osteopenia and osteoporosis reported in IBD patients. Furthermore, we provide evidence for an increased bone resorption accompanied by low bone formation in IBD patients. This imbalance of bone metabolism is likely to be one of the reasons for increased bone loss in IBD patients.

Absorptiometry, Photon↗
PubMed1993

Host factors predisposing to anaerobic infections.

Factors that predispose to infection in general, of course, may predispose to infection with anaerobes. Included in this category are diabetes mellitus, neutropenia, hypogammaglobulinaemia, malignancy, splenectomy, collagen vascular disease, cytotoxic drug therapy, corticosteroid therapy and other immunosuppression. However, even with these situations there may be certain, more specific, associations: anaerobic cholecystitis and anaerobic osteomyelitis in diabetics, neutropenic colitis, and the increased incidence of local anaerobic infections associated with carcinoma of the lung, colon and uterus. Conditions that lead to decreased redox potential more specifically predispose to infection with anaerobes. Included in this category are obstruction and stasis, tissue anoxia, tissue destruction, vascular insufficiency, prior aerobic infection, burns, foreign body implantation, and calcium salts in a wound (in association with fractures). Other specific clinical situations that predispose to anaerobic infections include leukaemia; oral, gastrointestinal, and female pelvic surgery; trauma at other sites; childbirth; aspiration pneumonia; human and animal bites; and therapy with agents with poor activity against anaerobes (e.g. aminoglycosides, quinolones). AIDS patients appear to be predisposed to severe periodontal disease and its complications.

Bacteria, Anaerobic↗
PubMed1998

[RETRACTILE MESOCOLONITIS: PATHOPHISIOLOGY AND COMPLICATIONS]

The mesentery and mesocolon are structures with suspensory functions of the small bowel and colon respectively. When they are involved by prominent fibroblastic proliferation tissue, this is know as retractile mesenteritis and retractile mesocolonitis. The retractile mesocolonitis is associated with sigmoid volvulus, and is a common finding in the rural areas of Puno (Peru). The common macroscopic appearance consists of a markedly thickened mesentery of rubbery consistency, and the retraction predisposing a twist of the bowel. The histologic features include fibrosis with massive accumulation of dense collagenous tissue. These lesions can be the expression of a reparative proccess that occurs in response to mesenteric injury of enteric bacteria (bacterial transiocation) or inflammatory response. Repeated attacks of bacterial colitis might lead to scarring of the mesocolon.

Journal Article↗
PubMed2007

Germinated barley foodstuff suppresses dextran sulfate experimental colitis in rats: the role of mast cells.

Recent studies have suggested that dietary fiber exerts a therapeutic effect on inflammatory bowel disease patients. The aim of this study was to evaluate the effects of a dietary fiber, germinated barley foodstuff (GBF), derived from the aleurone and scutellum fraction of germinated barley against dextran sulfate sodium (DSS)-induced experimental colitis in rats. Sprague-Dawley rats were fed a 3% DSS diet containing GBF or alpha-cellulose for 8 days. The mucosal damage (macroscopic and microscopic inflammation) was then quantified. In addition, we evaluated the alterations in the mucosal mast cells and connective tissues. GBF effectively prevented mucosal damage. In addition, GBF suppressed the infiltration of the mucosal mast cells, and prevented the distraction of both collagen and elastic fibers. These effects may be closely associated with its inhibitory effects on mucosal mast cells, and the destruction of the mucosal connective tissues.

Animals↗
PubMed1989

Mast cells in ulcerative colitis. Quantitative and ultrastructural studies.

The changes in the number and ultrastructure of mast cells were studied in 37 colonoscopical biopsies from patients with ulcerative colitis. Changes in the active stage of the disease and during remission were compared. Cell counts were performed on semithin sections stained with Giemsa after osmium tetroxide fixation. This method overcome the uncertain staining found after formalin fixation. Accumulation of mast cells accompanied by intense degranulation was found to be significant in the active stage of the disease. Two forms of degranulation were observed: discharge of the individual granules and protrusion and detachment of the cytoplasmic processes containing granules. The latter was a sign of rapid degranulation, as described earlier in animal experiments. Mast cells were closely associated with capillary blood vessels, Schwann cells, neural fibres, myofibroblasts and collagenous fibres, and were also present between epithelial cells. It is assumed that close topographic contact may also imply a functional correlation.

Adult↗
PubMed1997

The effect of prostaglandin E1 on experimental colitis in the rat.

