Intestinal Mucosa Of Patients Research Articles

Activation of CD40-CD154 co-stimulatory pathway and its correlation with disease activity in patients with inflammatory bowel disease

Objective To investigate the expression of CD40-CD154 co-stimulatory pathway in peripheral circulation and intestinal mucosa in patients with inflammatory bowel disease （IBD）, the difference between the expression of CD40-CD154 in patients with IBD and that in healthy controls, and the correlation between CD40-CD154 levels and disease activity. Methods A total of 62 patients with Crohn＇s disease （CD）, 64 patients with ulcerative colitis （UC） and 56 healthy controls were enrolled. Enzyme-Linked Immuno Sorbent Assay （ELISA）, SYBR-green real time PCR and immunohistochemical assay were respectively applied to evaluate expression of CD40-CD154 in plasma, mononuclear cells of peripheral blood and intestinal mucosa. Results Levels of CD40 （ P = 0. 000） and CD154 （P = 0. 001 ） in plasma, mononuclear cells of peripheral blood and intestinal mucosa were significantly higher in patients with CD and UC than in healthy controls. However, no correlation between disease activity and CD40-CD154 expression in peripheral circula- tion or intestinal mucosa was detected （ P 〉 0. 05 ）. Conclusion CD40-CD154 pathway activation is found in plasma, peripheral blood mononuclear ceils and intestinal mucosa in patients with IBD, but is not correlated with disease activity. Key words: Colitis, ulcerative ; Complement pathway; Crohn＇s disease

Significance of interleukin-27 expression in the intestinal mucosa of patients with inflammatory bowel disease

Significance of interleukin-27 expression in the intestinal mucosa of patients with inflammatory bowel disease

Study on activation of CD27-CD70 co-stimulatory pathway in patients with inflammatory bowel disease

Objective To investigate the expression of CD27-CD70 co-stimulatory pathway in peripheral circulation and intestinal mucosa of patients with inflammatory bowel disease, and to find the difference between the expression of CD27-CD70 in patients with inflammatory bowel disease and in healthy controls. Methods A total of 62 patients with Crohn's disease, 64 patients with ulcerative colitis and 56 healthy controls were enrolled. Enzyme-linked immunosorbent assay was applied to evaluate plasma CD27-CD70 protein expression in patients with inflammatory bowel disease and healthy controls. SYBR-green real time PCR was applied to access CD27-CD70 mRNA expression in peripheral blood mononuclear cells in patients with inflammatory bowel disease and healthy controls.And CD27-CD70 protein expression in intestinal mucosa was determined by immunohitochemistry.Results Plasma levels of CD27 (P=0. 025) and CD70 (P=0. 000) were significantly higher in patients with Crohn's disease than in healthy controls. However, CD27 (r= 0. 055, P= 0. 673) and CD70 (r= 0. 024, P = 0. 852) were not significantly associated with endoscopic disease activity in patients with Crohn's disease. Similarly, CD27 (P=0. 001) and CD70 (P=0. 000) were significantly higher in patients with ulcerative colitis than in healthy controls. And CD27 (r=0. 077, P=0. 547)and CDT0 (r=0.021, P=0. 869) were not significantly associated with endoscopic disease activity in patients with ulcerative colitis. Moreover, CD27 and CD70 mRNA expression in peripheral blood mononuclear cells were significantly higher in patients with Crohn's disease and ulcerative colitis than in healthy controls (all P=0. 000), and immunostaining indicated that CD27 and CD70 expression in intestinal mucosa were significantly higher in patients with Crohn's disease and ulcerative colitis than in healthy controls (all P=0. 000). Conclusions CD27-CD70 pathway activated in plasma, peripheral blood mononuclear cells and intestinal mucosa of patients with inflammatory bowel disease. However,plasma levels of CD27 and CD70 can not reflect endoscopic disease activity. Key words: Crohn's disease; Ulcerative colitis; Antigens; CD27; Antigens; CD70

Effect of compound Sophorae Flavescentis Jiechangrong capsule on expression of NF-κB p65 and STAT6 in the intestinal mucosa of patients with ulcerative colitis

