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PubMed2006

T cells climb on board Blimp-1.

B lymphocyte-induced maturation protein (Blimp)-1, a transcriptional repressor, has long been known to drive the terminal maturation of B cells into plasma cells. However, two recent studies reveal an unanticipated role for Blimp-1 in T-cell homeostasis. Blimp-1-deficient T cells exhibit enhanced proliferative and functional responses following activation, and induce spontaneous colitis. Hence, aside from its role in B-cell differentiation, Blimp-1 directs restraint among T cells.

Animals↗
PubMed1994

Cytomegalovirus colitis in HIV-1-infected patients: a prospective research in 55 patients.

OBJECTIVE: To determine criteria for the diagnosis of cytomegalovirus (CMV) colitis and to analyse stages of the course and prognosis of CMV colonic involvement in HIV-1-infected patients. DESIGN: Prospective search for CMV colonic involvement with systematic biopsies to search for CMV intranuclear inclusion bodies and for CMV culture. The evolution of CMV colonic involvement was estimated using further coloscopies and autopsy. SETTING: Infectious diseases department in a tertiary referral teaching hospital in Paris, France. PARTICIPANTS: Fifty-five consecutive patients with HIV-1 infection, who had not previously received anti-CMV drugs, and who had at least one coloscopy performed. RESULTS: According to initial coloscopy, colitis, either ulcerative or inflammatory, was found in nine (16%) out of the 55 patients, CMV intranuclear inclusions were present in the colon of four (7%) patients, and colonic cultures were positive for CMV in 15 (27%) patients. The results of the initial coloscopy showed a positive correlation between endoscopic colitis (either ulcerative or inflammatory), CMV inclusions and positive CMV culture from colonic biopsies. The absence of endoscopic ulcerative lesions had a 98% (49 out of 50) negative predictive value for recording CMV inclusions in the colon (95% confidence interval, 89-100). CMV inclusions were recorded in three out of five ulcerative colitis. Male homosexuality, HIV-1 infection stages IVB, C1, D or E, according to the Centers for Disease Control and Prevention classification, CD4 lymphocyte count < 200 x 10(6)/l and CMV viraemia also correlated positively with CMV colonic involvement. During the observation period (mean, 7.3 months), the estimated incidence of CMV colitis according to coloscopic studies was 13%. Deterioration in condition was the most frequent spontaneous evolution of CMV colonic infection, whereas anti-CMV treatment resulted in an improvement. Ulcerative lesions occurred earlier in patients with colonic CMV inclusions or positive colonic CMV culture than in patients without CMV colonic involvement at the initial coloscopy. CMV colitis occurred late in the course of HIV-1 infection, on average 4 months before death. The presence of CMV inclusions was an indicator of poor prognosis with earlier occurrence of CMV viraemia and retinitis and no survival after 9 months. CONCLUSIONS: These results confirm that the colon is a target organ for CMV in HIV-1-infected patients. Coloscopy should be used to diagnose CMV colitis, because of the close correlation between endoscopic and histological data (i.e., intranuclear inclusions). This combination allows us to propose an evolutive staging of CMV colonic involvement and provide stratification criteria to assess the efficacy of anti-CMV drugs.

AIDS-Related Opportunistic Infections↗
PubMed1986

[Ulcerative colitis caused by Histoplasma capsulatum in a patient with the acquired immunodeficiency syndrome].

The authors report a case of ulcerative colitis due to Histoplasma capsulatum in a previously healthy 35 year-old french geologist with acquired immune deficiency syndrome (AIDS). Gomori-Grocott and PAS stains and indirect immunofluorescence revealed Histoplasma capsulatum in colonic biopsies. The search for LAV antibody was positive. T-lymphocyte analysis revealed 10/mm3 OKT4 with OKT4/OKT8 ratio of 0.16. Histoplasmosis should be considered in subjects with ulcerative colitis according to the epidemiological context. In patients with AIDS relapses after discontinuation of treatment are to be expected and suppressive therapy with an imidazole derivative should probably be continued indefinitely.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Polyclonal nature of the intestinal mucosal lymphocyte populations in inflammatory bowel disease. A molecular genetic evaluation of the immunoglobulin and T-cell antigen receptors.

