Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied susceptibility to experimental systemic cryptococcosis in mice previously infected with the retroviral complex LP-BM5 (responsible for murine AIDS). LP-BM5 was inoculated to C57B1/6 mice by intravenous (i.v.) injection 8 weeks before an i.v. challenge with 4 x 10(3) CFU of Cryptococcus neoformans. Uninfected and singly infected mice were used as controls. LP-BM5 infection did not result in a significant increase in fungal burdens in the lungs or brains of co-infected animals compared to mice infected with C. neoformans alone. However, mortality was enhanced in the co-infected animals. The kinetics of splenocyte subsets differed in co-infected mice and LP-BM5-infected mice; the increase in CD4+, CD8+ and Ly5+ cells was only moderate in the former. Cytokine production by concanavalin A (Con A)-stimulated splenocytes from co-infected mice showed a marked decrease in the Th1 response (IFN-gamma, IL-2) and an increase in the Th2 response (IL-4, IL-10). Furthermore, cryptococcosis altered the course of MAIDS, inhibiting splenomegaly. This effect was not related to a decrease in ecotropic virus titres in the spleen or to improved in vitro responsiveness of spleen cells to Con A. The marked decrease in IFN-gamma production in co-infected animals could partly explain the inhibition of LP-BM5-induced splenomegaly. This model of murine retroviral infection does not seem to be suitable for studying cryptococcosis in immunosuppressed animals, but remains valuable for investigating in vivo interactions between two pathogens.
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PMID:Cryptococcus neoformans infection in mice previously infected with LP-BM5 MuLV, the agent of murine AIDS (MAIDS). 936 2

The lipophilic yeast Pityrosporum ovale is a member of the normal human cutaneous flora in adults but also associated with several skin diseases. In pityriasis versicolor, under the influence of predisposing factors, P. ovale changes from the round blastospore form to the mycelial form. A great problem in pityriasis versicolor is the high rate of recurrence and to avoid this a prophylactic treatment is mandatory. Pityrosporum folliculitis is a chronic disease characterized by pruritic follicular papules and pustules located primarily on the upper trunk, neck and upper arms. In direct microscopy clusters of round budding yeast cells are found. The disease responds rapidly to antimycotic therapy. There are now many studies indicating that P. ovale plays an important role in seborrhoeic dermatitis. Many of these are treatment studies showing a good effect of antimycotics paralleled by a reduction in number of organisms. Severe seborrhoeic dermatitis often difficult to treat is associated with AIDS. In peripheral blood from a high number of patients with seborrhoeic dermatitis we found an increase in number of natural killer T-cells and decreased PHA and Con-A stimulation. Secondary we found low serum IgG antibody titres in patients compared to controls. Other studies have found a reduced lymphocyte stimulation reaction when lymphocytes from patients with seborrhoeic dermatitis were stimulated with a P. ovale extract. Additionally, IL-2 and IFN gamma production by lymphocytes from patients was markedly depressed and IL-10 synthesis were increased after stimulation with P. ovale extract. The majority of adult patients with atopic dermatitis localized to the head, neck and scalp are prick-test positive to a protein P. ovale extract. One study showed that p. ovale extracts increased IL-4, IL-10 and IgE synthesis in patients with atopic dermatitis. There are also treatment studies indicating that antifungal treatment may be beneficial in these patients.
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PMID:Pityrosporum yeasts--what's new? 937 Jan 47