The effects of compound Sophorae Flavescentis Jiechangrong capsule (CSFJC) on the expression of nuclear factor-κB p65 (NF-κB p65) and signal transducer and activator of transcription 6 (STAT6) in the intestinal mucosa of patients with ulcerative colitis and the possible mechanism were investigated. Eighteen patients with ulcerative colitis were randomly divided into a traditional Chinese medicine (TCM) group (n = 11) treated by CSFJC and a western medicine (WM) group (n = 7) treated by Sulfasalazine tablets. The treatment duration lasted eight weeks. Before and after the treatment, the symptoms and the physical signs were observed, and the routine stool test, the colonoscopy, and pathological examination were performed in the two groups. The expression levels of NF-κB p65 and STAT6 were detected by using immunohistochemistry. The results showed that the total effective rate of the curative effectiveness in TCM and WM groups was 100% and 71.4%, respectively, and the total effective rate of colonic mucosa lesion in TCM and WM groups was 90.9% and 71.4%, respectively, with the differences being significant (all P<0.05). The total effective rate of syndromes of damp-heat blocking according to the TCM in TCM and WM groups was 90.9% and 71.4%, respectively. After the treatment, the expression of NF-κB p65 and STAT6 in the two groups was decreased, and the decrease of NF-κB p65 and STAT6 expression in TCM group was more significant than in WM group (P<0.05). It was concluded that CSFJC can inhibit the activation and expression of NF-κB p65 and STAT6 in the intestinal mucosa of patients with ulcerative colitis, which is a possible mechanism for CSFJC treating ulcerative colitis.

Long-term and acute effects of gliadin on small intestine of patients on potentially pathogenic networks in celiac disease

Celiac disease (CD) is a complex, immune-mediated intolerance to gliadin that develops in genetically susceptible individuals. Although the main driving force of the disease is an aberrant autoimmune response, several other pathogenic mechanisms, many still unidentified, are also involved. In order to describe at a network level the alterations provoked by a gliadin insult on the intestinal mucosa of patients, we compared the expression profiles of biopsies from 9 active and 9 treated patients (long-term effects of gliadin), and of 10 biopsies from gluten-free diet treated patients that were incubated in vitro with or without gliadin (acute effects) and integrated significantly altered transcripts into potentially pathogenic biological processes. Using information on Kyoto Encyclopedia of Genes and Genomes pathways and Gene Ontology terms represented among the differentially expressed genes, we observed important dysfunction in several complex networks, including those related to cell–cell communication, intracellular signaling, ubiquitin–proteasome system, cell cycle/apoptosis and extracellular matrix. The reconstruction of the role of these biological networks in the development of the intestinal lesion in CD provides a comprehensive picture of key events that contribute to the disease, and could point towards novel functional candidates that might be potential therapeutic targets or responsible for genetic susceptibility.

Expression of integrin alphavbeta6 in the intestinal epithelial cells of patients with inflammatory bowel disease.

Background and aims:The prevalence of inflammatory bowel disease (IBD) is about 0.05% in industrialized countries. The pathogenesis of IBD remains to be further understood. The present study aims to elucidate the expression of integrin αvβ6 in the intestinal mucosa of patients with IBD.Materials and Methods:Colonic biopsy was obtained from a group of IBD patients. The expression of αvβ6 in the intestinal mucosa was detected by Western blotting. Human colonic epithelial cell line T84 cells were stimulated by microbial antigen flagellin. The expression of αvβ6 in T84 cells was evaluated by quantitative RT-PCR and Western blotting.Results:The levels of αvβ6 in the intestinal mucosa were much lower than it in normal control subjects. The serum levels of myeloperoxidase (MPO) were higher in IBD patients that were negatively correlated with the levels of αvβ6 in the intestinal mucosa. The expression of αvβ6 was detectable in T84 cells at naοve status that could be upregulated by exposure to microbial antigen flagellin. Pretreatment with MPO dramatically suppressed the expression of αvβ6 in T84 cells.Conclusions:We conclude that the expression of αvβ6 was suppressed in IBD intestinal mucosa, which could be resulted from the high levels of MPO.