To define the clonality of the intestinal lymphocytes involved in the immune response of inflammatory bowel disease, we performed a molecular genetic analysis of the arrangement of the immunoglobulin and antigen-specific T-cell receptor genes of isolated lamina propria lymphocytes derived from resected intestinal specimens of 12 patients with Crohn's disease, 5 patients with chronic ulcerative colitis, and 7 patients with other gastrointestinal diseases. The sensitivity of this technique is sufficient to detect a monoclonal population when there is as little as 1% clonal expansion in a mixed cell population. In all these groups of patients, deoxyribonucleic acid from the non-T cells demonstrated only a germ-line gene pattern, and no non-germ-line rearrangements of immunoglobulin genes as assessed by an immunoglobulin-joining heavy-chain gene probe. Deoxyribonucleic acid from the lamina propria T cells showed a rearrangement pattern of the antigen-specific T-cell receptor beta- and gamma-chain genes that is characteristic of polyclonal T cells as assessed by T-constant beta- and T-joining gamma-gene probes. These results indicate that the lamina propria non-T and T-lymphocyte populations in inflammatory bowel disease and controls are polyclonal.

Adult↗
PubMed1988

Neutropenic colitis: evaluation with computed tomography.

The computed tomography findings of 10 patients with neutropenic colitis are described and illustrated. Seven of these patients had leukemia, one had lymphocytic lymphoma, and two had systemic lupus erythematosus. All patients had colon wall thickening which was either isodense with the normal bowel tissue or showed areas of intramural low density. Air in the thickened bowel wall was seen in six patients. These computed tomography findings in neutropenic patients with fever, abdominal pain, and diarrhea should suggest the diagnosis in most instances, resulting in prompt treatment of this usually life-threatening entity.

Adult↗
PubMed2004

Escherichia coli 0157:H7: an update on intestinal colonization and virulence mechanisms.

Cattle are a major reservoir of Escherichia coli 0157:H7, an important zoonotic pathogen that causes hemorrhagic colitis and hemolytic uremic syndrome (HUS). Colonization of cattle occurs predominantly in the large intestine, and may especially target follicle-associated epithelium (FAE) in the terminal rectum. Bacterial colonization involves induction of attaching-effacing (A/E) lesions, mediated by type III secreted proteins and an outer membrane protein called intimin. ToxB, encoded on plasmid pO157, contributes to adherence of E. coli O157:H7 through promotion of the production and/or secretion of type III secreted proteins. Production of type III secreted proteins and intestinal colonization appear to involve quorum-sensing mechanisms. In the human host, E. coli O157:H7 may have a preference for FAE in the distal small intestine. The H7 flagellum induces production of chemokines such as interleukin 8, and neutrophilic infiltration of the intestinal mucosa, which in turn may enhance Shiga toxin (Stx) uptake across the intestinal epithelium. Both Stx and cytokine responses play critical roles in the induction of the vascular lesions that underlie hemorrhagic colitis and HUS. In cattle, Stx binds to intestinal crypt cells and submucosal lymphocytes but not vascular endothelium. The role played by Stx in cattle may be to suppress mucosal immunity, yet enhance other effects that promote intestinal colonization.

Animals↗
PubMed2006

Structural adaptations in the murine colon microcirculation associated with hapten-induced inflammation.

BACKGROUND: Blood flowing across the vascular endothelium creates wall shear stress, dependent on velocity of flow and vessel geometry, that tends to disrupt lymphocyte-endothelial cell adhesion. OBJECTIVE: The microcirculation in a murine model of acute colitis was investigated to identify structural adaptations during acute colitis that may facilitate transmigration. METHODS: In 2,4,6-trinitrobenzenesulphonic acid-induced acute colitis, the infiltrating cells and colonic microcirculation was investigated by cellular topographic mapping, corrosion casting and three-dimensional scanning electron microscopy (SEM). Colonic blood velocimetry was performed using intravital microscopy. RESULTS: Clinical and histological parameters suggested a peak inflammatory response at 96 h (p<0.001). The infiltrating cells were spatially related to the mucosal capillary plexus by three-dimensional topographic mapping (p<0.001). In normal mice, corrosion casting and three-dimensional SEM showed a polygonal mucosal plexus supplied by ascending arteries and descending veins. After 2,4,6-trinitrobenzenesulphonic acid stimulation, three-dimensional SEM showed preserved branch angles (p = 0.52) and nominal vessel lengths (p = 0.93), but a significantly dilated mucosal capillary plexus (p<0.001). Intravital microscopy of the mucosal plexus showed a greater than twofold decrease in the velocity of flow (p<0.001). CONCLUSIONS: The demonstrable slowing of the velocity of flow despite an increase in volumetric flow suggests that these microvascular adaptations create conditions suitable for leucocyte adhesion and transmigration.

Acute Disease↗
PubMed1992

[Acute alveolitis due to mesalazine].

