Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged consumption of ethanol (ETOH) results in alterations of host defense via immune modulation, increasing susceptibility to infection. In the present study, effects of chronic dietary ETOH on cytokine production by splenocytes and thymocytes, splenocyte and thymocyte proliferation induced by mitogens, splenic natural killer cell activity, and antibody production (IgA and IgG) were examined. C57BL/6 mice were fed 5% ETOH v/v in the Lieber-DeCarli liquid diet for 11 weeks. Release of interleukin (IL)-2, IL-5, IL-6, IL-10, and interferon (IFN)-gamma produced by concanavalin A (Con A) stimulated splenocytes was significantly decreased, whereas secretion of IL-4 was slightly decreased by chronic dietary ETOH compared with controls. Production of tumor necrosis factor-alpha and IL-6 by lipopolysaccharide-stimulated splenocytes was significantly and slightly decreased by ETOH compared with controls, respectively. Splenocyte and thymocyte proliferation induced by Con A was significantly inhibited by ETOH, whereas splenocyte proliferation induced by lipopolysaccharide was not affected. Natural killer cell activity was significantly inhibited by ETOH compared with controls. The production of IgA and IgG by splenocytes were also significantly decreased by ETOH compared with controls. The levels of IL-2, IL-4, and IL-6 produced by Con A-stimulated thymocytes were significantly reduced by dietary ETOH compared with control, whereas production of IFN-gamma by thymocytes was not affected. Our results suggest that chronic dietary ETOH alters the cytokine release, thereby impairing immune response and T-cell maturation, which increase host susceptibility to infection.
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PMID:Influence of chronic dietary ethanol on cytokine production by murine splenocytes and thymocytes. 819 29

In this paper we report that macrophages can be stimulated to express detectable levels of IFN-gamma-specific mRNA. Macrophages from lipopolysaccharide (LPS)-responsive, C3H/OuJ mice are induced by LPS to increase steady-state levels of IFN-gamma-specific mRNA, while those from LPS-hyporesponsive C3H/HeJ mice are not. This interstrain variation is apparently the result of LPS-specific signal differences since macrophages derived from both Lpsn and Lpsd mouse strains are able to produce comparable levels of IFN-gamma-specific mRNA following stimulation with polyinosinic-polycytidylic acid. The identity of the cell type responsible for this IFN-gamma message appears to be the macrophage as IFN-gamma-specific mRNA was also detectable following T and natural killer cell depletion, in the LPS-stimulated RAW 264.7 cell line, and in a homogeneous population of mature macrophages propagated in vitro by stimulation of bone marrow progenitors with recombinant colony stimulating factor-1. Immunofluorescent staining of fixed and permeabilized LPS-stimulated macrophages confirmed the presence of immunoreactive IFN-gamma protein. The possible significance of IFN-gamma production by macrophages is discussed in the context of normal macrophage differentiation as well as the inflammatory immune response.
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PMID:Induction of IFN-gamma in macrophages by lipopolysaccharide. 826 Apr 52

This study was performed to examine the in vivo effects of a bolus of recombinant human growth hormone (r-hGH) on the human immune system. In a double blind placebo controlled cross over study, healthy volunteers were given 2 IU r-hGH as an intravenous infusion. r-hGH did not influence the subpopulations of blood mononuclear cells (BMNC), natural killer cell activity, in vitro proliferative responses or production of interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-2, IL-6, IL-8, tumor necrosis factor alpha (TNF alpha), TNF beta or interferon gamma in supernatants from BMNC stimulated with either lipopolysaccharide or phytohemagglutinin. However, two h after infusion a significant neutrocytosis occurred. It is concluded that a bolus infusion of r-hGH to healthy volunteers exerts only minor effects on the human immune system.
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PMID:Effects of an acute bolus growth hormone infusion on the human immune system. 828 61

The purpose of this study was to correlate cellular immune responses and cytokine production in vitro between patients with one or two primary malignant neoplasms. One hundred and ninety-three patients (110 patients with one primary malignant neoplasm (group I), and 83 patients with two primary tumors (group II), entered this study. Mononuclear cells isolated from peripheral blood were tested in the following tests: (a) proliferative responses in the autologous and allogeneic mixed lymphocyte reaction (auto- and allo-MLR respectively): (b) natural killer cell activity; (c) production of interleukin-2 during the allo-MLR, and (d) interleukin-1 beta production by lipopolysaccharide-stimulated monocytes. All these parameters were found to be decreased in cancer patients as compared to normal donors (p < 10(-3)). In addition, we were able to detect significant differences between the values obtained from patients in groups I and II (p < 10(-2)). These data suggest a further impairment in cancer patients' immune status after the diagnosis of a second malignancy.
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PMID:Comparison of immune parameters in patients with one or two primary malignant neoplasms. 843 63

