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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gastrointestinal tract plays a major role in the pathogenesis and pathophysiology of infection by the type 1 human immunodeficiency virus (HIV-1). It is a potential route for viral entry and it is the site of a number of complications, including both opportunistic infections and a primary HIV-induced enteropathy. Correspondingly, both in vivo and in vitro studies have demonstrated HIV infection of gastrointestinal cells of lymphoid and epithelial origin. HT-29, a human colonic epithelial cell line that is infectable with many HIV-1 strains, does not express CD4 protein or mRNA. Recent studies showed that antibodies recognizing a neutral glycolipid related to galactosylceramide (GalCer) in HT-29 cells inhibited HIV-1 infection of this cell line, extending previous findings in neural cells. In the current studies, we further analyzed the neutral glycolipids of HT-29 cells and showed that they contained authentic GalCer and that recombinant gp120 bound to this glycolipid. Moreover, by analyzing GalCer expression in clones derived from HT-29 and Caco-2 (another human colonic cell line), we observed that the level of expression of this glycolipid was associated with the sensitivity to HIV-1 infection. Subclones of Caco-2 did not express GalCer and were not infectable with any of three HIV-1 strains. These results strengthen the possibility that GalCer is an alternative receptor in CD4- cell lines. Furthermore, since GalCer is a major glycolipid in epithelial cells of the small intestine and colon, these results provide a structural basis for the binding of HIV-1 by gastrointestinal epithelial cells and the entry of the virus into those cells.
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PMID:Infection of colonic epithelial cell lines by type 1 human immunodeficiency virus is associated with cell surface expression of galactosylceramide, a potential alternative gp120 receptor. 846 78

Gastrointestinal dysfunction and wasting are frequent complications of human immunodeficiency virus (HIV) infection. Nutrient malabsorption, decreased digestive enzymes and HIV transcripts have been documented in jejunal mucosa of HIV-infected patients; however, the pathogenesis of this enteropathy is not understood. Rhesus macaques infected with simian immunodeficiency virus (SIV) also exhibit diarrhea and weight loss; therefore, we investigated the use of this animal model to study HIV-associated intestinal abnormalities. A retrospective study of intestinal tissues from 15 SIV-infected macaques was performed to determine the cellular targets of the virus and examine the effect of SIV infection on jejunal mucosal morphology and function. Pathological and morphological changes included inflammatory infiltrates, villus blunting, and crypt hyperplasia. SIV-infected cells were detected by in situ hybridization in stomach, duodenum, jejunum, ileum, cecum, and colon. Using combined immunohistochemistry and in situ hybridization, the cellular targets were identified as T lymphocytes and macrophages. The jejunum of SIV-infected animals had depressed digestive enzyme activities and abnormal morphometry, suggestive of a maturational defect in proliferating epithelial cells. Our results suggest that SIV infection of mononuclear inflammatory cells in intestinal mucosa may alter development and function of absorptive epithelial cells and lead to jejunal dysfunction.
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PMID:Simian immunodeficiency virus infection of the gastrointestinal tract of rhesus macaques. Functional, pathological, and morphological changes. 850 46

Autoimmune enteropathy is characterized by chronic secretory diarrhea, villous atrophy, associated autoantibodies, and a partial response to immunosuppression. Currently available therapy (including steroids and cyclosporine) has resulted in remission only in a subset of patients. We evaluated the effects of tacrolimus (FK506) in patients with autoimmune enteropathy refractory to steroids and cyclosporine. Three patients with diagnosed autoimmune enteropathy who continued to have intractable diarrhea despite treatment with steroids and/or cyclosporine were treated with oral tacrolimus. Despite documented histological villous atrophy and poor absorption of oral cyclosporine, therapeutic tacrolimus levels were easily achieved in all 3 patients. All patients showed clinical improvement as documented by decreased stool output and ability to be weaned off parenteral nutrition; response time ranged from 1 to 4 months after tacrolimus was begun. Histological improvement was noted in all patients, and the small bowel biopsy specimens of 2 of the 3 patients showed a return to normal. All patients have been followed up for at least 6 months and are in clinical remission; 1 has received a bone marrow transplant for underlying immunodeficiency. Tacrolimus is a useful drug in the treatment of autoimmune enteropathy, even in patients who have not responded to steroids or cyclosporine. No long-term follow-up of patients with autoimmune enteropathy treated with tacrolimus is currently available.
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PMID:Treatment of pediatric autoimmune enteropathy with tacrolimus (FK506). 869 5

