[Adenomyomatosis of the gallbladder].
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Adenomyoma↗
Biomedical subjects
K Kusugami
Publications and source records attributed to K Kusugami.
Phenotypic and functional characterization of T-cell lines generated from colonoscopic biopsy specimens in patients with ulcerative colitis.
Intestinal T-cell lines were generated from lamina propria mononuclear cells isolated from colonoscopic biopsies in ulcerative colitis patients and controls. In both ulcerative colitis and controls, expanded cells were constituted largely by T-cell receptor alpha beta+, CD4+, CD45RA- (helper), and CD8+, CD11b- (cytotoxic) phenotypes. T-cell receptor V beta gene usage was not significantly changed after cell expansion and no difference was observed between ulcerative colitis and controls. Ulcerative colitis cells, especially those derived from the patients with long-standing disease, showed significantly higher levels of cytotoxicity against the target cells, including those of colonic epithelial origin, and enhanced production of tumor necrosis factor-alpha and interferon-gamma after short incubation with anti-CD3 antibody. Generation of T-cell lines from colonoscopic biopsy specimens may be useful for detailed functional characterization of locally infiltrating T cells in ulcerative colitis patients.
Adolescent↗
Elevation of interleukin-6 in inflammatory bowel disease is macrophage- and epithelial cell-dependent.
Local interleukin-6 (IL-6) activity was studied using colonic mucosal tissues in inflammatory bowel disease (IBD) and inflammatory control patients. Active IBD specimens exhibited significantly higher IL-6 activity than control specimens in both cultures of isolated lamina propria mononuclear cells (LPMC) and mucosal tissues with an increased number of IL-6-producing cells. However, the activity in inactive IBD or inflammatory controls did not differ from controls. Northern blot analysis demonstrated IL-6 messenger RNA in LPMC and colonic epithelial cells isolated from active IBD specimens but not in control cells. Furthermore, immunofluorescent microscopic study of active IBD specimens showed more conspicuous staining of IL-6 in infiltrating LPMC (mostly CD68+ cells) and colonic epithelial cells. These results suggest that elevation of local IL-6 activity may be a characteristic feature of active IBD and both macrophages and colonic epithelial cells are the major cell types responsible for this phenomenon.
Adenocarcinoma↗
[Combination chemotherapy with FP versus FEP in patients with advanced gastric cancer. Research group of gastric cancer chemotherapy].
Forty-eight patients with unresectable gastric cancer were enrolled for a randomized trial of FP (n = 24) vs FEP (n = 24) combination chemotherapy with respect to their effects on survival period. Of these, excluding 7 patients, 21 in FP group were treated with 400 mg/m2 UFT po daily and 50 mg/m2 CDDP i.v. on days 1 and 8 every 4 weeks, and 20 in FEP group were treated with 400 mg/m2 UFT po daily, 50 mg/m2 etoposide iv and 50 mg/m2 CDDP i.v. on days 1 and 8 every 4 weeks. In FP group, 10 PR in primary lesions were observed with an overall response rate of 52.4%. In FEP group, 5 PR in primary lesions were observed with an overall response rate of 35.0%. Toxicities over Grade 3 were anorexia (35%), vomiting (25%), and leukopenia (12%), which were manageable. The 50% survival time in FP and FEP group was 233 and 176 days, respectively. Because of the high response rate and prolongation of the survival period, combination chemotherapy with FP seemed to be useful for the treatment of patients with advanced gastric cancer.
Adenocarcinoma↗
Impaired interleukin-2 production in active ulcerative colitis is reversed by calcium ionophore plus phorbol myristate acetate and related to altered intracellular Ca2+ responses.
Phytohemagglutin in (PHA)-induced IL-2 production in vitro by peripheral blood mononuclear cells (PBMC) and lamina propria mononuclear cells (LPMC) from patients with active UC (n = 24, n = 8, respectively) was significantly less than that in controls (n = 13, n = 8, respectively) and inactive patients (n = 11). In contrast, PBMC from inactive disease showed no significant difference when compared with the controls. Depressed IL-2 production in active UC was not reversed by the addition of anti-CD3 monoclonal antibody plus phorbol myristate acetate (PMA), but was largely reversed by adding calcium ionophore plus PMA. Using a fluorescent Ca2+ probe fura-2, we found that after PHA stimulation LPMC from patients with active UC showed a lower magnitude of rise in intracellular free calcium concentration ([Ca2+]i) than control cells. These results suggest that impaired PHA-induced IL-2 production in active UC may be related to some alterations of the early signaling events that cause elevation of the [Ca2+]i.
Adult↗
[Chlamydia trachomatis proctitis].
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Chlamydia Infections↗
[Chlamydia trachomatis proctitis].
