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PubMed2004

Efficacy of wogonin in the production of immunoglobulins and cytokines by mesenteric lymph node lymphocytes in mouse colitis induced with dextran sulfate sodium.

We previously examined wogonin, isolated from Scutellaria baicalensis, chemical mediators, and IgE by mesenteric lymph node (MLN) lymphocytes in rats. The present study explores the effect of wogonin on the MLN lymphocyte function of mice given orally at 20 mg/kg for 2 weeks with dextran sulfate sodium (DS)-induced colitis. The results indicate that IgA levels in MLN lymphocytes were high, while IgE was low, in mice given wogonin compared to those given water. Also, fecal IgA concentration of DS in the wogonin group mice was significantly higher than in the DS group. Concentrations of interferon-gamma and interleukin (IL)-2 of T cells by concanavalin A treatment was significantly higher in the wogonin fed group than in the normal group. Activation-induced IL-4, IL-5 and IL-10 secretion was lower in wogonin fed mice compared control mice after DS-induced colitis. For these reasons, we conclude that wogonin can alleviate the inflammation in DS-induced colitis brought about by an abnormal Th(2) response.

Animals↗
PubMed2002

Alteration in expression of beta 2 integrins on lamina propria lymphocytes in ulcerative colitis and Crohn's disease.

We have previously demonstrated by immunohistochemistry that mucosal expression of beta 2 integrins was enhanced in Crohn's disease and ulcerative colitis as compared to normal controls. We aimed, therefore, to determine whether there was a corresponding alteration in the expression of CD11a/CD18 (LFA-1), the primary lymphocyte beta 2 integrin, among the principal subsets of lamina propria lymphocytes (LPLs). Accordingly, LPLs were extracted from surgical resection specimens derived from patients with Crohn's colitis, ulcerative colitis, and from noninflamed controls. Following immunofluorescent staining, three-color flow-cytometry analysis identified LPLs on the basis of CD45 side scatter gating, which in turn, were further subdivided into CD4(+), CD8(+), and CD19(+) cells to account for the predominant T and B cells in the lamina propria. Expression patterns of CD11a, the alpha-subunit of LFA-1; CD18, the beta-subunit of LFA-1; and alpha d, a novel alpha-subunit of the beta 2 integrin family were assessed for each of these lymphocyte subsets. In Crohn's disease and ulcerative colitis there was an increased mean percentage expression of CD4(+) cells and CD11a(+) cells compared with noninflamed controls. CD11a was more likely to be expressed on CD4(+) cells in both Crohn's disease and ulcerative colitis and compared with controls and less expressed on CD19(+) cells. It is likely that an influx of CD4(+)11a(+) cells into the lamina propria accounted for these changes. These results suggest that although currently there is great interest in harnessing alpha 4 beta 7 in treatment of inflammatory bowel disease, further consideration should be given to the role of CD11a in these disease states.

Antigens, CD19↗
PubMed1990

The in vitro effect of corticosteroids on T-lymphocyte subpopulations in patients with ulcerative colitis.

T-lymphocyte subpopulations were measured in the blood of 20 patients with ulcerative colitis (11 in clinical remission and 9 in exacerbation) and 9 healthy persons, before and after in vitro incubation with dexamethasone. Although we found no significant differences in the helper/suppressor T cell ratio between patients and controls before in vitro incubation, addition of dexamethasone in culture induced a significant decrease of the ratio only in patients with ulcerative colitis in exacerbation. The percentage of natural killer cells before and after incubation with dexamethasone was not altered.

Adolescent↗
PubMed1997

Differences in immunophenotyping of mucosal lymphocytes between ulcerative colitis and Crohn's disease.

OBJECTIVES: Immunologic studies have characterized the numbers and types of inflammatory cells in diseased inflammatory bowel disease (IBD) mucosa but have yielded conflicting results regarding intestinal lymphocytes activation in IBD. We investigated the levels of lymphocytes subsets, interleukin-2 receptor, transferrin receptor, and T cell receptors in mainly isolated lamina propria lymphocytes. Including intraepithelial lymphocytes of normal colonic mucosa or IBD (ulcerative colitis and Crohn's disease) mucosa to understand the pathogenesis of IBD. We have results from this study. RESULTS: 1) In comparing ulcerative colitis with control, IL-2R (p < 0.05), TR (p < 0.01), and CD3/HLA-DR (< 0.05) showed a significant increase. 2) In comparing Crohn's disease with control, CD3 (P < 0.05), TCR alpha/beta (p < 0.01) and TCR gamma/delta (p < 0.05) showed a significant decrease. 3) In comparing Crohn's disease with ulcerative colitis, CD19 (p < 0.01), TR (p < 0.01), TCR alpha/beta (p < 0.01) and TCR gamma/delta (p < 0.05) showed a significant decrease. CONCLUSION: From these results, there are increased T cell markers, IL-2R, TR, and CD3/HLA-DR in UC, but differently, decreased CD3, TCR alpha/beta and TCR gamma/delta in CD compared with control. In addition, definitive differences in lymphocytes markers, CD19, TR, TCR alpha/beta and TCR gamma/delta, which are higher in UC than in CD, may elucidate the different immunopathogenesis between UC and CD.