The PBj14 isolate of simian immunodeficiency virus, SIVsmmPBj14, induces an acutely lethal disease in experimentally inoculated pigtailed macaques, that is characterized by severe enteropathy and extensive immune activation, particularly within gut-associated lymphoid tissue (GALT). Experiments were conducted to determine whether virally induced immune activation might promote the induction of apoptosis in GALT during acute SIVsmmPBj14 infection. In situ labeling studies revealed a significant increase in the number of apoptotic cells within GALT from macaques with acute SIVsmmPBj14 infection, compared to (i) other tissues from the same animals, (ii) GALT from virus-negative animals, or (iii) GALT from macaques that were sacrificed soon after infection with SIVmac239, which does not cause acutely lethal enteropathy. These findings were confirmed by biochemical assays of DNA fragmentation, using DNA laddering and ELISA techniques. Immunostaining experiments revealed a strong positive correlation between the extent of apoptosis and the degree of immune activation, as assessed either by the number of cells which contained nuclear (activated) RelA or by the number of cells immunoreactive for CD25, a T-cell activation marker. Additional analyses of SIV antigen expression revealed that the majority of the apoptotic cells were not productively infected by SIV (i.e., that they were bystander cells). Taken together, these findings support the hypothesis that SIVsmmPBj14 efficiently induces immune activation and that this results in extensive apoptosis within gut-associated lymphoid tissue during acute viral infection.
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PMID:Apoptosis correlates with immune activation in intestinal lymphoid tissue from macaques acutely infected by a highly enteropathic simian immunodeficiency virus, SIVsmmPBj14. 891 30

T-cell lymphomas in human immunodeficiency virus infections are rare, first case have being described in 1987, by Presant. Our purpose is to report the first T-cell Lymphoma case without epidermotropism in an HIV patient in Extremadura, and pioneer in Spain. Clinic extensive and histopathologic studies of cutaneous lesions were realized, including monoclonal antibodies tests. Peculiar clinical features were small bowel disease (MALT), gingiva, pericardium and skin involvement, with spontaneous resolution of skin nodules. Polychemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone was not effective, causing serious myelotoxicity. We outline the rarity of T-cell Lymphomas, the predominance of T4 phenotype, its relation with Epstein-Barr virus, the increase in 6-interleukin production, and the prognostic value of these factors, in correlation with advanced clinical status and unfavorable outcome.
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PMID:[Report of a case of T-cell peripheral lymphoblastic lymphoma in an HIV patient]. 913 37

A patient with a commun variable immunodeficiency (CVID) is hospitalized for chronic symptoms of malabsorption (weigh loss and diarrhea). The duodenal histology show a total villous atrophy. Investigations are negative and a gluten free diet is given. Symptoms of malabsorption disappear and improvement is histologically confirmed. Our observation suggest that the coincidence of gluten sensitive enteropathy and CVID is possible and clinicians should be aware of this association and should consider giving a gluten free diet. The sensitivity of serologic testing in this conditions is unknown.
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PMID:[Common variable immunodeficiency and total villous atrophy regressive after gluten-free diet]. 936 25

Intestinal lesions were studied in 32 rhesus monkeys experimentally infected with different strains of simian immunodeficiency virus SIVmac (251/32H, 251/32H-SPL and 251/MPBL) by light microscopy, transmission and scanning electron microscopy. A spectrum of primary and secondary manifestations of SIV-infection were detected. Primary changes included 'SIV-enteropathy' in 12 monkeys and virus-induced syncytial giant cell formation (GCF) of the intestine in two animals. A primary virus-induced enteropathy occurred both as only histologically visible 'SIV-enteropathy' and as 'AIDS-enteropathy' accompanied by clinical signs of enteritis. Secondary opportunistic infections (Balantidium coli, Cryptosporidium, Trichuris, Trichomonas, Spironucleus, Mycobacteria and Cytomegalovirus) were identified in 27 animals and three monkeys developed malignant lymphomas involving the intestinal tract. Compared to intestinal lesions in HIV-infected patients, differences were found concerning the incidence of GCF and the range of opportunistic infections, with cryptosporidium, cytomegalovirus and mycobacteria occurring in both SIV-infected macaques and AIDS patients. The present observations revealed that SIV-infected rhesus monkeys provide an excellent model both for studies on the pathogenesis of HIV-enteropathy and opportunistic infections and for the development of therapies against cryptosporidial, cytomegalovirus and mycobacteria infection. Comparison of three SIV-strains revealed differences in primary and secondary lesions observed: SIVmac251/MPBL was correlated with severe primary SIV-induced pathologic changes and SIVmac251-SPL-infected animals showed a higher incidence of malignant lymphomas.
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PMID:Intestinal manifestations of experimental SIV-infection in rhesus monkeys (Macaca mulatta): a histological and ultrastructural study. 939 15