A 66-year-old male developed lymphocytic alveolitis with bronchiolitis after 3 month's treatment with mesalazin for ulcerative colitis. The patient's symptoms disappeared after halting mesalazin and increasing the steroid dose, the reduced diffusing capacity ameliorated and the thoracic X-ray normalized. The question whether this was a case of pulmonary involvement in inflammatory bowel disease or a drug side effect.

Aged↗
PubMed1996

Induction of lymphocyte proliferation and severe gastrointestinal disease in macaques by a nef gene variant SIVmac239.

The molecularly cloned virus known as SIVmac239/YEnef causes extensive lymphocyte activation in unstimulated peripheral mononuclear cell cultures and induces an acute disease syndrome in macaque monkeys. Here we describe the histopathological and immunophenotypic changes and viral localization in peripheral lymph nodes, spleen, and gastrointestinal tract (including the gut-associated lymphoid tissue (GALT) in rhesus monkeys inoculated with SIVmac239/YEnet beginning at day 3 postinoculation (pi). The findings are compared with those of rhesus monkeys inoculated with the same dose of parental SIVmac239. Histopathological examination of peripheral lymphoid tissue and GALT demonstrated marked hyperplasia of T-cell-dependent regions and involution of germinal centers as early as day 7 pi. The most striking lesions were multifocal areas of lymphohistiocytic gastroenteritis and colitis. Cellular infiltrates peaked between day 7 and 14 pi and were composed primarily of CD3+ T lymphocytes and HAM-56+ monocyte/macrophages. Many of these inflammatory cells were also strongly immunoreactive for teh nuclear proliferation antigen Ki-67. Despite the presence of severe gastrointestinal pathology by day 7 pi, no significant difference in the numbers of virus-positive cells in the gastrointestinal tract was observed between these animals and SIVmac239-infected animals examined at the same time point. However, the distribution of virus in the gastrointestinal tract was markedly different, with virus localized to lymphoid nodules of GALT in SIVmac239-infected animals and restricted to areas of lymphohistiocytic gastroenteritis and colitis in animals infected with SIVmac239/YEnef. Our data indicate that the acute disease syndrome induced by SIVmac239/YEnef is not simply related to increased viral replication in the gastrointestinal tract but is likely due to inappropriate virus-induced T lymphocyte activation and proliferation in GALT and subsequent mucosal destruction.

Animals↗
PubMed2004

Blocking inducible co-stimulator in the absence of CD28 impairs Th1 and CD25+ regulatory T cells in murine colitis.

Several autoimmune disease models depend on an imbalance in the activation of aggressor T(h)1 and CD4(+)CD25(+) regulatory T (T(reg)) cells. Here we compare the requirement for signals through the co-stimulatory molecules CD28 and inducible co-stimulator (ICOS) in chronic murine colitis, a model for inflammatory bowel disease. We used a colitis model in which disease-causing CD45RB(hi) T cells alone or in combination with CD4(+)CD25(+) T cells from either CD28-deficient or wild-type donors were transferred into T cell-deficient animals, half of which were treated with ICOS-blocking reagents. Blocking ICOS on the surface of CD28-deficient T(h)1 cells abrogated development of colitis, whereas blocking CD28 or ICOS alone had little to no effect on disease induction. In contrast to T(h)1 cells, regulatory T cell functioning depended mostly on CD28 signaling with only a minor contribution for ICOS. We conclude that CD28 and ICOS collaborate to development of murine colitis by aggressor T(h)1 cells, and that CD28 is required for T(reg) cells, which should caution against the use of CD28-blocking reagents in inflammatory bowel disease.

Animals↗
PubMed1984

[Immunologic studies in patients with Crohn disease and ulcerative colitis].

To compare patients with Crohn's disease and patients with ulcerative colitis we have studied some immunological parameters (level of IgM, IgG and IgA in the serum, number of lymphocytes, E rosettes) and the immunological reactivity to antigens from colon carcinoma and to colon antigens prepared from healthy and from colon tissue altered by Crohn's disease (antigen specific rosette test, MEM-test, antibody titer). The results indicate a decreased proportion of T cells in both bowel diseases on the one hand, on the other hand a specific cell-meditated immune reaction to colon antigens could be observed in patients with Crohn's disease. In patients with ulcerative colitis such reactions are determined only in the acute phase of disease or in recidive. It remains to be elucidated whether these immunological reactions represent a basic pathogenetic factor in the onset of these diseases.

Antigens, Neoplasm↗
PubMed1992

Incidence and natural history of cytomegalovirus disease in patients with advanced human immunodeficiency virus disease treated with zidovudine. The Zidovudine Epidemiology Study Group.

