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PubMed1997

Induction of protective immunity and modulation of granulomatous hypersensitivity in mice using PIII, an anionic fraction of Schistosoma mansoni adult worm.

This study was performed in order to define Schistosoma mansoni antigens that are able to function as modulator agents in the granulomatous hypersensitivity to parasite eggs in BALB/c and C57BL/6 mice. A fraction of S. mansoni, designated PIII, derived from adult worm antigen preparation (SWAP) was obtained using anion-exchange chromatography on an FPLC system. Immunization of mice with PIII in the presence of Corynebacterium parvum and Al(OH)3 as adjuvant induced an immune response in this animals as determined by ELISA and spleen cell proliferation assays against S. mansoni antigens SEA, SWAP and PIII. In addition, PIII caused a significant degree of protection against a challenge infection in immunized mice as observed by the decrease on worm burden recovered from the portal system. We also showed that PIII profoundly inhibited the vigorous anamnestic granulomatous response to eggs in the liver and lungs. This suppression correlated with a significant decrease in granuloma size. From these results we conclude that the PIII preparation contains antigens that can mediate protective anti-parasite immunity and downregulate granulomatous hypersensitivity to S. mansoni eggs.

Adjuvants, Immunologic↗
PubMed1997

Multiple eruptive dermatofibromas in three men with HIV infection.

BACKGROUND: Multiple eruptive dermatofibromas (MEDF) are rare and their etiology is unknown. An association with immunosuppression has led to the speculation that they are the result of an abortive immunoreactive process. In the literature, there have been 5 isolated case reports of multiple dermatofibromas and human immunodeficiency virus (HIV) infection. Three of these cases had other immune modulators present (i.e. prednisone, systemic lupus erythematosus, alpha-interferon, UVB phototherapy). The other 2 cases had disseminated mycobacteriosis. OBSERVATIONS: A series of 3 men with HIV infection and MEDF is described. In contrast to previous case reports, our patients did not have other immune modulators besides HIV infection nor did they have disseminated mycobacteriosis. CONCLUSIONS: This series lends support to the speculation that MEDF may be associated with immunosuppression. Further study is needed to delineate the exact mechanism for this relationship. These patients presented within a 4-month period and illustrate the frequency at which MEDF may be seen in the HIV-positive population. As clinicians who care for patients with HIV infection, it is important to be aware that MEDF may be seen in this immunosuppressed population.

Adjuvants, Immunologic↗
PubMed1993

Immune response modulation by pentoxifylline in vitro.

Pentoxifylline (PTX) has recently been shown to modulate TNF-alpha production and to reduce the incidence and severity of all major complications after BMT, including mucositis, veno-occlusive disease, renal insufficiency, hypertension, and graft-versus-host disease. To analyze in detail the effect of PTX on immune complications after BMT, we investigated the immunomodulatory effect of PTX on immune responses in vitro. The continuous presence of PTX significantly reduced the proliferative response of PBMC to PHA stimulation and to alloantigens in a dose-dependent manner. Starting at concentrations of 100 micrograms/ml, PTX was able to inhibit and, at 1000 micrograms/ml, completely block mitogen-induced proliferation. Maximal inhibition of more than 90% (91 +/- 4%) was also observed at PTX concentrations of 1000 micrograms/ml in the mixed lymphocyte culture (MLR) and by addition on day 0. However, lower but still significant suppression (13 +/- 7%) was achieved at concentrations of 10 micrograms/ml PTX. The inhibitory capacity of PTX was increased by mAbs against TNF-alpha (34 +/- 5% additional suppression at 100 micrograms/ml PTX) and not reversed by the addition of rTNF-alpha. The effect of PTX on the generation of CTLs in vitro was studied in the cell-mediated lymphotoxicity assay. PTX (100 micrograms/ml) significantly inhibited (P = 0.0178) the in vitro generation of CTLs when PTX was added to the culture on day 0. PTX also showed profound modulatory properties in the NK assay, with a reduction of 23 +/- 3% in specific lysis at 10 micrograms/ml PTX and maximal reductions of 88 +/- 3% at 1000 micrograms/ml PTX. Immunomodulatory properties of PTX were not only associated with blockage of TNF-alpha, as shown by decreased mRNA expression and TNF-alpha values in the culture supernatants, but also with an impaired production of other cytokines and secondary messages such as IFN-gamma and neopterin. PTX treatment, however, did not affect IFN-alpha or IL-1 beta production, and IL-6 release was even increased. PTX, therefore, has profound immunomodulatory properties in vitro, which are associated with selective inhibition of cytokine release and can be enhanced by the addition of mAbs against TNF-alpha, but not reversed by the addition of rTNF-alpha.

