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Results for “immune modulation”

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At least 595 records · Page 33Linked to original sources

PubMed1984

IgG-induced experimental immune synovitis: hormonal modulation of in vitro splenic immune responses to homologous antigens.

The effect of oestrogen or anti-oestrogen administration on gross pathology and in vitro cell-mediated immune responses to homologous IgG, native and denatured interstitial collagens and PPD was studied in an IgG-induced rabbit model of immune synovitis. During induction of synovitis, rabbits were administered oestradiol valerate (0.075 mg/kg/day) or tamoxifen, an anti-oestrogen (2.0 mg/kg/day, high dose or 0.5 mg/kg/day, low dose) or placebo injections. Low dose tamoxifen administration was associated with significant improvement P less than 0.05 in immune synovitis with regard to gross pathology, when compared to placebo and the oestradiol treatment group. High dose tamoxifen treatment was not associated with significant improvement in observed synovitis. With regard to cell-mediated immune responses, spleen cells derived from immune synovitis rabbits were observed to increase 3H-thymidine uptake on incubation with native or denatured homologous collagens. Modulation of these immune responses to antigens was observed in anti-oestrogen treated rabbits with immune synovitis. In vitro cell-mediated immune responses to denatured type I, II and III collagens, PPD, as well as native type II and III collagens were not observed in the low dose tamoxifen treatment group. However, in vitro immune responses to these antigens were observed in spleen cell cultures from immune synovitis rabbits treated with either high dose tamoxifen or oestradiol valerate. The data suggest that in vivo anti-oestrogen administration can modulate the in vitro cell-mediated immune response to connective tissue constituents observed in immune synovitis. Concomitant with reduced immune responses is a significant reduction in the observed lesions of the inflammatory response.

Animals↗

PubMedDate not supplied

Neural modulation of immunity: conditioning phenomena and the adaptability of lymphoid cells.

The behavioral conditioning of alterations in the immune response is one pillar supporting the growing edifice of central nervous system (CNS) modulation of immunity. The mechanisms underlying such conditioning phenomena are not understood. In this communication, we attempt to develop a theoretical position based on the concept of phenotypic and functional adaptability of lymphoid cells. We propose that these cells can learn to associate responsiveness to antigens and to other "immunoactive" agents, with responsiveness to signals originating in the CNS delivered via neuroendocrine or autonomic nervous channels. Neural/endocrine signals act on the immune system in conjunction with immunological stimuli, in a way that leads to "storage" of the association (memory) of these two kinds of stimuli in the immune system rather than in the brain.

Animals↗

PubMed2006

In vivo heparan sulfate treatment alters the immune response of normal and LLC-bearing mice.

Despite the large amount of research dedicated to the understanding and treatment of tumor growth, the majority of cancers continue to lack effective therapeutic options. As in the case of most solid tumors, growth requires evasion of the host immune system. Our previous work using the Lewis Lung Carcinoma (LLC) model of tumor bearing (TB)-mice has shown several tumor-induced immune suppressing effects to be present. These effects include a decreased T-cell proliferative response to Con A and altered cytokine secretion patterns that favor neither a Th1 nor a Th2 response. To address these immune alterations, immune modulating approaches have been a central area of study. Of the many potential immune modulating compounds, we believe promising therapeutic potential lies in the heparin family. Heparan sulfate (HS), in particular, has been shown to increase T-cell proliferative response in non TB-mouse splenocytes as well as promotion of a beneficial Th1 response. In this paper, we studied the potential of HS to decrease tumor burden via in vivo treatment of TB-mice. Results showed both normal and TB-mice splenocytes had a dose response change in proliferation as a result of HS treatment. Furthermore, splenocytes from HS treated TB-mice showed a potentially beneficial decrease in basal level proliferation. On gross examination, HS treatment produced a decrease in tumor surface necrosis with a visible (2 +/- 1.8%) surface necrotic area in treated mice as opposed to a (43 +/- 16%) surface necrotic area in untreated mice. HS treatment decreased TB-mice splenomegaly when comparing mice spleen weights in treated (0.3 +/- 0.05 g) vs. untreated (0.14 +/- 0.02 g) groups. These results show a potential role of HS as an immune modulating agent with antitumor properties.

