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At least 901 records · Page 50Linked to original sources
PubMed2005

Leptin ameliorates burn-induced multiple organ damage and modulates postburn immune response in rats.

The present study was designed to determine whether exogenous leptin reduces remote organ injury in the rats with thermal burn trauma. Leptin (10 microg/kg) or saline was administered intraperitoneally after burn injury, and the rats were decapitated at either 6 or 24 h. Plasma samples of 24-h burn group were assayed for the determination of monocyte and neutrophil apoptosis. Thermal injury increased tissue-associated myeloperoxidase (MPO) activity and microscopic damage scores in the lung, liver, stomach, colon and kidney of both 6- and 24-h burn groups. In the 6-h burn group, leptin reduced microscopic damage score in the liver and kidney only, while damage scores in the 24-h burn group were reduced in all the tissues except the lung. Also, in both burn groups, leptin reduced elevated MPO activity in all tissues except the lung. The percentage of mononuclear cells was significantly reduced at the 24 h of burn injury, while the granulocyte percentage was increased. Leptin treatment, however, had no significant effect on burn-induced reversal of white blood cell ratios. On the other hand, burn-induced increase in the death of mononuclear cells and granulocytes was significantly reduced in leptin-treated rats. The results of the present study suggest that leptin may provide a therapeutic benefit in diminishing burn-induced inflammation and associated multiple organ failure.

Animals↗
PubMed2006

IL-18 as critical co-stimulatory molecules in modulating the immune response of ITAM bearing lymphocytes.

NK cells responses are controlled by inhibitory and activating cell surface receptors. Inhibitory receptors serve to moderate NK activity by dampening cytokine release and cytotoxicity if activating ligands are also triggered by interaction with their receptors on the NK cells. This dampening effect is critical to prevent wide scale self destruction. These studies have focused on cytokine signaling in the context of an environment where ITAM bearing receptors are triggered on NK, NKT and T cells. Our findings indicate that cytokines are an important co-stimulatory signal that is needed to maximize the host innate immune response.

Animals↗
PubMed2005

The use of Th1 cytokines, IL-12 and IL-23, to modulate the immune response raised to a DNA vaccine delivered by gene gun.

Unlike intramuscular injection, gene gun delivery of DNA drives a strong type 2 response. In an effort to counter this, we have genetically fused the type 1 cytokines, IL-12 and IL-23, to the hemagglutinin (HA) gene from influenza APR/8/34, and delivered these DNA constructs to Balb/c mice. Gene gun delivery of the HA gene was able to induce antibody production by all vaccinated mice. Linking of IL-12 caused almost complete suppression of immune responses whereas mice vaccinated with IL-23HA showed long-lived IgG1 antibody levels. Splenocytes from IL-23HA vaccinated mice also tended to produce more IL-5 and IFNgamma after restimulation in vitro than splenocytes from HA vaccinated mice. While codelivery of IL-23 did not change the type of immune response it may increase its longevity following vaccination.

Animals↗
PubMed2004

Reduction in arthritis severity and modulation of immune function in tissue factor cytoplasmic domain mutant mice.

Tissue factor (TF), a transmembrane receptor for plasma factor VII(a), is the main initiator of the coagulation cascade. It has also been implicated in noncoagulant processes, including inflammation. The function of the TF cytoplasmic domain was studied in mice in which 18 of the 20 cytoplasmic amino acids were deleted. This mutation (TF(deltaCT/deltaCT)) is not associated with alterations in blood coagulation. Arthritis was induced by intra-articular injection of methylated bovine serum albumin (mBSA) in mice preimmunized with mBSA. Arthritis severity was significantly reduced in TF(deltaCT/deltaCT) mice compared to wild-type mice, including reductions in synovitis, synovial exudate, cartilage degradation, and bone damage. A marked reduction in synovial interleukin (IL)-1beta and IL-6 mRNA was also observed. Serum anti-mBSA IgG1, but not IgG2a, was increased in mutant mice. Cutaneous delayed-type hypersensitivity and antigen-induced T-cell proliferation were reduced in TF(deltaCT/deltaCT) compared to wild-type mice. A significant down-regulation of lipopolysaccharide-induced IL-1, tumor necrosis factor, IL-6, macrophage migration inhibitory factor, and matrix metalloproteinase-13 mRNA was observed in immunized, but not in naive TF(deltaCT/deltaCT) macrophages ex vivo. These data suggest a significant role for the cytoplasmic domain of TF in the regulation of the immunoinflammatory responses, a murine arthritis model, and macrophage function.

Animals↗
PubMed2003

Asian and Siberian ginseng as a potential modulator of immune function: an in vitro cytokine study using mouse macrophages.