Prostaglandin E1 (PGE1) is known to have a strong vasodilator effect and to block coagulation and inflammation in high concentrations. The aim of this study has been to investigate whether PGE1 has an inhibitory effect on inflammation in experimental colitis. Experimental colitis was produced by rectal instillation of 10% acetic acid in 60 rats. These were divided into prostaglandin (PG) (n = 30) and control groups (n = 30). Twelve hours later, an intraperitoneal injection of 2 micrograms PGE1 in 1 ml saline was given to the PG group and 1 ml saline to the control group. This was repeated daily and the animals were sacrificed in groups of 10 on the 3rd, 7th and 10th day. Histopathological examination and hydroxyproline determination for assessment of collagen synthesis were performed. PGE1 significantly decreased inflammation on third day with the hydroxyproline level significantly higher in the PG group compared with the control group (p < 0.05). This difference was however not significant at the 7th and 10th day. The present study supports a beneficial role for prostaglandin E1 in reducing the severity of colonic inflammation following chemically induced colitis but only in the early stages of development.

Alprostadil↗
PubMed1983

Stromal cell changes in human colorectal adenomas and carcinomas. An ultrastructural study of fibroblasts, myofibroblasts, and smooth muscle cells.

Structural changes in stromal cells during the development of human colorectal carcinomas were studied by light and electron microscopy. The results were as follows: Stromal cells of the lamina propria in control subjects consisted principally of resting fibroblasts. Stromal fibroblasts were mildy activated in adenomas with mild -moderate atypia, and more markedly in adenomas with severe atypia (carcinoma in situ). In invasive adenocarcinomas, (a) desmoplastic reaction was induced, (b) stromal fibroblasts proliferated significantly and were activated showing enlarged nuclei and abundant rough endoplasmic reticulum, and (c) some smooth muscle cells were endowed with well-developed rough endoplasmic reticulum in their axial cytoplasm, resulting in a similar appearance to "myofibroblasts". Stromal fibroblasts in ulcerative colitis and proctitis were also activated. Morphometric analysis revealed that activated fibroblasts significantly increased the areas of their nuclei and cytoplasm, and the perimeter of rough endoplasmic reticulum. These activated fibroblasts suggested a higher production of collagen and other connective tissue proteins. Bundles of microfilaments of actin type were readily found in fibroblasts in all cases examined. These filaments were most remarkable in the fibroblasts in the desmoplastic stroma of invasive adenocarcinoma and were considered to be one of the basic components of these cells. Relationships between fibroblasts, "myofibroblasts", and smooth muscle cells are discussed.

Adenocarcinoma↗
PubMed1990

Giant inflammatory polyps associated with idiopathic inflammatory bowel disease. An ultrastructural study of five cases.

Five cases of giant inflammatory polyps associated with idiopathic inflammatory bowel disease are reported. Polyps produced intestinal obstruction in three cases; consequently, surgery was performed. In a further two cases, intestinal bleeding was improved by endoscopic polypectomy. Electron microscopy showed fibroblasts, myofibroblasts, mast cells, lymphocytes, collagen fibers, capillaries, and venules. Remnants of the original mucosal epithelial cells, smooth muscle cells, and hypertrophic autonomous nerve plexuses were noted. Nerve fibers were interwoven with the matrix of the polyps. Mast cells were closely linked with vessels, nerves, and collagen fibers. They may have an important role in the excessive granulation, angiogenesis, and fibrotic process in giant inflammatory polyps.

Adult↗
PubMed2003

Increased serum bone sialoprotein concentrations in patients with Crohn's disease.

INTRODUCTION: Impaired calcium homeostasis and/or the administration of corticosteroids are considered to be among the factors contributing to the pathogenesis of osteopenia in patients with inflammatory bowel disease. There is an increasing evidence suggesting that certain pro-inflammatory cytokines may also directly influence the bone metabolism in these patients. Routine measurement of bone mass and loss usually include dual energy X-ray absorptiometry as well as urinary and serum assessment of collagen crosslinks. More recent studies include likewise the detection of bone sialoprotein into a specific diagnostics of bone turnover. PATIENTS AND METHODS: We investigated 47 patients with inflammatory bowel disease (Crohn's disease N = 41, ulcerative colitis N = 6) and 17 healthy volunteers to assess and compare serum levels of bone sialoprotein and other routine parameters of bone turnover. Bone sialoprotein levels were measured by using a recently described radioimmunoassay. RESULTS: In comparison to the control group, bone sialoprotein and urinary crosslinks were significantly increased only in patients with Crohn's disease, while other markers of bone turnover (e. g. alkaline phosphatase, carboxylterminal propeptide of typ I procollagen, urinary deoxypyridinoline, vitamin D, phosphate and calcium) did not differ significantly between the patients' groups. CONCLUSION: According to these data, increased serum bone sialoprotein concentrations seem to be an additional valuable and sensitive marker of bone resorption in patients with Crohn's disease.

Adult↗
PubMedDate not supplied

Growth hormone in inflammatory bowel disease.