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Adolescent↗
Phenotypic and functional analysis of lamina propria mononuclear cells from colonoscopic biopsy specimens in patients with ulcerative colitis.
Phenotypic and functional analysis was performed with lamina propria mononuclear cells (LPMCs) isolated from colonoscopic biopsies in 27 patients with ulcerative colitis (UC). The proportion of T lymphocytes displaying HLA-DR antigens, interleukin 2 (IL-2) receptor, and transferrin receptor was greater in active UC than in control diseases. When LPMCs were cultured with IL-2 or phytohemagglutinin for 72 h, there were no significant differences in the proportion of cells bearing these activation markers between active UC and controls. The proportion of CD56+ cells and lymphokine-activated killer (LAK) cell activity was lower in LPMCs from active UC than in control cells, and depletion of CD56+ cells from control lamina propria cells essentially eliminated LAK cell activity. Mucosal T lymphocytes may be activated in vivo during active inflammation in UC, and lower levels of intestinal LAK cell activity may be related to the decrease of CD56+ cells under these conditions.
Adolescent↗
Effects of water-immersion-induced stress and intraperitoneal administration of brain-gut peptides upon immunoreactive thyrotropin-releasing hormone and prostaglandin E2 concentrations in the rat stomach.
The effects of water-immersion-induced stress and intraperitoneal (i.p.) administration of selected neuropeptides on the levels of thyrotropin-releasing hormone (TRH) and prostaglandin E2 (PGE2) were studied in the rat stomach. Water-immersion caused a significant decrease immunoreactive-TRH (ir-TRH) concentrations in the stomach, and a significant increase in ir-TRH concentrations in the gastric juice. The concentrations of PGE2 were significantly increased at 0.5-4 hrs, and significantly decreased at 6-8 hrs after water-immersion. In the experiment of i.p. administration of selected neuropeptides, the level of ir-TRH in the stomach was significantly decreased after VIP injection, whereas it was significantly increased after beta-endorphin injection. The concentration of PGE2 was significantly decreased in the stomach after i.p. administration of TRH and VIP. However, it did not change after beta-endorphin injection. These results indicate that some neuropeptides may participate in regulating the endogenous level of PGE2 and that these interrelations between neuropeptides and PGE2 may be important as ulcerogenic factors in stress ulcers induced by water-immersion in the rat.
Animals↗
Loss of interleukin-2-producing intestinal CD4+ T cells in inflammatory bowel disease.
Interleukin-2 activity of intestinal lamina propria mononuclear cells is decreased in Crohn's disease and ulcerative colitis patients compared with control patients with noninflammatory bowel disease. Factors that might be responsible for this phenomenon were investigated. Most interleukin-2 activity was produced by helper (CD4+) T cells. These were present in comparable numbers in both inflammatory bowel disease and control cultures, but the frequency of interleukin-2-producing cells was significantly (3-4 times) lower among Crohn's disease and ulcerative colitis than control cells. In agreement with this finding, levels of interleukin-2 messenger RNA were substantially decreased in both forms of inflammatory bowel disease compared with controls. Mucosal CD8+ T cells and plastic-adherent cells were unable to suppress interleukin-2 activity by autologous or allogeneic CD4+ T cells. The rate of interleukin-2 absorption was similar for inflammatory bowel disease and control cells. Induction of interleukin-2 by different stimuli (phorbol ester, phytohemagglutinin, or anti-CD3 monoclonal antibody) before or after incubation under basal conditions ("resting") failed to normalize the capacity to generate interleukin-2 by Crohn's disease and ulcerative colitis cells. Prostanoids (prostaglandin E2 and 6-keto-prostaglandin F1 alpha) were produced in large amounts in cultures of inflammatory bowel disease cells, but inhibition by indomethacin failed to restore interleukin-2 activity to control levels. Finally, supernatants from Crohn's disease and ulcerative colitis cell cultures failed to suppress interleukin-2 production by control CD4+ T cells. Our results show that the low interleukin-2 activity detected in inflammatory bowel disease mucosa is not caused by activated suppressor cells, excessive lymphokine utilization or immune stimulation, a defective response to activation signals, or production of inhibitory substances. Rather, the low interleukin-2 activity appears to be related to a loss of interleukin-2-producing mucosal CD4+ T cells. It is concluded that abnormalities of intestinal CD4+ T-cell function are associated with the immunopathogenesis of Crohn's disease and ulcerative colitis.
Adolescent↗
Impaired regulation of natural killer cells in immunoglobulin synthesis by peripheral blood mononuclear cells from patients with ulcerative colitis.