Adjuvants, Immunologic↗

PubMed2004

Endotoxin-induced chorioamnionitis modulates innate immunity of monocytes in preterm sheep.

The preterm fetus is immune naive and has immature innate immune function. Although the preterm fetus is frequently exposed to chorioamnionitis, the effects of exposure of the fetal lung to inflammation on innate immune responses are unknown. Using the fetal sheep model of chorioamnionitis, cord blood monocytes were isolated from preterm lambs 1 to 14 days after intra-amniotic endotoxin injection, cultured for approximately 16 hours, and challenged with endotoxin in vitro. Compared with monocytes from adult sheep, the preterm monocytes produced less H(2)O(2) and interleukin-6, and toll-like receptor 4 expression was decreased. Three days after intra-amniotic endotoxin exposure, preterm monocyte responses to in vitro endotoxin challenge demonstrated decreased H(2)O(2) and interleukin-6 production and decreased CD14 and major histocompatibility complex class II expression. Preterm monocyte responses 7 to 14 days after endotoxin tended to exceed those of adults and preterm control animals indicating augmented function. In contrast, a second intra-amniotic endotoxin injection 7 days after the initial endotoxin exposure suppressed monocyte function at 14 days. The fetal monocytes demonstrated patterns of responses consistent with endotoxin tolerance (immune paralysis) as well as maturation of function. Modulation of fetal innate immune responses by exposure to inflammation may alter subsequent immune adaptation after birth.

Amnion↗

PubMed1995

Alcohol modulation of immune function: clinical and experimental data. Veterans Affairs Cooperative Study Groups 119 and 275.

In both animal and human studies, ethanol seems to modulate host immune function. In a variety of animal studies, ethanol has been shown to decrease lymphocyte function and number. In human studies of patients with alcoholic hepatitis, these abnormalities were also seen with specific correlation with protein malnutrition. Hepatic pathological lesions were also correlated with lymphocyte subset infiltration. However, peripheral blood lymphocytes did not correlate consistently with hepatic histopathology.

Animals↗

PubMed1998

Cyclophosphamide given after active specific immunization augments antitumor immunity by modulation of Th1 commitment of CD4+ T cells.

BACKGROUND AND OBJECTIVES: In order to evaluate the regulatory effect of cyclophosphamide (CPA) on active specific immunization (ASI)-induced antitumor immunity, we examined the timing of CPA (100 mg/kg) with ASI, and focused on whether CPA given after ASI augments antitumor immunity by modulation of Th1 commitment of CD4+ T cells. METHODS: We examined the effect of CPA combined with ASI using sonicated tumor supernatant (SS) and recombinant interleukin-1 beta (rIL-1 beta). RESULTS: Survival of i.p. tumor inoculated mice after ASI (days -12, -9, and -6) followed by 100 mg/kg CPA (day -3) (ASI-CPA) was significantly prolonged compared with that of mice treated with ASI alone, whereas CPA (day -15) treatment before ASI (CPA-ASI) completely abrogated the survival prolongation by ASI alone. In early stage (day 0) after ASI-CPA treatment, the CD4+ T cells were determined to play an important role in the protective immunity for the following reasons: 1) the CD4+/CD8+ ratio of spleen cells from immunized mice was higher than that of the control or CPA alone treated group; and 2) the tumor neutralizing activity of fresh spleen cells was abrogated by CD4+ T-cell depletion in vitro. CD4+ T cells of mice treated with ASI-CPA produced more interferon (IFN)-gamma and IL-2 and less IL-4 than those of the ASI alone group. CONCLUSIONS: These results suggest that the protective immunity induced by ASI was augmented through the modification of the Th1 and Th2 balance by CPA injection after ASI.