Adult↗
PubMed1990

[Analysis of subsets of colonic mucosal lymphocyte in ulcerative colitis by two color flow cytometry].

To assess how the immunological events occur in the colonic mucosa in patients with ulcerative colitis, it is thought to be important to evaluate the subpopulations and/or subsets of mucosal lymphocytes. In this point of view, we assayed those by lymphocyte isolation techniques and two color flow cytometry. Although our results showed no disease-specific abnormalities of the percentages of CD3, CD4, CD8, CD20, and HLA-DR (+) cells in PBL (peripheral blood lymphocyte) nor CML (colonic mucosal lymphocyte), these subsets of CML appeared to be altered according to the grade of severity of inflammation. In our cases, the HLA-DR (+) cell and CD4 population were larger in severely inflamed mucosa. Furthermore, fluorescence intensities of HLA-DR antigen of CD20 population in CML were greater than those in PBL. These results suggest that the B cell-mediated mechanisms may play an important role in maintaining the severe inflammation, and the clinical significance of these studies are discussed.

Adolescent↗
PubMed1989

Lymphocytic enterocolitis in patients with 'refractory sprue'.

We describe a patient with refractory sprue with malabsorption, a flat small-bowel biopsy specimen unresponsive to a gluten-free diet, and colonic biopsy specimens consistent with lymphocytic (microscopic) colitis. To investigate further the relation between celiac disease and lymphocytic or collagenous colitis (a similar and possibly related entity), we examined colorectal and small-bowel biopsy specimens in patients indexed histologically as having celiac disease who have been seen at The Johns Hopkins Hospital since 1958. Of 135 indexed patients, 21 had colorectal biopsies. Colorectal biopsy specimens were abnormal in 7 of the 21 patients. Four patients had biopsy specimens resembling lymphocytic colitis, 2 patients had acute colitis, and another patient had both lymphocytic and acute colitis. No patients had collagenous colitis. Three of the patients with lymphocytic colitis and celiac-like changes of the small bowel never responded to a gluten-free diet and may represent a distinctive panintestinal disease for which the term "lymphocytic enterocolitis" with malabsorption is proposed.

Adult↗
PubMed1993

[Evaluation of activated T cells among isolated colonic mucosal lymphocytes in ulcerative colitis--using three color flow cytometry].

In present study, the subsets of activated (HLA-DR+) lamina propria T cells were evaluated in ulcerative colitis (UC) mucosa using three-color flow cytometry. Activated suppressor-inducer T cells (T(si)), helper T cells (Th) and cytotoxic T cells (Tc) were increased in affected mucosa of UC patients not given steroid hormones (SH) compared with in the normal control mucosa. It was supposed that the increase of activated T(si) was the secondary change of inflammation, because this change was demonstrated in non-IBD colitis too. However, the increase of activated Th and Tc might indicate the immunological abnormalities related to the pathogenesis of UC, because these changes were demonstrated only in UC, not in non-IBD colitis. On the other hand, no increase of these activated T cells were demonstrated in affected mucosa of UC patients given SH, perhaps reflecting the immuno-suppressive effect of SH.

Adolescent↗
PubMed2002

Mice lacking T and B lymphocytes develop transient colitis and crypt hyperplasia yet suffer impaired bacterial clearance during Citrobacter rodentium infection.