The combination of polymorphisms within MCP‐1 and IL‐1β associated with ulcerative colitis

Monocyte chemoattractant protein-1 (MCP-1) is a chemokine involved in monocyte recruitment to sites of inflammation. Raised level of MCP-1 has been widely demonstrated in the intestinal mucosa of patients with ulcerative colitis (UC), suggesting an important role of MCP-1 in the pathogenesis of UC. The -2518A/G polymorphism in the promoter region of MCP-1 gene affecting its transcriptional activation has been reported recently. In order to assess the potential role of this polymorphism in UC, we examined its distribution in 162 unrelated UC patients and 203 healthy controls. In addition, considering the gene regulatory association between interleukin-1beta (IL-1beta) and MCP-1, we further examined whether the gene polymorphisms between MCP-1 and IL-1beta exert synergetic effects on risk of UC. Our results show that the distribution of MCP-1 genotype or allele frequencies between UC patients and controls was not significantly different; however, the association between the polymorphism of MCP-1 -2518 GG and the polymorphism of IL-1beta-511 T in UC patients is significant (OR 2.062, 95% CI 1.034-4.113, P = 0.038). This is the first report describing the association between MCP-1 polymorphism and UC, and our data suggest that the MCP-1 -2518 polymorphism itself does not represent an independent genetic risk factor for UC. In contrast, the combination polymorphisms between MCP-1 and IL-1beta can increase UC risk significantly, which might help us understand the molecular mechanism underlying the development of UC.

Síndrome del intestino irritable y enfermedad inflamatoria intestinal: ¿alguna conexión?

Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders and is that with the greatest socioeconomic impact worldwide. Diagnosis of IBS is based on clinical criteria that have been modified over time, the Rome II criteria being those that are currently followed. Some of the symptoms of IBS are similar to those in patients with inflammatory bowel disease (IBD), which can hamper or delay diagnosis. The use of inflammatory markers in stools (such as calprotectin) may help to distinguish between these two entities. A possible connection between IBS and IBD could be based on five points: (i) both disorders have similar symptoms; (ii) symptoms often overlap in the same patients; (iii) IBS and IBD have a common familial aggregation; (iv) some predisposing factors, such as a history of acute gastroenteritis, play a role in both disorders, and (v) importantly, signs of microinflammation are found in the bowels of patients with IBS. With regard to this latter point, an increase in inflammatory cells has been found in the intestinal mucosa of patients with IBS and, more specifically, mastocytes have been found to be increased in the jejunum and colon while CD3 and CD25 intraepithelial lymphocytes have be observed to be increased in the colon. Moreover, activated mastocytes are increased near to nerve endings in patients with IBS and this finding has been correlated with the intensity of both intestinal symptoms (abdominal pain) and psychological symptoms (depression and fatigue). A good model of microinflammation is post-infectious IBS, since the timing of the onset of the infectious process is known. In patients with post-infectious IBS, an increase in intraepithelial lymphocytes and enterochromaffin cells is initially found, which is reduced over time; consequently, although the symptoms of IBS persist, after 3 years no differences are detected in the number of inflammatory cells between IBS patients and controls. Among the various factors that can favor the development of IBS in these patients, two host-dependent mechanisms are most closely implicated in the physiopathology of IBS: polymorphism of the genes codifying pro- or anti-inflammatory cytokines and psychological factors such as anxiety, depression, somatization and neuroticism at the time of the acute infection. In view of all of the above, the similarities between IBS and IBD are probably more than mere coincidence and may reflect distinct manifestations of a broad spectrum of inflammation in the colon.

Differential expression and regulation of ADAM17 and TIMP3 in acute inflamed intestinal epithelia

The acute phase of Crohn's disease (CD) is characterized by a large afflux of polymorphonuclear leukocytes (PMNL) into the mucosa and by the release of TNF-alpha. Conversion of inactive TNF-alpha into an active form requires the cleavage of a transmembrane TNF-alpha precursor by the TNF-alpha-converting enzyme (ADAM17), a protease mainly regulated by the tissue inhibitor of metalloproteinase 3 (TIMP3). The aim of the present study was to investigate in an in vitro model of PMNL transepithelial migration and in the intestinal mucosa of patients with CD the expression and regulation of ADAM17 and TIMP3 in intestinal epithelial cells (IEC). ADAM17 and TIMP3 expression was analyzed by Western blotting, RT-PCR, confocal microscopy, and immunohistochemistry by using the T84 model and digestive biopsies. ADAM17 expression in IEC was increased at a posttranscriptional level during the early phase (from 2 to 4 h) of PMNL transepithelial migration whereas TIMP3 was only increased 24 h later. TNF-alpha induced an early upregulation of ADAM17 in T84 cells, whereas PMNL adhesion, H(2)O(2), or epithelial tight junction opening alone did not affect the amount of ADAM17. Immunohistochemistry of intestinal biopsies revealed that strong expression of ADAM17 was associated with a high activity of CD. In contrast, TIMP3 was very poorly expressed in these biopsies. ADAM17 and TIMP3 profiling did not correlated with the NOD2/CARD15 status. The ADAM17 activity was higher both in the early phase of PMNL transepithelial migration and in active CD. These results showed early posttranscriptional upregulation of ADAM17 in IEC linked to PMNL transepithelial migration and a high activity of CD.