Animals↗

PubMed2005

Vaccinia viruses with a serpin gene deletion and expressing IFN-gamma induce potent immune responses without detectable replication in vivo.

In a continuing effort to develop safe and efficacious vaccine and immunotherapeutic vectors, we constructed recombinant vaccinia virus (rVV) vaccines lacking either the B13R (SPI-2) or the B22R (SPI-1) immune-modulating gene and coexpressing IFN-gamma. B13R and B22R are nonessential VV immune-modulating genes that have antiapoptotic and antiinflammatory properties with sequence homology to serine protease inhibitors (serpins). IFN-gamma is a cytokine with potent immunoregulatory, antineoplastic, and antiviral properties. We observed that these rVVs with a deletion in a serpin gene and expressing IFN-gamma replicated to high titers in tissue culture yet were avirulent in both immunocompromised and immunocompetent mice with no detectable viral replication in these animals. A single immunization elicited potent humoral, T helper, and cytotoxic T cell immune responses in mice despite the absence of any detectable virus replication in vivo. IFN-gamma coexpression and the inactivation of one or more VV immune-modulating genes provide an optimized method for increasing the safety while maintaining the efficacy of rVV vaccines. This strategy provides a method for developing highly safe and efficacious vaccines for smallpox and other diseases and immunotherapeutic vectors.

Animals↗

PubMed1998

Nutritional modulation of immunity and the inflammatory response.

The metabolic derangements of the injured or stressed patient are governed by multiple factors that partially include the severity of insult, preexisting illnesses, available energy reserves, and appropriateness of intervention. The normal response to injury is further characterized by the release of proinflammatory and antiinflammatory mediators that exert potent effects on cellular and organ function. Although brief periods of starvation and catabolism are tolerable in otherwise healthy individuals, protracted nutritional deprivation can manifest as immunocompromise, irreversible organ injury, and late mortality. Moreover, patients with severe injuries or preexisting illnesses who exhibit exaggerated inflammatory responses may be further predisposed to such deleterious consequences following the insult. The optimal supply of appropriate nutrients and substrates in such circumstances has often been championed as a necessary means of restoring proper cellular metabolism, wound healing, immune competence, and proper organ function. However, much debate surrounds the present efficacy of nutritional therapy in modulating the immune response associated with injury and stress. This article seeks to assess the merits of nutritional therapeutics in the injured patient through available biological and clinical evidence.

Animals↗

PubMed2006

Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b.

BACKGROUND: There have been indications that common Angiotensin Receptor Blockers (ARBs) may be exerting anti-inflammatory actions by directly modulating the immune system. We decided to use molecular modelling to rapidly assess which of the potential targets might justify the expense of detailed laboratory validation. We first studied the VDR nuclear receptor, which is activated by the secosteroid hormone 1,25-dihydroxyvitamin-D. This receptor mediates the expression of regulators as ubiquitous as GnRH (Gonadatrophin hormone releasing hormone) and the Parathyroid Hormone (PTH). Additionally we examined Peroxisome Proliferator-Activated Receptor Gamma (PPARgamma), which affects the function of phagocytic cells, and the C-CChemokine Receptor, type 2b, (CCR2b), which recruits monocytes to the site of inflammatory immune challenge. RESULTS: Telmisartan was predicted to strongly antagonize (Ki asymptotically equal to 0.04 nmol) the VDR. The ARBs Olmesartan, Irbesartan and Valsartan (Ki asymptotically equal to10 nmol) are likely to be useful VDR antagonists at typical in-vivo concentrations. Candesartan (Ki asymptotically equal to 30 nmol) and Losartan (Ki asymptotically equal to 70 nmol) may also usefully inhibit the VDR. Telmisartan is a strong modulator of PPARgamma (Ki asymptotically equal to 0.3 nmol), while Losartan (Ki asymptotically equal to 3 nmol), Irbesartan (Ki asymptotically equal to 6 nmol), Olmesartan and Valsartan (Ki asymptotically equal to 12 nmol) also seem likely to have significant PPAR modulatory activity. Olmesartan and Irbesartan (Ki asymptotically equal to 9 nmol) additionally act as antagonists of a theoretical model of CCR2b. Initial validation of this CCR2b model was performed, and a proposed model for the Angiotensin II Type1 receptor (AT2R1) has been presented. CONCLUSION: Molecular modeling has proven valuable to generate testable hypotheses concerning receptor/ligand binding and is an important tool in drug design. ARBs were designed to act as antagonists for AT2R1, and it was not surprising to discover their affinity for the structurally similar CCR2b. However, this study also found evidence that ARBs modulate the activation of two key nuclear receptors-VDR and PPARgamma. If our simulations are confirmed by experiment, it is possible that ARBs may become useful as potent anti-inflammatory agents, in addition to their current indication as cardiovascular drugs.