Crohn's disease and ulcerative colitis are inflammatory diseases of the gastrointestinal tract characterized by chronic relapsing inflammation and catabolism. Growth hormone/insulin-like growth factor-I axis is important in inflammatory bowel disease, because of the effects on epithelial cell kinetics, collagen deposition and immunomodulation. The potential of growth hormone as a therapeutic option in inflammatory bowel disease has been proven in various clinical settings. Acquired growth hormone resistance in inflammatory bowel disease seems to be mediated by a combination of undernutrition and active inflammation. In particular, proinflammatory cytokines, such as TNF-a and interleukin-6, have been implicated as potential mediators of growth hormone resistance. The introduction of anti-TNF-alpha monoclonal antibodies has proven very efficacious in patients with inflammatory bowel disease. By reducing cytokines levels in inflammatory cells of intestinal mucosa, infliximab could interfere with cytokine-induced growth hormone resistance. Recent in vivo data have shown that acquired growth hormone resistance in patients with inflammatory bowel disease may be reversed after the administration of anti-TNF-alpha therapy.

Animals↗
PubMed2001

Chronic use of non-steroidal anti-inflammatory drugs does not alter colonic mucosa of patients without diarrhoea.

BACKGROUND: Several types of colitis can be NSAID-induced, but whether chronic use of NSAIDs alters colonic mucosa in patients without diarrhoea is not known. PATIENTS AND METHODS: Biopsy specimens of rectal mucosa were taken in six patients with rheumatoid arthritis without diarrhoea receiving NSAIDs (group 1, n=6). Patients with rheumatoid arthritis without diarrhoea not receiving NSAIDs (group 2, n=9), and patients undergoing surveillance colonoscopy (group 3, n=23) served as controls. In all patients from the three study groups, intraepithelial lymphocyte count and apoptotic cell count were assessed, and sub-epithelial collagen band thickness was measured. Leucocyte population of lamina propria was evaluated semi-quantitatively. HLA-DR and CD25 expression of mucosal cells was appreciated by immunohistochemistry. RESULTS: Intraepithelial lymphocyte count was in the normal range in all three group patients, and not statistically different between groups. Apoptotic epithelial cell count was not different between groups. Sub-epithelial collagen band thickness was normal in all the patients. No patient had a marked infiltration of lamina propria by leucocytes, and HLA-DR and CD25 were normally expressed in all patients. CONCLUSION: These results from a small sample of patients suggest that patients without diarrhoea receiving NSAIDs on a long-term basis do not develop microscopic or inflammatory colitis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

ADAM15 upregulation and interaction with multiple binding partners in inflammatory bowel disease.

A disintegrin and metalloproteinase (ADAM)15 is upregulated in some tissues undergoing remodeling. This glycoprotein is characterized by adhesive function through its interaction with members of the integrin family and protease properties. The goal of this work was to describe the tissue distribution of ADAM15 and its spatial relationship with its known binding partners in inflammatory bowel disease. ADAM15 expression was examined using frozen tissues from eight patients with ulcerative colitis or Crohn's disease and four normal colons by immunohistochemistry, immunoblotting and quantitative reverse transcription-polymerase chain reaction. In addition expression of alpha5beta1- and alphavbeta3-integrins, VE-cadherin, alpha-smooth muscle actin (alpha-SMA) and collagen IV was examined using immunohistochemistry and confocal microscopy. In the normal colon, ADAM15 was expressed by all epithelial cells throughout the crypt and by pericryptic myofibroblasts coexpressing alpha-SMA and collagen IV. ADAM15 was also expressed by endothelial cells and vascular myocytes in all layers of the intestinal wall as well as by nonvascular myocytes of the muscularis mucosae and muscularis propria. In inflammatory bowel diseases, ADAM15 was strongly upregulated at the mRNA level and expressed only as an active form as shown by immunoblotting analysis. Parallel to its upregulation, ADAM15 expression was found both at the plasma membrane and in the cytoplasm of epithelial cells in acute attacks of the disease. In the crypt abcesses, ADAM15-positive epithelial cells were in close contact with alpha5beta1-integrin-positive leukocytes localized between these cells and in the crypt lumen. In the regenerative areas, ADAM15-positive epithelial cells were in close contact with alpha5beta1- and alphavbeta3-positive pericryptic myofibroblasts. In endothelial cells, VE-cadherin was decreased. In contrast, ADAM15 was strongly expressed by endothelial cells and was in close contact with alpha5beta1-positive leukocytes. There is a differential expression of ADAM15 in epithelial cells during inflammatory bowel disease compared with the normal colon. In addition, the spatial relationships with its binding partners suggest a role for ADAM15 in the differentiation of regenerative colonic mucosa as well as in leukocyte transmigration across epithelial and endothelial barriers.

ADAM Proteins↗