Infection of rhesus monkeys with SIV leads to AIDS-like symptoms. Similar to human AIDS patients, some monkeys develop B cell non-Hodgkin lymphoma (NHL). We determined transcription of cytokine genes regulating the activation of B and T cells, which play a role in intratumoral immune surveillance. Therefore, we compared the transcription of the cytokine genes encoding IL-2, IL-4, IL-6, IL-10, IFN-gamma, TNF-alpha, and TGF-beta1, and the Epstein-Barr virus-encoded BCRF 1 gene, in cells from five monkey and two human tumor specimens. The immune-suppressive IL-10 and TGF-beta1 genes were predominantly transcribed in all tumor specimens analyzed. Cytokine gene transcription patterns appeared to be similar in human and animal tumor cells. The transcription patterns corresponded to their histological classification as diffuse large-cell lymphoma according to the REAL classification and as immunoblastic or centroblastic tumors according to the Kiel classification. The determination of cytokine gene transcription pattern in the NHL may improve our understanding of pathogenesis and immune surveillance in this heterogeneous group of tumors. Our data show that SIV-associated NHLs of rhesus monkeys are comparable to human HIV-1-associated EBV-positive non-Hodgkin lymphoma.
AIDS Res Hum Retroviruses 1997 Dec 10
PMID:Cytokine gene transcription in simian immunodeficiency virus and human immunodeficiency virus-associated non-Hodgkin lymphomas. 943 Feb 51

Reports on plasma concentrations of tumor necrosis factor alpha (TFN-alpha), interleukin 6 (IL-6), IL-10, and IFN-alpha in AIDS patients are contradictory. An alternative approach for the estimation of cytokine production is the measurement of lipopolysaccharide (LPS)-stimulated cytokine production in whole blood. We compared plasma concentrations of these cytokines, soluble TNF receptor (sTNFr) types I and II, and LPS-stimulated cytokine production in whole blood from clinically stable AIDS patients (n = 6) and healthy controls (n = 6). The plasma concentrations of TNF-alpha and sTNFr-II were higher in AIDS patients compared with controls (mean [95% CL]: TNF-alpha, 24 [17-31] and 8 [1-16] pg/ml, respectively, p < 0.01; sTNFr-II, 6.8 [4.6-9.0] and 3.2 [2.4-4.0] ng/ml, respectively, p < 0.01). The plasma concentrations of sTNFr-I and IL-10 were not different between AIDS patients and controls. Neither IL-6 nor IFN-alpha was detectable in any plasma sample. LPS-stimulated production in whole blood of TNF-alpha, IL-6, IL-10, and IFN-alpha was not different between AIDS patients and controls at any combination of LPS concentration (0, 0.1, 0.5, 1, 10, 100, and 1000 ng/ml) and duration of stimulation (0, 4, 8, and 24 hr). It is concluded that the plasma concentrations of TNF-alpha and sTNFr-II, but not of IL-6, IL-10, IFN-alpha, and sTNFr-I, are higher in AIDS patients compared with controls. The production of cytokines in LPS-stimulated whole blood does not provide information additional to the measurements of plasma concentrations.
AIDS Res Hum Retroviruses 1998 Jan 20
PMID:In vitro production of cytokines in whole blood versus plasma concentrations of cytokines in AIDS. 946 22

T cell receptor (TCR) triggering via superantigens induces decreased proliferative responses and increased apoptosis in T cells from HIV-infected patients compared with controls. Our aim was to delineate the role of intrinsic T cell defects, of APC dysfunction and of cytokines and costimulatory signal dysregulation in the deficient responses of CD4+ and CD8+ T cells from HIV+ subjects to the superantigen Staphylococcus enterotoxin A (SEA). Proliferation and IL-2R alpha up-regulation on SEA-stimulated CD4+ and CD8+ T cells in whole blood were reduced in HIV+ subjects with CD4 counts < 500, compared with controls. Neither addition of IL-2, IL-12 or phorbol myristate acetate (PMA) nor neutralization of endogenous IL-10, tumour necrosis factor-alpha (TNF-alpha), TNF-beta or transforming growth factor-beta (TGF-beta) could restore the decreased activation by SEA. Possible intrinsic T cell defects were studied by presenting SEA on HLA-DR-transfected Chinese hamster ovary (CHO) cells, co-expressing LFA3 and/or CD80, to purified T cells. In this system CD8+ T cells from most HIV+ patients were hyporesponsive with regard to IL-2 production, IL-2R alpha up-regulation and proliferation, whereas clearly reduced responses were only shown in CD4+ T cells from AIDS patients. Similarly, apoptosis was increased in CD8+ T cells from all patients, but only in CD4+ T cells from AIDS patients. During HIV infection, the responses to TCR triggering through SEA are deficient in both T cell subsets. The intrinsic defect appears earlier during disease progression in purified CD8+ T than in CD4+ T cells, it occurs in conjunction with both CD2 and CD28 costimulation, and it is correlated with increased levels of apoptosis.
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PMID:Superantigen activation of CD4+ and CD8+T cells from HIV-infected subjects: role of costimulatory molecules and antigen-presenting cells (APC) 947 54