Immunoglobulin (Ig) synthesis, natural killer (NK) cell activity, and lymphokine production by peripheral blood mononuclear cells (PBMC) were studied in 34 patients with ulcerative colitis (UC). Levels of Ig produced by PBMC were significantly higher in patients with active UC as compared to controls. However, there were no significant differences in Ig-synthesis between patients with inactive UC and controls. NK cell activity was significantly decreased in patients with active UC as compared to controls, and a significant negative correlation was observed between the level of IgA and NK cell activity in patients with UC. Reconstitution experiments demonstrated that CD56+ cells from controls suppressed the levels of IgA, when added to the culture containing a constant number of B cells and CD4+ cells. In contrast, CD56+ cells from patients with active UC completely lacked the capacity to suppress IgA production. In addition, the activities of interleukin-2 and interferon-gamma were significantly decreased in patients with active UC. The present study suggests that immunoregulatory abnormality of NK cells exists in patients with UC and impaired NK cell activity may be related to increased Ig-synthesis observed in these patients.
Adult↗
Interleukin 2 and interferon-gamma activities of mononuclear cells from regional lymph nodes in patients with gastric cancer.
The interleukin 2 (IL-2) and interferon-gamma (IFN-gamma) activities of regional lymph node mononuclear cells (LNMC) were studied in 22 patients with gastric cancer. Regional LNMC could produce high levels of IL-2 and IFN-gamma independent of the disease extension or the location of the lymph nodes. The activities of peripheral blood mononuclear cells (PBMC) from cancer patients were decreased especially in advanced disease compared to controls. The lymph node CD4+ cells were responsible for the bulk of IL-2 activity, whereas both CD4+ and CD8+ cells were equally capable of producing IFN-gamma. The proportion of T cells in LNMC was similar to that seen in PBMC, however, CD4+ cells predominated over CD8+ cells in the lymph nodes, contributing to higher activities of IL-2 and IFN-gamma in LNMC. Furthermore, significant cytotoxic activity could be induced from PBMC using the culture supernatant derived from autologous LNMC in cancer patients. This study suggests that regional lymph nodes are strategically located near the tumor and the local cells are capable of producing high levels of IL-2 and IFN-gamma.
CD4-Positive T-Lymphocytes↗
Intestinal immune reactivity to interleukin 2 differs among Crohn's disease, ulcerative colitis, and controls.
When stimulated by the lymphokine interleukin 2, human intestinal mucosal mononuclear cells mediate lymphokine-activated killer cell activity. When supplied with optimal doses of exogenous interleukin 2, lamina propria mononuclear cells isolated from inflammatory bowel disease and control tissue display comparable levels of cytotoxicity in vitro. However, cultures of Crohn's disease- and ulcerative colitis-derived cells contain significantly decreased interleukin 2 activity, suggesting that in vivo the availability of interleukin 2 may be limited, perhaps resulting in impaired cytotoxic function. To test this hypothesis, lamina propria mononuclear cells from inflammatory bowel disease and control patients were stimulated to produce endogenous interleukin 2, which was then used to induce autologous lymphokine-activated killer cells. When tested against K562 and Daudi target cells, Crohn's disease cells, despite producing only one-third of the amount of interleukin 2 generated by control cells, exhibited comparable levels of cytotoxicity. In contrast, ulcerative colitis cells produced substantially less interleukin 2 and exhibited remarkably low lymphokine-activated killer cell activity. When the same cells were supplied with an amount of human recombinant interleukin 2 equivalent to the average titer found in control cultures, similar results were obtained, and Crohn's disease cells even showed a significantly greater cytolytic activity than controls. These results suggest that the observed differences in lymphokine-activated killer cell activity cannot be attributed to the level of interleukin 2 alone, and that response to this lymphokine is different among Crohn's disease, ulcerative colitis, and control intestine. In Crohn's disease, there is either an increased number of interleukin 2-responsive cells or an exacerbated reactivity to interleukin 2. In ulcerative colitis, a loss of interleukin 2-responsive cells, a hyporesponsiveness to interleukin 2, or both might be present. In conclusion, this study demonstrates that reactivity to interleukin 2 distinguishes inflammatory bowel disease from control intestinal mononuclear cells, and, under appropriate experimental conditions, it can be used to uncover abnormalities of intestinal immunity.
Adolescent↗
Expression of HLA-DR antigens in inflammatory bowel disease mucosa: role of intestinal lamina propria mononuclear cell-derived interferon gamma.