Biopterins↗
PubMed2001

Nutritional modulation of immune function.

The inflammatory response to injury and infection, although an essential part of immune function, carries the risk of severe tissue depletion and immunosuppression. These outcomes increase morbidity and delay recovery. Evidence is accumulating that single-nucleotide polymorphisms in the genes controlling pro-inflammatory cytokine production adversely influence the response. Immunonutrition provides a means of modulating the inflammatory response to injury and infection, and thereby improves clinical outcome. n-3 Polyunsaturated fatty acids (n-3 PUFA), glutamine, arginine, S amino acids and nucleotides are important components of immunonutrient mixes. While animal model studies suggest that all these components may exert a beneficial effect in patients, the number of large randomized placebo-controlled trials utilizing immunonutrition is fairly limited and the observed effects are relatively small. Meta-analyses suggest that while immunonutrition may not reduce mortality rates, a reduction in hospital length of stay, decreased requirements for ventilation and lower infection rates are achieved by this mode of nutrition. The present paper discusses some underlying reasons for the difficulty in demonstrating the clinical efficacy of immunonutrition. Paramount among these reasons is the antioxidant status and genetic background of the patient. A number of studies suggest that there is an inverse relationship between inflammation and T-cell function. Immuno-enhancive effects have been shown in a number of studies in which n-3 PUFA, glutamine and N-acetyl cysteine have been employed. All these nutrients may exert their effects by suppressing inflammation; n-3 PUFA by direct suppression of the process and glutamine and N-acetyl cysteine by acting indirectly on antioxidant status. Glutamine and nucleotides exert a direct effect on lymphocyte proliferation. Preliminary data suggests that not all genotypes are equally sensitive to the effects of immunonutrition. When further studies have been conducted to discern the precise interaction between each individual's genotype of relevance to the response to injury and infection, and immunonutrients, the level of precision in the application of immunonutrition will undoubtedly improve.

Animals↗
PubMed1999

Emergence of unusual cytogenetic abnormalities under interferon-alpha therapy in patients with chronic myelogenous leukemia.

New treatments that may change the course of a disease or have potential carcinogenicity can result in the emergence of new cytogenetic or clinical disorders. We report here the cytogenetic evolution of 52 cases of Philadelphia (Ph)-positive myelogenous leukemia (CML) receiving interferon-alpha (IFN-alpha) therapy compared with that of 59 Ph-positive CML cases treated with busulfan (BU) or hydroxyurea (HY). Twenty-one percent of the CML patients receiving IFN-alpha displayed unusual secondary abnormalities, among which alteration of the long arm of chromosome 3, del(7), and del(9) were recurrent. The frequency of these unusual secondary changes was significantly higher than in CML cases after Bu or Hy treatment (P = 0.02). Three of the 11 IFN-alpha-treated CML patients displayed cytogenetic evolution in the chronic phase and, in two cases, the cytogenetic findings were transient, inasmuch as they disappeared upon withdrawal of IFN-alpha. In addition, a majority of cytogenetic abnormalities involved chromosome 3 at bands 3q21 and 3q26, which corresponds to the locus of EVI1, a gene implicated in the development or progression of human myeloid leukemias. Possible explanations include: toxicity of IFN-alpha by effect on bone marrow stroma, immune-modulating effects of IFN-alpha, and mutagenic effects of IFN-alpha. The mechanisms underlying these cytogenetic changes remain to be elucidated. However, our data suggest that IFN-alpha induces additional cytogenetic abnormalities even in the chronic phase through its immune-modulating effects and that these unusual cytogenetic abnormalities do not alter the history of CML.

Adolescent↗
PubMed2006

Multiple opioid receptors on immune cells modulate intracellular signaling.