The bacterial pathogen Citrobacter rodentium belongs to a family of gastrointestinal pathogens that includes enteropathogenic and enterohemorrhagic Escherichia coli and is the causative agent of transmissible colonic hyperplasia in mice. The molecular mechanisms used by these pathogens to colonize host epithelial surfaces and form attaching and effacing (A/E) lesions have undergone intense study. In contrast, little is known about the host's immune response to these infections and its importance in tissue pathology and bacterial clearance. To address these issues, wild-type mice and mice lacking T and B lymphocytes (RAG1 knockout [KO]) were infected with C. rodentium. By day 10 postinfection (p.i.), both wild-type and RAG1 KO mice developed colitis and crypt hyperplasia, and these responses became more exaggerated in wild-type mice over the next 2 weeks, as they cleared the infection. By day 24 p.i., bacterial clearance was complete, and the colitis had subsided; however, crypt heights remained increased. In contrast, inflammatory and crypt hyperplastic responses in the RAG1 KO mice were transient, subsiding after 2 weeks. By day 24 p.i., RAG1 KO mice showed no signs of bacterial clearance and infection was often fatal. Surprisingly, despite remaining heavily infected, tissues from RAG1 KO mice surviving the acute colitis showed few signs of disease. These results thus emphasize the important contribution of the host immune response during infection by A/E bacterial pathogens. While T and/or B lymphocytes are essential for host defense against C. rodentium, they also mediate much of the tissue pathology and disease symptoms that occur during infection.

Animals↗
PubMed1999

Lymphocytic and Collagenous Colitis: Medical Management.

When possible, patients taking nonsteroidal anti-inflammatory medications should discontinue them when the diagnosis of microscopic colitis is made. Although there is no direct evidence of its efficacy, a trial of elimination of caffeine or lactose or both should be undertaken. Nonspecific antidiarrheal agents (eg, loperamide, diphenoxylate) may be administered, but appear to be largely ineffective in this population. An aminosalicylate should be initiated at full therapeutic dose (2 to 4 g daily) as the first-line therapy. Because sulfasalazine appears to be associated with a high incidence of adverse effects in patients with microscopic colitis, other derivatives of 5-aminosalicylate (5-ASA) are preferred. Bile salt-binding agents such as cholestyramine or colestipol appear to be effective alternatives for patients who are either unresponsive to or intolerant of aminosalicylates. Systemic corticosteroids are an effective treatment for microscopic colitis, but may offer only transient improvement in symptoms. Given their potential adverse effects, corticosteroids should be reserved for patients with refractory disease in whom aminosalicylates and bile salt-binding agents have failed. Other agents that may be effective include antibiotics, bismuth subsalicylate, budesonide, pentoxifylline, octreotide, and methotrexate. Although these agents can be considered in unusual cases, the cumulative clinical experience with them in this setting is relatively limited. Surgical intervention, with either fecal stream diversion or subtotal colectomy, shows promise as an intervention of last resort. In refractory cases of microscopic colitis, strong consideration should be given to excluding a concomitant diagnosis of celiac disease, bacterial overgrowth, or chronic infection.

Journal Article↗
PubMed2005

[What is inflammatory bowel disease?].

Inflammatory bowel diseases are chronic conditions of unknown origin that result from continuous or intermittent inflammation of a part of the intestinal wall. The main classic types of IBD are ulcerative colitis, Crohn's disease and indeterminate colitis that cannot be classified accurately as ulcerative colitis or Crohn's disease with pure colonic involvement. The two main subtypes of microscopic colitis, namely lymphocytic and collagenous colitis, fulfill the criteria that define IBD and should be considered as true IBD.

Colon↗
PubMed1994

The use of proliferating cell nuclear antigen (PCNA) expression and intraepithelial lymphocyte count in the differential diagnosis of inflammatory bowel disease.

Colonic biopsies of 283 patients with Crohn's disease (CD), ulcerative colitis (UC), infectious colitis (IC) lymphocytic colitis (LC) and controls for patients with either CD or UC, matched for age and sex, were evaluated with respect to the number of intraepithelial lymphocytes (IEL) and PCNA (cyclin) positive crypt epithelia. The IEL count of patients with LC differed significantly from all other patient groups, indicating that this condition bears no relation to the other diseases. Our patients with histologic diagnosis of LC had no uniform clinical presentation and the significance of this characteristic increase in IEL is unclear. The mean value of PCNA positive crypt epithelia in the lower crypt half was significantly higher in UC patients than in CD patients. PCNA counts in patients with IC or LC were not different from values in UC patients. PCNA counts in CD patients overlapped frequently with those in UC patients. This parameter thus fails to distinguish between CD and UC in individual patients and, though not investigated by us, is unlikely to be effective in the differential diagnosis in patients with a provisional diagnosis of indeterminate colitis.

Adult↗