Amino Acid Sequence↗

PubMedDate not supplied

Modulation of immune responses by surface polysaccharides of Candida albicans.

Fungal polysaccharides, especially those from the cell wall of the nonpathogenic yeast Saccharomyces cerevisiae, have been investigated as modulators of immune function for many years. More recently, because surface-associated components are known to be elaborated and circulate during serious episodes of candidiasis, investigators have taken interest in the opportunistic fungus Candida albicans. This review emphasizes the immunomodulatory activities of mannan and cell wall-derived glycoproteins from C. albicans. Mannan extracted with hot citrate buffer has been shown in an antibody-forming cell assay to be a heterogeneous mixture with components capable of enhancing or suppressing antibody responses when administered to mice at or near the time of immunization with type III pneumococcal polysaccharide (SSS-III), a T helper cell-independent antigen, or with sheep erythrocytes (SRBC), a T helper cell-dependent antigen. The components responsible for these opposing effects have been separated on the basis of size or charge by column chromatography. Two similar cell wall glycoproteins, removed from isolated cell walls by different procedures, induced enhancement only of the immune response to SSS-III and SRBC. The mechanism(s) by which these polysaccharides effect modulatory activity has not been elucidated. The enhancing property does not appear related to a direct mitogenic effect on lymphocytes or to stimulation of the production of B cell growth factors or interleukin 2.

Animals↗

PubMed1990

A role for the autonomic nervous system in modulating the immune response during mild emotional stimuli.

The role of the autonomic nervous system in the modulation of the immune response to emotional stimuli, was established in rats subjected to the passive avoidance test. An increase in splenic primary antibody response directed against SRBC was found after exposure of rats to the passive avoidance apparatus (novelty). Both local surgical denervation of the spleen and beta-receptor blockade (timolol, 1 mg/kg i.p. 1 h prior to testing) prevented the increase in primary antibody response.

Animals↗

PubMed1979

Immune response modulation by colonization of germfree rats with Propionibacterium acnes.

Propionibacterium acnes (oral and/or parenteral administration) had a modulating effect on antibody-and cell-mediated immune responses of germfree (GF) and monoassociated (MA) rats. In conventionally reared rodents, parenteral injection of killed P. acnes stimulated the splenic plaque-forming cell response to sheep erythrocytes. However, in GF rats and in rats monoassociated with viable P. acnes, parenteral injection of killed P. acnes antigen inhibited the plaque-forming cell response to sheep erythrocytes. When compared with the responses of GF control rats, splenocytes from GF rats parenterally injected with P. acnes antigen had a decreased in vitro blastogenic response to phytohemagglutinin and concanavalin A and an increased blastogenic response to homologous bacterial antigens. Conversely, a parenteral injection of P. acnes antigen into P. acnes MA rats resulted in an increased splenocyte blastogenic response to phytohemagglutinin and concanavalin A but not to homologous (P. acnes) antigens. Thus the presence or absence of intestinal antigenic stimuli (in MA and GF rats) had a modulating effect on the immune response to a parenteral injection of P. acnes antigen.