In 1979, Joseph Wybran reported his insights into the existence of different opioid receptor subtypes on T-cells. He observed that morphine and methionine enkephalin had different effects on human T-cell rosetting to sheep red blood cells. Since that time, a wide array of laboratories have shown that opiate alkyloids and opioid peptides exert pleiotropic effects on immune cell function. These compounds are immunomodulators, modifying immune responses to extracellular stimuli such as mitogens, antigens, and antibodies that cross-link the T-cell receptor. It has been demonstrated that cells involved in host defense and immunity express mRNA transcripts encoding the various opioid receptors originally described in neuronal tissues. Molecular imaging approaches have demonstrated the regulated expression of both delta and kappa opioid receptors, predominantly on T-cells. Moreover, atypical opiate and opioid binding sites are present on these cells. This review will consider the evidence for both classical and atypical opioid receptors and their effects on signaling within immune cells; our emphasis is the T-cell and its delta opioid receptor.

Animals↗
PubMed1987

[Study of abscopal effect and cellular infiltration of tumor nests using less-fractionated, large-dose radiation].

As reported by several authors, abscopal effect and favorable cellular infiltrations into the tumor nest caused by irradiation suggest the existence of cell immunity in the host. In our present study, as first step to elucidate the mechanism of the fact mentioned above, effects of radiation with a single dose irradiation was estimated in terms of the increase of survival rate and the inhibition of pulmonary metastasis, i.e. abscopal effect in the mice of irradiated tumor burden. Therefore, we examined the resected and pulmonary specimen after irradiation histopathologically. We also examined the effects of the administration of immune modulator PSK and OK-432. Results; 1) Increase of survival rate and inhibition of pulmonary metastasis were observed in groups of mice with inoculated tumor and with again inoculated tumor treated by a single dose irradiation, compared to either the control groups. 2) Also administration of immune potentiator with radiation enhanced the survival rate and inhibition of pulmonary metastasis in all experimental protocols. 3) Remarkable cellular infiltrations of tumor nest after irradiation were observed, and these cellular infiltrations suggest participation of immunoreaction. In the group of using immune modulator, the cellular infiltrations were observed more remarkable than the other groups. 4) Optimal radiation dose was proved to be 30 Gy in this study.

Animals↗
PubMed1988

Aspects of cytokine induced modulation of immunity and inflammation with emphasis on interleukin 1.

Interleukin 1 (IL 1) contributes to both acute and chronic inflammatory processes. Purified IL 1 by itself is only one of the signals that induces local inflammation. The contribution of IL 1 to local inflammatory reactions is influenced by exogenous stimuli, antagonists such as steroid hormones and TGF beta (tissue growth factor beta) and agonists such as TNF (tissue necrosis factor). IL 1 production is depressed by glucocorticoids, but glucocorticoids induce expression of receptors for IL 1 on selected cell types including B lymphocytes and fibroblasts. Thus, complex interactions between hormones and cytokines modulate immunological and inflammatory responses.

Animals↗
PubMed2005

Mycophenolate mofetil (MMF): firing at the atherosclerotic plaque from different angles?

Atherosclerosis is characterized by a persistent, low-grade inflammatory state in which immune cell activation is inseparably linked to plaque formation and destabilization. The T-lymphocyte in particular has emerged as a pivotal player throughout the course of atherogenesis. As a consequence, the concept that immune modulation is a suitable target for cardiovascular prevention is currently an important focus of research. Mycophenolate mofetil (MMF) has emerged as a non-competitive inhibitor of inosine monophosphate dehydrogenase (IMPDH) that exerts cytostatic effects, particularly on proliferating T-lymphocytes. In addition, MMF has other immune-modulating effects, such as downregulation of the expression of adhesion molecules and attenuation of monocyte and macrophage responses. Given the added benefit that MMF is well tolerated, this immunosuppressive agent constitutes an attractive candidate for the modulation of inflammatory activation in atherogenesis. The present review provides an overview of the potential anti-atherogenic properties of MMF.

Animals↗
PubMed1997

Antiviral immune responses modulate the nature of central nervous system (CNS) disease in a murine model of multiple sclerosis.