Cryptosporidium parvum is a coccidian parasite that causes diarrheal disease in animals and humans. Severe cryptosporidial infections were noted in young adult rats immunosuppressed with the glucocorticosteroid dexamethasone (DEX). B-cell and T-cell responses to the mitogens lipopolysaccharide and concanavalin A, respectively, were depressed in the DEX-treated rats. In addition, DEX treatment suppressed serum IgG levels, in vitro IgG production, and natural killer cell activities. Previous results have shown that DEX-immunosuppressed rats treated with dehydroepiandrosterone (DHEA) exhibit significant reductions in cryptosporidiosis as determined by monitoring oocyst shedding in the feces and parasite colonization of the small intestine. Results from this study indicated that B- and T-cell responses to their respective mitogens, serum IgG levels, and in vitro IgG production were greater in DHEA-treated immunosuppressed rats than in untreated DEX-immunosuppressed rats infected with C. parvum. Similar results were demonstrated in DHEA-treated versus normal control rats infected with C. parvum. These results suggest that the effects of DHEA in reducing cryptosporidiosis are the result of a potentiation of the immune system in the immunosuppressed rats.
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PMID:Effects of dehydroepiandrosterone in immunosuppressed rats infected with Cryptosporidium parvum. 850 92

Our previous work has shown that cells of the immune system produce a growth hormone (GH) molecule similar to that secreted by the pituitary. In the present studies, we evaluated the possibility that normal spleen cells producing GH transferred to dwarf mice could stimulate their growth. The results showed that normal spleen cells alone or spleen cells treated with growth-hormone-releasing hormone (GHRH) did not appear to significantly stimulate the growth of dwarf mice. Spleen cells activated in vitro with concanavalin A or lipopolysaccharide and then transferred to dwarf mice, or thymus cells alone, were also without effect, whereas GH alone stimulated growth as expected. Serum levels of insulin-like growth factor-I (IGF-I) and IGF-I-liver RNA were undetectable in control dwarf mice and dwarf mice receiving spleen cells, whereas serum levels of IGF-I increased after treatment of dwarf mice with GH. The immune system of dwarf mice receiving spleen cells, however, was significantly altered. Spleen cells from dwarf animals showed enhanced immunoglobulin, interleukin (IL)-6, IL-2, and interferon-gamma production whereas no significant change was apparent in natural killer cell activity. Despite the absence of the pit-1 protein in dwarf mice, their spleen and thymus cells retained the ability to produce almost as much lymphocyte GH as normal. Overall, the findings support the idea that the pit-1 protein in lymphocytes of dwarf mice may not be obligatory for the expression of lymphocyte GH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the administration of growth-hormone-producing lymphocytes on weight gain and immune function in dwarf mice. 852 85

The subpopulation of strongly CD14-positive (CD14++) monocytes and monocytes coexpressing the CD16 antigen and low levels of CD14 (CD14+/CD16+ cells) were isolated by fluorescence-activated cell sorting (FACS) followed by stimulation with lipopolysaccharide (LPS) at 1 micrograms/mL. Polymerase chain reaction (PCR) after reverse transcription of isolated mRNA (RT-PCR) revealed similar levels of tumor necrosis factor (TNF) transcripts in both subpopulations. By contrast, transcripts for interleukin-10 (IL-10) were only detectable in CD14++ monocytes, whereas CD14+/CD16+ cells produced no detectable IL-10 transcripts after 4 hours. Only after 16 hours of LPS stimulation was a low level of IL-10 transcripts discernible in CD14+/CD16+ monocytes. The same pattern was seen at the protein level in that TNF in LPS-stimulated supernatants was comparable for both subpopulations, whereas IL-10 was detected in CD14++ monocytes but not in CD14+/CD16+ cells. To avoid interference of cell activation by CD14 and CD16 antibodies, cells were also isolated based on the high and low level of CD33 antigen expression. Again, weakly CD33-positive cells, which comprise the CD14+/CD16+ cells, showed no or only minimal IL-10 mRNA. When comparing blood monocyte subpopulations with alveolar macrophages (AM), AM showed high levels of LPS-stimulated TNF, whereas IL-10 transcripts were undetectable. Our data show that CD14+/CD16+ blood monocytes produce high levels of proinflammatory cytokines like TNF, whereas the anti-inflammatory IL-10 is low or absent, a pattern similar to what is seen in AM.
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PMID:Differential cytokine expression in human blood monocyte subpopulations: a polymerase chain reaction analysis. 854 64