Administration, Oral↗

PubMed1996

Buspirone, a serotonin receptor agonist, increases CD4 T-cell counts and modulates the immune system in HIV-seropositive subjects.

OBJECTIVE: We have previously shown that drugs that decrease intracellular cAMP levels increase/restore the proliferative and cytotoxic capacity of T cells from HIV-seropositive subjects in vitro. Buspirone, a serotonin receptor agonist, indirectly decreases intracellular cAMP levels in T cells and has the same increasing/restoring effect on T-cell proliferation in lymphocytes from HIV-seropositive subjects in vitro. DESIGN: Buspirone was given as a single high dose to six HIV-seropositive subjects, or as continuous medication with increasing dosage over 6 weeks to nine HIV-seropositive subjects, with CD4 T-cell counts of 150-300 x 10(6)/l. RESULTS: Significant increases in CD4 T cells, CD4 percentage and CD4/CD8 ratio were found 1 week after a single high dose of buspirone was administered. With continuous administration, a significant increase in CD4 T cells was observed after 1 and 4 weeks. Serum HIV RNA showed a significant decrease 1 h after a single dose of buspirone was administered. With continuous administration of buspirone, plasma HIV RNA first increased within the first 2 weeks of treatment and then decreased towards and below baseline concurrently with a significant decrease in CD8T cells. The proliferative T-cell response to poke weed mitogen and membrane expression of IL-2R increased significantly during continuous treatment with a significant decrease in expression of HLA-DR on CD8+ T cells. Development of "flu-like' symptoms, so severe that two patients withdrew from the study and two patients ceased medication before time, was a clinical indication of modulation of the immune system by buspirone. CONCLUSION: The study shows that buspirone modulates the immune system and leads to changes in the CD4 and CD8 T-cell numbers, functional capacity, cell maturation and viral load.

Adult↗

PubMed1999

Modulation of immune response with ornithine A-ketoglutarate in burn injury: an arginine or glutamine dependency?

Enterally administered ornithine alpha-ketoglutarate (OKG) is an efficient complement of nutritional support in trauma situations, especially after burn injury. A typical feature observed in this intense catabolic state is insufficient production of glutamine (Gln) and arginine (Arg), two amino acids (AAs) involved in the immune response. As OKG in vivo metabolism generates these two AAs, we investigated, in burned rats, the action of OKG with regard to modulation of immunity. Male Wistar rats were randomly allocated to four groups. On day 0, 12 rats were burned with boiling water (20% body surface area). After a 24-h fast, they were enterally refed for 48 h using Osmolite, as a low-calorie low-nitrogen regimen, supplemented with either 5 g OKG x kg(-1) x d(-1) (n = 6) or an equivalent amount of nitrogen in the form of glycine (n = 6). Non-burned pair-fed controls treated with glycine (n = 6) and healthy rats fed ad libitum (n = 6) were also studied. Nitrogen balance was assessed from daily measurement of total nitrogen excretion. On day 3, thymus, Anterior tibialis muscle and proximal jejunum weights were recorded. Muscle and intestinal AA concentrations were also quantified. OKG counteracted (P<0.01) the thymic involution that occurs with burn injury, and increased the concentrations of Gln and Arg in both the muscle (P<0.01 and P<0.05, respectively) and the jejunum (P<0.01 for Gln). When all groups were taken together, a positive correlation was found between thymus weight, and Gln and Arg muscle concentrations (r = 0.71, P<0.001 and r = 0.58, P<0.01, respectively). Furthermore, as expected, OKG improved nitrogen balance. As it is known that total number of thymocytes parallels thymic weight, and as Gln and Arg are essential nutrients for activated immune cells, our results suggest that Gln and Arg derived from OKG are responsible for the immunomodulating properties of this molecule in burn injury.

Animals↗

PubMed1997

Morphine induces splenocyte apoptosis and enhanced mRNA expression of cathepsin-B.