The spectrum of disease is influenced by factors related to both the pathogen and the host, as well as the end points used in defining disease. In this article, the issue of disease resistance versus susceptibility will be examined in the framework that genetic manipulation of either the pathogen or the host immune response alters the balance from disease protection towards pathogenesis. The response of the host may trigger both a protective and a pathogenic immune response. The failure to mount a protective immune response predisposes the pathogen to persistence, which then becomes the target for immunopathology. This review will examine the factors involved both in virus-mediated pathogenesis and in disease protection in the Theiler's model of human multiple sclerosis. By manipulating the character of the virus pathogen and the specificity of the immune response, the entire spectrum of human demyelinating disease is reproduced.

Animals↗
PubMed2004

Immunonutrition and cancer.

The immune system is the body's primary defence against invading pathogens, non-self components and cancer cells. Inflammatory processes, including the release of pro-inflammatory cytokines and formation of reactive oxygen and nitrogen species, are an essential part of these processes. Although such actions are usually followed rapidly by anti-inflammatory effects, excessive production of pro-inflammatory cytokines, or their production in the wrong biological context may lead to situations of chronic inflammation. Whether such conditions arise as a result of exogenous chemicals, invading pathogens or disease processes, the long-term implications include an increased risk of cancer. A number of nutrients have the ability to modulate immune response and counter inflammatory processes. Zinc, epigallocatechin galate (EGCG), omega-3 polyunsaturated fatty acids and probiotics all act differently to modulate immune response, but all appear to have the potential to protect against cancer development and progression. We suggest that immunonutrition may provide a less invasive alternative to immunotherapy in protection against cancers associated with chronic inflammation.

Diet↗
PubMed1994

Leukocyte reduction of cellular blood components. Effectiveness, benefits, quality control, and costs.

Cellular blood components contain passenger donor leukocytes. Transfusion of passenger leukocytes may be associated with alloimmunization to leukocyte antigens, febrile transfusion reactions, refractoriness to platelet transfusion, severe pulmonary dysfunction, graft-vs-host disease, the transmission of infectious diseases, and immune modulation. Advanced leukocyte-reduction filters enable the removal of up to 99.9% of leukocytes from cellular blood components. Clinical trials suggest that the use of leukocyte-reduction filters may prevent or diminish the probability of febrile transfusion reactions, alloimmunization, and cytomegalovirus infection, but controversy exists regarding the effectiveness of leukocyte reduction in preventing immune modulation. There is no evidence that available techniques will prevent graft-vs-host disease. Cost-benefit analyses support the use of leukocyte-reduction filters for well-defined indications. Standards for leukocyte reduction of red blood cells have been defined, but issues regarding the quality control of leukocyte-reduced blood components require additional study.

Cost-Benefit Analysis↗
PubMed1990

A complex component modulating immune-deficient cells in leprosy patients leading to loss of viability of Mycobacterium leprae--a possible vaccine.

Macrophages from peripheral blood of leprosy patients, both multi-bacillary and paucibacillary are unable to kill phagocytosed Mycobacterium leprae due to their inability to produce superoxide (O2-) and hydroxyl radicals (OH.). The macrophages from healthy individuals are able to kill M. leprae along with release of O2- and OH. radicals. The deficiency in the macrophages of both types of leprosy patients is removed by activation of these cells when exposed to a culture supernatant obtained after stimulation of peripheral blood mononuclear cells from the same patients with delipidified cell components of M. leprae which are most likely cell wall proteins. The activation of macrophages also leads to recognition of whole live M. leprae as an antigen by cells from lepromatous patients. This activation of the phagocytes by delipidified cell components is blocked by cyclosporin A, indicating the possible role of several steps involved in immune activation of cells. The observations thus indicate the significant ability of delipidified cell components to eliminate the deficiencies in the macrophages from leprosy patients and restore them to behave like the cells from healthy individuals. Considering all these, it is suggested that delipidified cell components could be potential modulators, and are probably capable of functioning as a vaccine for leprosy.

Adjuvants, Immunologic↗
PubMed2005

Histidine-rich glycoprotein: A novel adaptor protein in plasma that modulates the immune, vascular and coagulation systems.