Patients with advanced human immunodeficiency virus (HIV) infection are susceptible to infections with Mycobacterium avium complex (MAC). Interleukin (IL)-10 may impair immunity to MAC; therefore, the effect of different MAC preparations on IL-10 production was examined in mononuclear cell cultures from HIV-infected patients. IL-10 levels in cultures for 26 patients were higher than those in 20 control cultures. The highest IL-10 levels were found in cultures from patients with the most advanced HIV disease. Monocytes were the major IL-10 producers, while little IL-10 could be attributed to Th2 lymphocytes. Cultures for patients produced reduced levels of tumor necrosis factor-alpha and normal levels of IL-12; the production of these cytokines increased after neutralization of IL-10. Circulating IL-10 was higher in HIV-infected patients than in controls, with the highest levels in the AIDS group. Elevated monocyte/macrophage-derived IL-10 production may contribute to the high susceptibility to MAC infection seen in patients with advanced HIV disease.
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PMID:Enhanced interleukin-10 production in response to Mycobacterium avium products in mononuclear cells from patients with human immunodeficiency virus infection. 949 36

The present study analyses the ability of HIV-1 to modulate IL-10 production in cells of monocyte-macrophage lineage cultured in the presence of macrophage colony-stimulating factor (M-CSF). Both monocytes and macrophages spontaneously produced low amount of IL-10. Lipopolysaccharide (LPS) induced a strong IL-10 response in fresh monocytes and in M-CSF-treated macrophages. In contrast, macrophages cultured in the absence of M-CSF exhibited a marked decrease in their susceptibility to LPS stimulation. M-CSF increased the IL-10 response of macrophages to LPS by enhancing both the expression of membrane-bound CD14, the protein that serves as LPS receptor, and the sensibility of CD14-expressing cells to LPS stimulation. Neither spontaneous nor LPS-induced expression of IL-10 was modulated in monocytes and macrophages by infection with eight monocytotropic strains, as demonstrated by ELISA and cytofluorimetric analysis. In contrast, all the HIV-1 strains primed macrophages for an increased IL-6 response to LPS stimulation. To determine whether IL-10 production was associated with in vivo infection, monocytes from AIDS individuals were analysed for IL-10 production. We found that neither spontaneous nor LPS-induced IL-10 production were different between healthy controls and HIV-infected patients. Taken together, these data strongly suggest that HIV-1 infection of monocytes-macrophages does not play a significant role in the regulation of IL-10 in infected patients. This study also emphasizes the role of M-CSF activation in the regulation of the cytokine response in macrophages.
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PMID:HIV-1 does not alter in vitro and in vivo IL-10 production by human monocytes and macrophages. 956 97