Morphine has been demonstrated to modulate immune function. We studied whether morphine modulates apoptosis of splenocytes. Splenocytes were isolated from control and morphine treated rats. Splenocytes isolated from morphine treated rats showed increased percentage (P < 0.001) of apoptosis when compared to splenocytes isolated from untreated rats (control, 4.7 +/- 1.0% apoptotic splenocytes/field vs. morphine, 47.8 +/- 3.4% apoptotic splenocytes/field). These results were further confirmed by gel electrophoresis as well as by end-labeling DNA of splenocytes isolated from control and morphine treated rats. Splenocytes from morphine treated rats showed a classical ladder pattern with integer multiples of 180 base pairs. Splenocytes from morphine treated rats also showed increased mRNA expression of cathepsin-B, a gene associated with active cell death. These results suggest that morphine may also be modulating immune function by enhancing apoptosis of splenocytes.

Animals↗

PubMed2005

Effects of sugar cane extract on the modulation of immunity in pigs.

The experiment was aimed to test the efficacy of sugar cane extract (SCE) on the modulation of pig immunity under field conditions. The SCE preparation consisted of sugar cane extract (20%) and oilcake of rice bran (80%). SCE (500 mg/kg of body weight per day) was fed to weanling pigs on 3 consecutive days per week for 4 weeks. The results showed a significant enhancement of cytotoxicity of natural killer (NK) cells and phagocytosis by neutrophils and monocytes, compared to untreated pigs. The enhancement of NK cell function may have protected against porcine reproductive respiratory syndrome (PRRS), as there was a reduction in seroconversion rates in treated pigs. Moreover, SCE-treated pigs showed a 7.87% growth enhancement compared with untreated controls. Thus SCE produces an immunostimulative effect on porcine innate immunity that may provide protection against pathogens.

Analysis of Variance↗

PubMed2004

Novel aspects of signaling and ion-homeostasis regulation in immunocytes. The TRPM ion channels and their potential role in modulating the immune response.

In just a few years, the discovery and subsequent characterization of several members of the TRPM family of cation channels have provided us with surprising new insights into unknown aspects of cellular ion-homeostasis regulation. This includes reports about ADP-ribose functioning as a novel intracellular second messenger and gating molecule of the Ca(2+)-permeable TRPM2 channel, studies demonstrating the central role of mouse TRPM5 in taste signaling, as well as the unexpected involvement of TRPM6 and TRPM7 in regulating Mg(2+)-homeostasis, or the cool properties of TRPM8 acting as a cold and menthol sensor in sensory neurons. At least four of the eight known TRPM proteins have been shown to be present in the immune context: TRPM1 (melastatin), TRPM2, TRPM4 and TRPM7. Although we currently lack animal models allowing a detailed assessment of the potential involvement of TRPM family members in modulating the immune response, the powerful combination of molecular and cellular biology, biochemistry, and electrophysiology have provided the first clues as to how these molecules could contribute to immunity.

Animals↗

PubMed1987

Stress-related modulation of immunity: a review of human studies.

The assumption that life changes and stressful events can alter host defense is based mainly on studies of changes in a variety of immune and inflammatory reactions. Whether those changes also confer an increased susceptibility to infectious agents and neoplasms, or modify the course of such diseases, is still less well substantiated. Nonetheless, psychological and neural modulation of immunity has recently been possible to approach from a mechanistic viewpoint. For instance, generation of a variety of lipid mediators from arachidonic acid may be under control of dietary and endocrine factors that can be affected by stress. Since these lipids, eg, lipoxygenase products, are potent regulators of leukocyte functional responses, their significance as one of several mechanisms is discussed. The role of various neuropeptides in leukocyte function has only recently been discovered. Since the release of, eg, substance P, enkephalins, and endorphins, which all have modulating effects on leukocyte functional responses, is under neural control and can occur in the vicinity of immunocompetent cells, they might constitute one of several links between the mind and the immune system.

Communicable Diseases↗