Data were analyzed from a multicenter observational cohort study of 1002 persons with AIDS or AIDS-related complex (ARC) and total CD4 cell count < 0.25 x 10(9)/L treated with zidovudine between April 1987 and April 1988. Cytomegalovirus (CMV) disease developed in 109 patients (10.9%), with a 2-year actuarial risk of 15%. Manifestations included retinitis (93 patients), esophagitis (10), colitis (8), gastritis (1), hepatitis (1), and encephalitis (1). The probability of CMV disease at 2 years for patients with initial counts < 0.1 x 10(9)/L was 21.4%, compared with 10.3% for patients with initial counts > or = 0.1 x 10(9)/L (P < .001). By proportional hazards analysis, baseline CD4 cell count < 0.1 x 10(9)/L, enrollment diagnosis of AIDS, and homosexuality were significantly associated with subsequently developing CMV disease. Median survival after diagnosis of CMV disease was 173 days, and CMV was an independent predictor of death. CMV contributes to AIDS-related morbidity and mortality. As new anti-CMV drugs become available, prophylaxis should be targeted at individuals with CD4 cell counts < 0.1 x 10(9)/L.

AIDS-Related Opportunistic Infections↗
PubMed1997

An ICAM-1 antisense oligonucleotide prevents and reverses dextran sulfate sodium-induced colitis in mice.

Mice treated p.o. with 5% dextran sodium sulfate develop a mild to moderate colitis characterized by focal areas of inflammation and crypt abscesses. Immunohistological analysis of colons from dextran sodium sulfate-treated mice revealed an increased expression of intercellular adhesion molecule 1 (ICAM-1) and infiltration of lymphocyte function antigen 1-positive cells. A murine-specific antisense oligonucleotide, ISIS 3082, was used to determine the role of ICAM-1 expression in the development of colitis. Prophylactic treatment of dextran sodium sulfate-treated mice with ISIS 3082 reduced the clinical signs of colitis in a dose-dependent manner, with maximal effects occurring at a dose of 1 mg/kg/day. Reductions in ICAM-1 immunostaining and infiltrating leukocytes were observed in colons of animals treated with 1 mg/kg ISIS 3082. Scrambled control oligonucleotides failed to modify the course of the disease. The ICAM-1 oligonucleotide also diminished the clinical severity of colitis in mice with established colitis. The toxicity of ISIS 3082 was assessed in normal CD-1 mice by administering the oligonucleotide intravenously every other day for 2 weeks. At pharmacologically relevant doses of ISIS 3082 (1 and 10 mg/kg), there were no signs of toxicity with respect to body and organ weights, clinical chemistry or hematology. At a dose of oligonucleotide 20- to 100-fold greater than maximal pharmacological doses, the oligonucleotide produced an increase in liver and spleen weights; a mild chronic inflammation in liver, lung and lymph nodes; monocytosis and an elevation of serum liver transaminases. These data suggest that an antisense oligonucleotide that reduces ICAM-1 expression could be effective in the therapy of inflammatory bowel disease in humans and that such an oligonucleotide would be safe at pharmacologically relevant doses.

Animals↗
PubMed1980

Transfer of colon inflammatory disease from immune to normal guinea pigs by lymphocytes.

Lymphocytes from guinea pigs which had been immunized with a saline extract of rabbit colon in complete Freund's adjuvant were transferred to normal guinea pigs of the same strain. 19% of the donors and 42% of the recipients developed histologic alterations of the colon. Recipients of killed lymphocytes from immune animals, normal lymphocytes, or animals immunized with an unrelated antigen had normal tissue histology. Thus, a cell-mediated immune response directed to an antigen found in a saline extract of colon is a factor in the pathogenesis of this experimental model of immunologically mediated colon disease.

Animals↗
PubMed1991

Nonspecific radiographic abnormalities in collagenous colitis.

Collagenous colitis (CC) is characterized clinically by a chronic, watery diarrhea. Pathologically, there is a chronic lymphocytic infiltrate with abnormal thickening of the subepithelial collagen layer. This disease occurs predominantly in females, and is more frequent in the elderly. Previous clinical studies suggest that radiographic examination of the colon is of no value in this condition. We reviewed five cases of CC all of whom had colon examination within 2 weeks of the biopsy. Two of our patients showed evidence of mucosal granularity and irregularity of the rectosigmoid on double-contrast barium enema (DCBE). One patient had nodularity of the rectal wall on single-contrast colon examination. Two patients had no inflammatory changes evident on colon examination. These radiographic changes are nonspecific and may be seen in other forms of colitis, particularly ulcerative colitis and nonspecific proctitis.

Adolescent↗