Expression of cluster of differentiation antigen-14 in intestinal mucosa of patients with inflammatory bowel disease and its implication

Expression of cluster of differentiation antigen-14 in intestinal mucosa of patients with inflammatory bowel disease and its implication

Clinicopathological significance of eosinophil granulocyte infiltration in the intestinal mucosa of patients with ulcerative colitis

Clinicopathological significance of eosinophil granulocyte infiltration in the intestinal mucosa of patients with ulcerative colitis

Degeneration of the Pericryptal Myofibroblast Sheath by Proinflammatory Cytokines in Inflammatory Bowel Diseases

Inflammatory bowel diseases (IBDs) are characterized by remodeling of the intestinal mucosa, which is associated with excessive cytokine release. Previous studies have shown that the epithelium in the crypt region of the mucosa in patients with Crohn's disease is susceptible to proinflammatory cytokines. We investigated whether the subepithelial myofibroblasts in this region were affected by these inflammatory conditions. Immunofluorescence and immunohistochemistry were performed on inflamed and uninflamed specimens from patients with IBD to detect alpha-smooth muscle actin (alphaSMA), desmin, and tenascin-C. The effects of the proinflammatory cytokines interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma were analyzed in human intestinal myofibroblast cultures by immunoblotting and apoptosis assays. Immunofluorescence analysis revealed decreased levels of the extracellular matrix molecule tenascin-C in pericryptal sheaths and alphaSMA in the immediate vicinity of the crypts in the inflamed specimens, indicating that the myofibroblast pericryptal sheath is affected by proinflammatory cytokines. Although individual cytokines did not affect myofibroblast proliferation or survival, cytokine combinations triggered caspase-dependent apoptosis. alphaSMA levels were reduced significantly in cells exposed to cytokines, either alone or in combination, suggesting dedifferentiation of myofibroblasts. Proinflammatory cytokines did not affect tenascin-C expression, suggesting that the decrease observed in the inflamed mucosa resulted from myofibroblast apoptosis. The subepithelial myofibroblasts of the epithelial sheath are disrupted in the intestinal mucosa of patients with IBD. A loss of myofibroblasts appears to result from the susceptibility of these cells to proinflammatory cytokines.

Altered Th1/Th2 cytokine profiles in the intestinal mucosa of patients with inflammatory bowel disease as assessed by quantitative reversed transcribed polymerase chain reaction (RT-PCR).

Cytokines serve a central function as key factors in the regulation of the intestinal immune response and mediation of tissue damage in inflammatory bowel disease (IBD). Abnormalities in the expression of immunoregulatory cytokines such as IL-2, IL-4, IL-10 and interferon-gamma (IFN-gamma) may indicate a dysregulation of intestinal immunity probably associated with pathogenic events. Therefore, cytokine mRNA concentrations were determined in the mucosa of patients with IBD at sites of active (n = 13) and inactive (n = 12) ulcerative colitis (UC), active (n = 11) and inactive (n = 11) Crohn's disease (CD) and in control patients (n = 14) using quantitative RT-PCR. IL-10 mRNA concentrations were significantly increased in patients with both active UC (P < 0.001) and active CD (P < 0.005) compared with control patients. IFN-gamma mRNA concentrations were also significantly increased both in patients with active UC (P < 0.02) and active CD (P < 0.05) compared with control patients, whereas IL-2 mRNA levels were significantly (P < 0.02) increased only in active CD. IL-4 mRNA expression in the intestinal mucosa was frequently below the detection limit. Our results demonstrate that chronic intestinal inflammation in patients with CD is characterized by an increase of Th1-like cytokines. Furthermore, the increased IL-10 mRNA expression at sites of active IBD suggests that IL-10 is an important regulatory component involved in the control of the inflammatory response in inflammatory bowel disease.

The cytokine interleukin 21: a new player in coeliac disease?

In this issue of Gut ,1 Fina et al demonstrate that interleukin 21 (IL21) expression is increased in the intestinal mucosa of patients with active coeliac disease (CD) but not...