BACKGROUND: Ginseng is a widely used herbal product in China, other Asian countries, and in the Unites States. There is a traditional belief that ginseng stimulates immune functions. In this study, the innate effects of Asian and Siberian ginsengs on cytokines and chemokines produced by cultured macrophages were examined. MATERIALS AND METHODS: The effects of Asian and Siberian ginseng on cytokines and chemokines produced by cultured macrophages were examined. Mouse macrophages (J774A.1) were incubated with Asian or Siberian ginseng at varying concentrations (1, 10, 100, and 1000 microg/ml) for 24 h and then harvested for RNA isolation. The expression levels of IL-1beta, IL-12, TNF-alpha, MIP-1 alpha, and MIP-2 mRNA were measured by quantitative PCR. RESULTS: Our data showed that Asian ginseng induced a statistically significant increase in IL-12 expression at both mRNA and protein levels. However, the minor twofold increase is probably biologically insignificant. No significant increase of IL-12 by Siberian ginseng was observed at any dose level studied. No significant change in IL-1beta, IL-15, TNF-alpha, or MIP-1alpha mRNA was observed by either Asian or Siberian ginseng treatment. CONCLUSIONS: Our data showed statistically significant differential regulation of IL-12 by Asian ginseng. Siberian ginseng did not show a statistically significant increase. We conclude that both Asian ginseng and Siberian ginseng cannot significantly stimulate innate macrophage immune functions that influence cellular immune responses. Therefore, contrary to the popular belief, Asian and Siberian ginseng may not stimulate immune function.

Adjuvants, Immunologic↗
PubMed1998

Modulation of immune cell function following fluoxetine administration in rats.

Fluoxetine (FLX) and other specific serotonin uptake inhibitors (SSRIs) have become the drugs of choice for treating depression. However, only a limited number of studies have addressed the effects of FLX on immune cell function. Our lab has measured the effects of both acute and chronic FLX administration on two functions of cell-mediated immunity, mitogen-induced lymphocyte proliferation (MILP) and natural killer cell cytolytic activity (NKCA). In this article we report that acute FLX administration (10 mg/kg) resulted in a dose- and time-dependent decrease in MILP and NKCA. MILP was more sensitive than NKCA to FLX, requiring lower doses for inhibition; however, the effects were more transient. Following chronic FLX administration, these effects were no longer observed, suggesting that an apparent tolerance to these particular measures of cell-mediated immunity had developed. Finally, a single microinjection of FLX directly into the lateral ventricle produced similar suppressive effects on MILP and NKCA, suggesting that the immunomodulatory mechanism may have a central component.

Analysis of Variance↗
PubMed1997

Modulation of immune cell function by the autonomic nervous system.

This review discusses some of the major findings implicating the autonomic nervous system in the regulation of immune function. The sympathetic nervous system, the primary focus of this line of research, directly innervates the major lymphoid organs, and physiological release of sympathetic neurohormones at these sites has been documented. Leukocytes have been shown to express receptors for catecholamines, as well as neuropeptide Y, and studies in vitro and in vivo have indicated that occupation of these receptors by the appropriate ligands produces functional changes in immunological cells. Finally, altered sympathetic regulation may underlie some of the immunological abnormalities observed in chronic stress, clinical depression, and ageing.

Animals↗
PubMed1997

Modulation of immune cell populations and activation markers in the pathogenesis of African swine fever virus infection.

African swine fever (ASF) virus induces immune cell alterations that may be detected by changes in peripheral blood cells phenotypic antigens and activation markers which were examined by flow cytometry, analyzing both cell proportion and/or expression intensity of superficial antigens. These studies were conducted in pigs with experimental acute of chronic ASF infection to determine whether changes among important surface activation markers and phenotypic antigens, and their correlative lymph node status, reflected similar or disparate aspects of immune pathology. In acute infection produced by virulent viruses, macrophage and B lymphocyte populations decreased in peripheral blood after a short activation period at the beginning of the infection. A significative decrease of interleukin 2 receptor (IL 2R) expression was also observed in those pigs. These variations correlated with lymph node cell depletion due to an intense lymphoid cell death by apoptosis, affecting mainly the B lymphocyte subpopulation as determined by immunohistochemistry. Nevertheless, pigs infected with an attenuated isolate undergoing chronic persistent infection, presented a distinct pattern of modification, according with a different clinicopathological evolution. Changes consisted in systemic immune activation coincident with the highest viremia titer, with an augmentation in CD8+ T lymphocyte, macrophage, and B cell populations, and MHC (major histocompatibility complex) antigens. Percentage elevation of circulating immune subpopulations was accompanied by cell accumulation with lymphoid hyperplasia but a conserved distribution of B lymphocytes in lymphoid organs of chronically infected pigs.

Acute Disease↗
PubMed2000

Gestational nicotine exposure alone or in combination with ethanol down-modulates offspring immune function.