Preincubation of peripheral blood lymphocytes with the microtubule disturbing agents estramustine (ETMN; n = 7, final conc. 20 microM) or taxol (TX; n = 13, final conc. 10 microM), resulted in a statistically significant inhibition of natural killer cell activity [(NKCA); baseline (x +/- SD; expressed as percentage of specific chromium release) of 32.2 +/- 30.5 and 34.4 +/- 27.7 and drug treated samples of 13.9 +/- 19.9 and 12.5 +/- 20.8, respectively; Student's paired t-test p < 0.005]. Furthermore, most individual values for NKCA in the drug preincubated samples were at least 20% below the same subject baseline lytic function (except for TX sample No.1), and NKCA was non detectable in 4 out of 7 and 5 out of 13 samples (pretreatment with either ETMN or TX< respectively). The use of other concentrations and different preincubation times for these chemotherapeutic agents also produced NKCA inhibition, which was time and dose dependent. Preincubation with lipopolysaccharide (LPS; n = 16, final conc. 50 micrograms/ml), an endotoxin prominently involved in the etiology of septic shock, resulted in a statistically significant enhancement of NKCA [baseline (x +/- SD; expressed as percentage of specific chromium release) of 25.4 +/- 20.4 and LPS treated sample of 36.6 +/- 17.4, respectively; Student's t paired t-test p < 0.005]. At least a 20% increase in NKC lytic function over its own baseline value was recorded for each and everyone of the samples tested with LPS.2+ the pathophysiology associated with septic shock.
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PMID:Studies of natural killer cell activity in a drug-free, healthy population. Response to a challenge with taxol, estramustine and lipopolysaccharide. 855 26

Research from our laboratory has demonstrated that the presentation of an aversive conditioned stimulus produces pronounced suppression of several in vitro measures of immune status. The present study was designed to evaluate the role of central corticotropin-releasing hormone (CRH) in the mechanisms mediating these conditioned effects. The aversive conditioned stimulus was a distinct environment that had previously been associated with electric footshock. Lewis rats received intraventricular administration of either buffered saline or a dose of the CRH-selective receptor antagonist alpha-helical CRH(9-41) (0, 0.5, 5, or 50 micrograms) prior to exposure to the aversive conditioned stimulus or home cage control treatment. The aversive conditioned stimulus produced decreases in splenic natural killer cell activity, splenocyte responsiveness to the mitogens concanavalin A (ConA), phytohemagglutinin (PHA), lipopolysaccharide (LPS), and the combination of ionomycin and phorbol myristate acetate (PMA), blood leukocyte responsiveness to ConA and PHA, and the production of interleukin-2 and interferon-gamma by activated splenocytes. The conditioned stimulus also produced an increase in plasma levels of corticosterone. Pretreatment with alpha-helical CRH(9-14) completely blocked the conditioned stimulus-induced suppression of natural killer cell activity. The CRH antagonist had no attenuative effect on the conditioned suppression of splenocyte or blood leukocyte proliferation in response to mitogens, or the production of interleukin-2 or interferon-gamma by activated splenocytes. There was also no effect of alpha-helical CRH(9-14) on the conditioned stimulus-induced increase in plasma corticosterone. These findings suggest that conditioned stimulus-induced suppression of natural killer cell activity is mediated by a mechanism that involves activity at central CRH receptors, and that this conditioned modulation is independent of HPA activation. Furthermore, these results indicate that the mechanisms involved in conditioned stimulus-induced suppression of proliferative or cytokine production responses are distinct from those involved in the modulation of natural killer cell activity.
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PMID:Corticotropin-releasing hormone is involved in conditioned stimulus-induced reduction of natural killer cell activity but not in conditioned alterations in cytokine production or proliferation responses. 855 20

The present study examined the involvement of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis in the immunomodulatory effects of acute morphine treatment in rats. Chlorisondamine, a ganglionic blocker, was used to assess the involvement of sympathetic and sympathoadrenal activity. Adrenalectomized rats were used to assess the involvement of the adrenal cortex, which is regulated primarily by hypothalamic-pituitary-adrenal axis activity, and the adrenal medulla, which is regulated primarily by sympathetic activity. The results showed that both chlorisondamine and adrenalectomy antagonize morphine's suppressive effects on the proliferative response of splenic lymphocytes to concanavalin A (Con A), lipopolysaccharide or ionomycin/phorbol myristate acetate. Chlorisondamine, but not adrenalectomy, antagonizes morphine's suppressive effects on phytohemagglutinin (PHA)-stimulated proliferation of splenic lymphocytes and interferon-gamma production by stimulated splenocytes. Adrenalectomy, but not chlorisondamine, blocks morphine's suppressive effects on the proliferative response of blood lymphocytes to Con A or PHA. Neither chlorisondamine nor adrenalectomy alters morphine's suppressive effect on splenic natural killer cell cytotoxicity. Collectively, these results suggest that sympathoadrenal activity is involved in the suppressive effects of acute morphine treatment on the proliferative response of splenic T and B cells to Con A, lipopolysaccharide or ionomycin/phorbol myristate acetate. Morphine's suppressive effects on the proliferative response of splenic T cells to PHA and the production of interferon-gamma by stimulated splenocytes also involve sympathetic activity, but not sympathoadrenal activity. The results suggest further that morphine's suppressive effects on the proliferative response of blood T cells to Con A or PHA do not involve sympathetic activity, but rather adrenocortical activity. Neither sympathetic nor adrenocortical activity appears to be involved in morphine's suppressive effect on splenic natural killer cell cytotoxicity.
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PMID:Evidence for sympathetic and adrenal involvement in the immunomodulatory effects of acute morphine treatment in rats. 862 40


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