Expression of Toll-like receptors in the intestinal mucosa of patients with inflammatory bowel disease

Evaluation of: Frolova L, Drastich P, Rossmann P, Klimesova K, Tlaskalova-Hogenova H. Expression of Toll-like receptor 2 (TLR2), TLR4, and CD14 in biopsy samples of patients with inflammatory bowel diseases: upregulated expression of TLR2 in terminal ileum of patients with ulcerative colitis. J. Histochem. Cytochem. 56(3), 267–274 (2007).Inflammatory bowel disease (IBD) consists of Crohn’s disease, which involves not only the large intestine but also the small intestine, and ulcerative colitis, which only involves the large intestine. The dysregulation of innate and adaptive intestinal immune responses to bacterial microbiota is believed to be highly involved in the pathogenesis of IBD. Toll-like receptors (TLRs) play a key role in microbial recognition in innate immunity and control the adaptive immune responses. Among the TLRs, TLR2 recognizes bacterial lipoprotein and peptidoglycan, whereas TLR4 and its coreceptor, CD14, recognize lipopolysaccharide. The expression levels of TLR2 or TLR4 have been shown to be limited in the intestine of healthy volunteers, suggesting a minimalization of the recognition of microbiota in the intestinal lumen. The paper under evaluation highlighted the expression levels of TLR2, TLR4 and CD14 in the terminal ileum, cecum and rectum of IBD patients (19 Crohn’s disease and 20 ulcerative colitis patients) and of 20 healthy volunteers. The authors suggested that the dysregulation of TLR2, TLR4 and CD14 expression in different parts of the intestinal mucosa might, therefore, play a crucial role in the pathogenesis of IBD.

Down-Regulation of the Monocarboxylate Transporter 1 Is Involved in Butyrate Deficiency During Intestinal Inflammation

Butyrate oxidation is impaired in intestinal mucosa of patients with inflammatory bowel diseases (IBD). Butyrate uptake by colonocytes involves the monocarboxylate transporter (MCT) 1. We aimed to investigate the role of MCT1 in butyrate oxidation deficiency during colonic inflammation. Colonic tissues were collected from patients with IBD or healthy controls and from rats with dextran sulfate sodium (DSS)-induced colitis. The intestinal epithelial cell line HT-29 was treated with interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). MCT1 expression was analyzed by real-time reverse-transcription polymerase chain reaction, Western blot, and immunofluorescence. Butyrate uptake and oxidation in HT-29 cells was assessed using [(14)C]-butyrate. The mechanism of MCT1 gene regulation was analyzed by nuclear run-on and reporter gene assays. MCT1 messenger RNA (mRNA) and protein levels were markedly decreased in inflamed colonic mucosa of IBD patients and rats. In HT-29 cells, down-regulation of MCT1 mRNA and protein abundance by IFN-gamma and TNF-alpha correlated with a decrease in butyrate uptake and subsequent oxidation. IFN-gamma and TNF-alpha did not affect MCT1 mRNA stability but rather down-regulated gene transcription. We demonstrate that the cytokine response element is located in the proximal -111/+213 core region of the MCT1 promoter. The data suggest that butyrate oxidation deficiency in intestinal inflammation is a consequence of reduction in MCT1-mediated butyrate uptake. This reinforces the proposition that butyrate oxidation deficiency in IBD is not a primary defect.

The Satiety Factor Apolipoprotein A-IV Modulates Intestinal Epithelial Permeability through its Interaction with α-Catenin: Implications for Inflammatory Bowel Diseases

Apolipoprotein A-IV (apoA-IV), an intestinally and cerebrally synthesized satiety factor and anti-atherogenic plasma apolipoprotein, was recently identified as an anti-inflammatory protein. In order to elucidate whether intestinal apoA-IV exerts similar repair function as its hepatic homologue apolipoprotein A-V (apoA-V), apoA-IV-interactive proteins were searched and in vitro functional studies were performed with apoA-IV overexpressing cells. ApoA-IV was also analyzed in the intestinal mucosa of patients with inflammatory bowel diseases (IBD), together with other genes involved in epithelial junctional integrity. A yeast-two-hybrid screening was used to identify apoA-IV-interactors. ApoA-IV was overexpressed in Caco-2 and HT-29 mucosal cells for colocalization and in vitro epithelial permeability studies. Mucosal biopsies from quiescent regions of colon transversum and terminal ileum were subjected to DNA-microarray analysis and pathway-related data mining. Four proteins interacting with apoA-IV were identified, including apolipoprotein B-100, alpha1-antichymotrypsin, cyclin C, and the cytosolic adaptor alpha-catenin, thus linking apoA-IV to adherens junctions. Overexpression of apoA-IV was paralleled with a differentiated phenotype of intestinal epithelial cells, upregulation of junctional proteins, and decreased paracellular permeability. Colocalization between alpha-catenin and apoA-IV occurred exclusively in junctional complexes. ApoA-IV was downregulated in quiescent mucosal tissues from patients suffering from IBD. In parallel, only a distinct set of junctional genes was dysregulated in non-inflamed regions of IBD gut. ApoA-IV may act as a stabilizer of adherens junctions interacting with alpha-catenin, and is likely involved in the maintenance of junctional integrity. ApoA-IV expression is significantly impaired in IBD mucosa, even in non-inflamed regions.