Prenatal nicotine exposure has been shown to disrupt the development of a number of peripheral organs. In the current study, we examined the effects of gestational nicotine exposure, alone or in combination with ethanol exposure, on offspring immune function. Timed pregnant rats were treated with either nicotine (6 mg/kg/day) from gestation day 4-20 using subcutaneously implanted osmotic mini-pumps or ethanol administered in the drinking water (15% w/v) from gestation day 10-20. The combined exposure group received both treatments. The ability of offspring T and B cells to proliferate in response to nonspecific stimulation by Concanavalin A or lipopolysaccharide, respectively, was determined on postnatal days 9, 15, 22, 29, 64, and 86. Offspring splenocyte beta(2)-adrenoceptor binding was also measured. Nicotine or nicotine+ethanol suppressed splenocyte responsiveness to Concanavalin A or lipopolysaccharide which was similar in timing and magnitude to that seen with ethanol alone. Splenocytes from these groups remained subresponsive to stimulation well into adulthood. The combined drug treatment caused an overall reduction in spleen beta-adrenergic receptor binding whereas the individual drug treatments did not alter the development of spleen beta-adrenergic receptors.Our results indicate that prenatal nicotine exposure can cause long-term suppression of the proliferative response of offspring immune cells. Moreover, the effects of nicotine+ethanol may cause more severe deficits in adulthood.

Animals↗
PubMed2001

Modulating the immune response with dendritic cells and their growth factors.

Different subsets of dendritic cells (DCs) appear to play a role in determining the specific cytokines secreted by T helper (Th) cells. A model is proposed that links together factors such as the pathogen, microenvironment, DCs and T cells in a mechanism that results in a flexible determination of T-cell polarization.

Adjuvants, Immunologic↗
PubMed2002

Superoxide dismutase as modulator of immune function in American white shrimp (Litopenaeus vannamei).

The immunomodulatory action of superoxide dismutase (SOD) and its possible use as an indicator of immune responses in American white shrimp (Litopenaeus vannamei) were studied. Juvenile shrimp were immersed in aerated beta-glucan and sulfated polysaccharide solutions for 6 h. SOD activity in haemocytes and muscle was quantified to evaluate whether beta-glucan and sulfated polysaccharide induce immunostimulatory activity. Haemocytes and muscle showed similar increased levels of SOD activity (1.5- and 1.4-fold that of control, respectively). Total haemocyte count decreased within the first 24 h after challenge with immunostimulants, but total haemocyte count and total soluble haemocyte protein increased over normal values after 48-120 h. Single immunostimulation with beta-glucan and sulfated polysaccharide is sufficient to generate an increase in the antioxidant activity of L. vannamei SOD.

Adjuvants, Immunologic↗
PubMed2000

Modulation of immune function by dietary lectins in rheumatoid arthritis.

Despite the almost universal clinical observation that inflammation of the gut is frequently associated with inflammation of the joints and vice versa, the nature of this relationship remains elusive. In the present review, we provide evidence for how the interaction of dietary lectins with enterocytes and lymphocytes may facilitate the translocation of both dietary and gut-derived pathogenic antigens to peripheral tissues, which in turn causes persistent peripheral antigenic stimulation. In genetically susceptible individuals, this antigenic stimulation may ultimately result in the expression of overt rheumatoid arthritis (RA) via molecular mimicry, a process whereby foreign peptides, similar in structure to endogenous peptides, may cause antibodies or T-lymphocytes to cross-react with both foreign and endogenous peptides and thereby break immunological tolerance. By eliminating dietary elements, particularly lectins, which adversely influence both enterocyte and lymphocyte structure and function, it is proposed that the peripheral antigenic stimulus (both pathogenic and dietary) will be reduced and thereby result in a diminution of disease symptoms in certain patients with RA.

Antigens↗
PubMed1998

Modulation of immune responses to parasitoids by polydnaviruses.

Parasitoids are parasites that invariably kill their host. Polydnaviruses are injected by parasitoid wasps into the body cavity of their insect host and cause immunosuppression, allowing the parasitoid to develop in the absence of encapsulation. One of the targets of the polydnaviruses are the haemocytes of the host, which undergo significant changes in response to entry of the virus. In some systems, haemocyte apoptosis is induced, or haemocyte clumping may be seen; in others, the cells round up and fail to adhere to a substrate. Effects on haemocytes may be transitory or permanent (cell death). Various polydnavirus gene products have been identified that interfere with normal haemocyte function. Phenoloxidase activity also is inhibited during parasitism, and the effect is inducible by polydnavirus. In some systems, venom components may act synergistically with polydnavirus in mediating the virally-induced effects on the host immune system. Polydnaviruses are powerful influences on the host immune system, which serve to permit successful development of the parasitoid without triggering the host immune response.

Animals↗