The expression of HLA-DR antigens on the surface of immune cells is crucial for appropriate antigen presentation and a normal immune response. In the intestinal mucosa involved by Crohn's disease and ulcerative colitis the expression of HLA-DR antigens is increased in both immune and nonimmune cells, a phenomenon probably mediated by soluble factors, such as interferon gamma, produced by locally activated mononuclear cells. This study investigated the production of interferon gamma by inflammatory bowel disease and control intestinal lamina propria mononuclear cells, and the ability of this endogenously produced lymphokine to induce expression of HLA-DR antigens on the monocytic cell lines U937 and ML3. After in vitro stimulation with interleukin 2 or phytohemagglutinin, but not spontaneously, lamina propria mononuclear cells produced variable amounts of interferon gamma, and their culture supernatants could induce de novo expression of HLA-DR antigens on the monocytic indicator cells. When the mononuclear cells were derived from inflammatory bowel disease mucosa, both the amount of interferon gamma present in the supernatants and the number of HLA-DR-positive cells induced by these supernatants were decreased as compared to controls. These results suggest that, in inflammatory bowel disease, interferon gamma may not be the only mediator of HLA-DR induction in the gut and that other soluble factors or agents, alone or interacting with interferon gamma, may also be responsible for this event, resulting in the enhanced HLA-DR antigen expression observed in the inflamed intestinal mucosa.
Adult↗
Natural killer, lymphokine-activated killer and interferon-gamma producing activities of peripheral blood- and regional lymph node-mononuclear cells in 23 cases of colorectal cancer.
Natural killer (NK) activity, lymphokine-activated killer (LAK) activity and interferon-gamma (IFN-gamma) producing activity of peripheral blood mononuclear cells (PBMC) and regional lymph node mononuclear cells (LNMC) were studied in 23 previously untreated cases of colorectal cancer. NK and LAK activities were significantly lower in LNMC than in PBMC. Patients showed depressed NK and LAK activities in PBMC. In the Dukes C group, especially, both NK activity and LAK activity decreased compared to control patients. NK and LAK activities of PBMC decreased as the grade of invasion to lymphatic channels progressed. LAK activity positively correlated with NK activity in PBMC. Patients with high LAK activity showed high IFN-gamma production in both controls and Dukes A . B patients. However, in Dukes C patients, no relationship between LAK activity and IFN-gamma production was observed. We conclude that the depressed NK and LAK activities of PBMC reflect the local lymphatic invasion and that IFN-gamma involvement in LAK cell generation is impaired in advanced cancer patients. More fundamental studies should be carried out before clinical trials of adoptive immunotherapy using LAK cells, because LAK activity is not induced sufficiently in advanced cancer.
Aged↗
Effect of recombinant gamma interferon on natural killer cell activity in patients with gastric cancer.
We investigated the effect of recombinant interferon-gamma (rIFN-gamma) in vitro on natural killer (NK) cell activity of peripheral blood lymphocytes (PBL) in patients with gastric cancer. Thirty untreated patients with gastric cancer and eleven healthy donors were studied. NK cell activity in healthy donors was 38.6 +/- 5.2%. In patients with gastric cancer, NK cell activity was 32.4 +/- 3.9% in stage I, 35.5 +/- 7.1% in stages II and III, and 22.4 +/- 3.9% in stage IV. NK cell activity in stage IV patients was significantly lower than in healthy controls or gastric cancer patients in stages I-III. After stimulation by rIFN-gamma, NK cell activity increased in all groups, and in stage IV patients NK cell activity recovered to normal levels. However, there was no significant increase in the proportion of Leu 7 positive or Leu 11 positive cells in PBL. In conclusion rIFN-gamma enhances the activity of NK cells, but does not increase the number of active NK cells.
Cytotoxicity Tests, Immunologic↗
[A case of ulcerative colitis with pyoderma gangrenosum].
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Adult↗
Minute carcinoid tumor of the stomach: report of two cases and review of the Japanese literature.
Two cases of minute carcinoid tumor of the stomach were reported and 167 cases of gastric carcinoid in Japan up to December 1984 were reviewed. In Case 1, two carcinoid tumors of the body were found as sessile polyps of 4.2 and 4.8 mm in diameter, respectively, the latter having been detected two years previously. Case 2 had 60 polypoid lesions on the body and the fundus, ranging from 1.0 to 4.5 mm in diameter. In both cases the tumor invasion was limited to the mucosa and submucosa, although many micronests were found around the polypoid lesions. Among 167 cases of gastric carcinoid in Japan, 12 were 5 mm or less in size and 12 were 6 to 10 mm in size. In the former cases, there was no metastasis while in the latter, metastasis to the lymph nodes was found in 25.0%. We propose that the minute gastric carcinoid should be defined as a tumor not exceeding 5 mm in size with the invasion limited to the mucosa or submucosa. In addition, we emphasized that radical gastrectomy should be performed even for the minute carcinoid tumor because of its multicentricity and invasiveness.
Adult↗