Rotavirus and Celiac Disease: Clues to the Pathogenesis and Perspectives on Prevention

Rotavirus and Celiac Disease: Clues to the Pathogenesis and Perspectives on Prevention

Predictive value of mucosal TNF-α transcripts in steroid-refractory Crohnʼs disease patients receiving intensive immunosuppressive therapy

Concentrations of proinflammatory cytokines are increased in the intestinal mucosa of patients with active Crohn's disease (CD). In a prospective study we investigated whether cytokines can predict long-term remission (>6 months) in patients with steroid-refractory CD receiving treatment with infliximab or cyclophosphamide, followed by azathioprine or methotrexate. Cytokine transcripts were quantified using real-time polymerase chain reaction (PCR) in mucosal biopsies from 19 patients with active, steroid-refractory CD before and 8 weeks after initiation of therapy. Patients were treated with cyclophosphamide (monthly treatment of 750 mg cyclophosphamide intravenously) or infliximab (5 mg/kg body weight) and were followed until relapse of the disease. Statistical analysis was performed to identify predictive factors to discriminate between patients with or without long-term remission. Seventeen out of 19 patients achieved remission of the disease, two patients were nonresponders, while six out of 17 patients exhibited an early recurrence. Pretreatment TNF-alpha, IL-18, MRP-14, and IL-8 transcripts were significantly correlated with long-term remission. While several cytokines, most importantly MMP-1, determined after 8 weeks were able to predict patients achieving long-term remission, only a decrease of TNF-alpha levels after 8 weeks was predictive. Overall, statistical analysis identified lower pretreatment TNF-alpha levels as the strongest predictor of long-term remission among baseline variables. Quantification of mucosal TNF-alpha transcripts prior to therapy allows identification of patients achieving long-term remission upon immunosuppression with infliximab or cyclophosphamide. Real-time PCR might have considerable potential in the analysis of disease activity and subsequent clinical management of patients with immunosuppressive therapies.

Abnormal Fatty Acid Pattern in Intestinal Mucosa of Children With Celiac Disease Is Not Reflected in Serum Phospholipids

Celiac disease (CD) is characterized by chronic inflammation of the small intestinal mucosa with disturbed epithelial transport. The fatty acid (FA) composition of intestinal membranes is important for epithelial function, and disturbances may contribute to the pathophysiology of the disease. We aimed to evaluate whether the intestinal mucosal FA status was reflected in serum phospholipids of patients with CD. Samples were obtained from 7 pediatric patients with active CD showing mucosal atrophy, 6 pediatric patients with CD in remission, and 11 control pediatric patients with morphologically healthy intestinal mucosa. Small intestinal biopsies were obtained using a Watson biopsy capsule under fluoroscopic control. Blood samples were collected on the same morning after an overnight fast. Tissue phospholipids were isolated by high-performance liquid chromatography, and FAs were analyzed by capillary gas-liquid chromatography. Serum phospholipid FA showed marginal differences between the patients with CD and the controls. Significant differences were observed in mucosa with active CD compared with controls. Linoleic acid (18:2n-6) level was decreased, whereas those of its derivatives were elevated, indicating increased transformation of n-6 FA. Mead acid (20:3n-9) level was increased, with an increased ratio of Mead acid to arachidonic acid (20:4n-6) levels, suggesting essential fatty acid deficiency. The n-3 FA levels were not significantly changed. During remission, the FA pattern of the intestinal mucosa was mainly similar to that in controls. The FA abnormality of intestinal mucosa in patients with active CD was not reflected in serum values. Altered FA content may contribute to the pathophysiology of the disease because FAs are important for enzymes and for the transport and receptor functions of epithelial membranes.