Vaccination of HIV-infected individuals increases HIV viral load, reduces CD4 cell counts, and might influence disease progression. Because these deleterious effects are postulated to be secondary to a direct activation of T lymphocytes induced by the immunogen, we compared immunologic and virologic effects of a T cell-dependent and a T cell-independent vaccine. Seventeen HIV-infected children were immunized with influenza (FLU) (T cell-dependent) or pneumococcal (PNEUMO) (T cell-independent) vaccines. HIV viral load and type 1 (IL-2 and IFN-gamma) and type 2 (IL-4 and IL-10) cytokine production were evaluated before and 7, 14, and 28 days after vaccination. Slopes of CD4 cell counts analyzed 6 months before and 6 months after vaccination were not significantly different. HIV viral load increased in both groups of children despite the fact that type 1 cytokine production and the type 1-to-type 2 ratio increased in FLU-vaccinated but not in PNEUMO-vaccinated patients. Thus, an increase in HIV viral load in the absence of T cell activation (as measured by cytokine production) was observed in PNEUMO-vaccinated children. Because polysaccharides of the bacterial cell wall stimulate TNF-alpha production by monocyte-macrophages and TNF-alpha was shown to stimulate HIV replication directly on activation of NF-kappa b after binding the long terminal repeat (LTR) sequences of HIV, we measured TNF-alpha production and observed a significant increase in both groups of vaccines. These data suggest that an increase in HIV viral load can be observed in vaccinated HIV-infected children even independent of direct antigen-induced activation of T lymphocytes, and that augmented production of TNF-alpha might play a role in this phenomenon.
AIDS Res Hum Retroviruses 1998 Jun 10
PMID:Immunization with both T cell-dependent and T cell-independent vaccines augments HIV viral load secondarily to stimulation of tumor necrosis factor alpha. 964 72

Increase Th2 cytokine production may contribute to some clinical manifestations of HIV infection, and studies have suggested that IL-13 rather than IL-4 is involved in these conditions. We directly tested this hypothesis by administrating IL-13 to SIV-infected macaques. SIV-infected rhesus macaques received a daily subcutaneous injection for 21 days of either IL-13 (10 microg/kg/day) or a placebo. The four macaques treated with IL-13 experienced body weight loss (9.95 +/- 0.71%) related to intestinal tract damage: they all suffered from a complete atrophy of duodenal villi. This was presumably due to premature epithelial cell death: proliferating Ki67+ cells in glandular crypts were as numerous as in control animals, but many epithelial cells developed apoptosis. The duodenal mucosa was infiltrated with cells expressing CD56 and PEN5, two markers of NK cells, and there was a deregulation of local cytokine and chemokine production characterized by a decrease in IL-10 gene expression (25% of controls) and an increase in gene expression for IFN-gamma (4-fold control), MIP-1alpha (8-fold control), and MIP-1beta (13-fold control). Thus, IL-13 can induce digestive epithelial cell injury in vivo in primates infected with a retrovirus. Therefore, its role should be considered in digestive manifestations of HIV infection as well as in other disorders associated with intestinal epithelial atrophy.
AIDS Res Hum Retroviruses 1998 Jun 10
PMID:Administration of interleukin 13 to simian immunodeficiency virus-infected macaques: induction of intestinal epithelial atrophy. 964 77

HIV-1 Tat protein, which trans-activates HIV-1 expression, exerts many effects on host immune function. Meanwhile, PBMCs and pulmonary macrophages from HIV-1-infected patients produce only a small amount of IL-12, which plays an essential role in the development of helper T type 1 (Th1) cells, and in the generation of cytotoxic T lymphocytes. We examined the possibility that Tat suppresses IL-12 production by PBMCs from healthy donors. Tat significantly inhibited IL-12 production by human PBMCs stimulated with Staphylococcus aureus Cowan 1 strain (SAC) at concentrations between 5 and 40 ng/ml. Immunoabsorption by using polyclonal antibody to Tat abolished the suppression of the IL-12 production by Tat. Tat at the same concentrations did not affect IL-10, IL-6, or TNF-alpha production. Other HIV-1 proteins (Nef and gp120) did not influence IL-12 production. Tat also suppressed the expression of mRNA encoding the p40 chain of IL-12, whereas it did not affect the expression of mRNA encoding IL-10 and beta-actin. IL-12 production by monocytes, separated from PBMCs by the adhesion method, was also inhibited by Tat. These results suggest that Tat protein is one of the main causes of decreased IL-12 production by PBMCs (mostly by monocytes) from HIV-1-infected individuals.
AIDS Res Hum Retroviruses 1998 Jul 01
PMID:HIV type 1 Tat protein inhibits interleukin 12 production by human peripheral blood mononuclear cells. 967 Dec 13


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