Human immunodeficiency virus (HIV)-infected patients display severe impairments of gastrointestinal functions, including diarrhea and malabsorption, even in the absence of opportunistic infections. Since HIV-1 proteins and nucleic acids have been detected in several cell types of the intestinal mucosa, it has been postulated that HIV-1 itself could alter enterocytic functions. In the present study, we analyzed the effect of HIV-1 on the differentiation process of the epithelial intestinal cell clone HT-29-D4, which mimics the maturation of enterocytes along the crypt-villus axis of the small intestine. We found that HIV-1 infection impairs cellular differentiation (i) by affecting the barrier function of the epithelium, as evidenced by a decrease in the transepithelial electrical resistance, and (ii) by inhibiting the activity of one major glucose absorption function, i.e., sodium/glucose cotransport. At the morphological level, HIV-1 infection of HT-29-D4 cells was associated with the formation of lumina, which are representative of a defect in cellular organization. These morphofunctional perturbations induced by HIV-1 could be mimicked by nocodazole, a microtubule-disrupting agent. Correspondingly, HIV-1 exposure of HT-29-D4 cells evoked a massive disruption of microtubules, as revealed by alpha-tubulin indirect immunofluorescence staining. A similar effect was observed after incubation of the cells with either recombinant gp120 or a monoclonal antibody against galactosylceramide (GalCer), the intestinal receptor for HIV-1 gp120, suggesting that the effect of HIV-1 was mediated by the binding of gp120 to GalCer. Based on these data, we propose that HIV-1 may selectively alter enterocytic functions through a direct effect on the intracellular architecture of the cells. In contrast with previous theories for HIV-1 enteropathy, our data support the concept that HIV-1 may perturb intestinal functions without necessarily infecting intestinal epithelial cells.
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PMID:Direct effect of type 1 human immunodeficiency virus (HIV-1) on intestinal epithelial cell differentiation: relationship to HIV-1 enteropathy. 940 May 96

Body wasting, protein catabolism, and hypoalbuminemia are complicating features of the acquired immunodeficiency syndrome (AIDS). Given their multifactorial causes, the contributing role of intestinal protein loss has not yet been fully elucidated. To quantify enteric protein leakage, determination of fecal alpha 1-antitrypsin (AAT) excretion has been established as an accurate and reliable endogenous marker. We estimated AAT concentration by standard immune nephelometry in duplicate random stool samples of 49 patients with AIDS, and we compared it to that of 43 patients with chronic inflammatory bowel disease and to 34 healthy controls. When compared with healthy persons, patients with AIDS had increased fecal AAT excretion regardless of current opportunistic intestinal infections and fecal AAT excretion similar to that of patients with quiescent chronic inflammatory bowel disease. The ratio of fecal and serum AAT concentration was not different between AIDS patients and healthy controls, although it was consistently increased in those with chronic inflammatory bowel disease. Significant intestinal protein leakage occurs in patients with AIDS, probably due to primary impairment of gut permeability. Enteric protein loss may be an important feature of human immunodeficiency virus-associated enteropathy with altered mucosal barrier function.
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PMID:Intestinal protein leakage in the acquired immunodeficiency syndrome. 941 42

Honduras has at least five-times more human immunodeficiency virus (HIV)-infected individuals than any other country in Central America. The relationship between HIV status and the presence of intestinal parasites in this part of the world is unknown. This study presents the results from a prospective, comparative study for the presence of parasites in 52 HIV-positive and 48 HIV-negative persons in San Pedro Sula, Honduras. Infection with HIV was determined by microagglutination and confirmed by Western blot analysis. Parasites were detected in stools using formalin-ether concentration, and Kinyoun and trichrome staining. Age, sex, and clinical state of HIV infection were recorded for each study participant. Our results indicate that Cryptosporidium parvum and Strongyloides stercoralis, which are intracellular or live in the mucosa, were found exclusively in persons infected with HIV. In comparison, the prevalence of the extracellular parasites Giardia lamblia, Ascaris lumbricoides, and Trichuris trichiura was significantly higher (P < 0.05) in persons who were HIV-negative. Trichuris worms are in contact with the gut epithelium and less so with the mucosa, whereas Strongyloides lives within the gut mucosa. It is possible that changes in the gut epithelium due to HIV infection do not affect the mucosa and therefore would not affect Strongyloides. We conclude that infection with HIV may selectively deter the establishment of certain intestinal parasites. This may be due to the fact that HIV-induced enteropathy does not favor the establishment of extracellular parasites. Intracellular and mucosal dwelling organisms, however, may benefit from pathologic changes and reduced local immune responses induced by the virus, which, in turn, may lead to higher prevalence among HIV-infected individuals.
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PMID:Intestinal parasitic infections in human immunodeficiency virus (HIV)-positive and HIV-negative individuals in San Pedro Sula, Honduras. 957 87


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