Histidine-rich glycoprotein (HRG) is an abundant plasma glycoprotein that has a multidomain structure, interacts with many ligands, and has been shown to regulate a number of important biological processes. HRG ligands include Zn(2+) and haem, tropomyosin, heparin and heparan sulphate, plasminogen, plasmin, fibrinogen, thrombospondin, IgG, FcgammaR and complement. In many cases, the histidine-rich region of the molecule enhances ligand binding following interaction with Zn(2+) or exposure to low pH, conditions associated with sites of tissue injury or tumour growth. The multidomain nature of HRG indicates that it can act as an extracellular adaptor protein, bringing together disparate ligands, particularly on cell surfaces. HRG binds to most cells primarily via heparan sulphate proteoglycans, binding which is also potentiated by elevated free Zn(2+) levels and low pH. Recent reports have shown that HRG can modulate angiogenesis and additional studies have shown that it may regulate other physiological processes such as cell adhesion and migration, fibrinolysis and coagulation, complement activation, immune complex clearance and phagocytosis of apoptotic cells. This review outlines the molecular, structural, biological and clinical properties of HRG as well as describing the role of HRG in various physiological processes.

Animals↗
PubMed1999

A monoclonal antibody directed against the murine macrophage surface molecule F4/80 modulates natural immune response to Listeria monocytogenes.

Whole spleen cell cultures from SCID mice release high levels of IFN-gamma when exposed to heat-killed Listeria monocytogenes (HKL). This microbe-induced and T cell-independent response depends on both macrophages (MPhi) and NK cells: HKL-stimulated MPhi release TNF-alpha and IL-12, which together activate NK cells for IFN-gamma release. We show here that this cytokine-mediated activation cascade can be modulated by a mAb against the MPhi surface glycoprotein F4/80. HKL-induced IL-12, TNF-alpha, and IFN-gamma in SCID whole spleen cell cultures was inhibited by coincubation with anti-F4/80 mAb whereas IL-1 and IL-10 were enhanced. Both effects were apparent at mRNA and protein release levels. Whereas inhibitory activities were F4/80 Ag specific, stimulatory effects were Fc dependent and nonspecific. Furthermore, cytokine inhibition by anti-F4/80 was only apparent when MPhi and NK cells were present simultaneously and in close vicinity, indicating that direct cell-to-cell contact is a prerequisite. These data suggest a novel pathway for microbe-induced MPhi/NK cell interaction involving direct cell-to-cell signaling and give the first evidence for a functional role of the MPhi surface glycoprotein F4/80.

Adjuvants, Immunologic↗
PubMed1999

Serum autoantibodies to brain in Landau-Kleffner variant, autism, and other neurologic disorders.

OBJECTIVE: Etiologically unexplained disorders of language and social development have often been reported to improve in patients treated with immune-modulating regimens. Here we determined the frequency of autoantibodies to brain among such children. DESIGN: We collected sera from a cohort of children with (1) pure Landau-Kleffner syndrome (n = 2), (2) Landau-Kleffner syndrome variant (LKSV, n = 11), and (3) autistic spectrum disorder (ASD, n = 11). None had received immune-modulating treatment before the serum sample was obtained. Control sera (n = 71) were from 29 healthy children, 22 with non-neurologic illnesses (NNIs), and 20 children with other neurologic disorders (ONDs). We identified brain autoantibodies by immunostaining of human temporal cortex and antinuclear autoantibodies using commercially available kits. RESULTS: IgG anti-brain autoantibodies were present in 45% of sera from children with LKSV, 27% with ASD, and 10% with ONDs compared with 2% from healthy children and control children with NNIs. IgM autoantibodies were present in 36% of sera from children with ASD, 9% with LKSV, and 15% with ONDs compared with 0% of control sera. Labeling studies identified one antigenic target to be endothelial cells. Antinuclear antibodies with titers >/=1:80 were more common in children with ASD and control children with ONDs. CONCLUSION: Children with LKSV and ASD have a greater frequency of serum antibodies to brain endothelial cells and to nuclei than children with NNIs or healthy children. The presence of these antibodies raises the possibility that autoimmunity plays a role in the pathogenesis of language and social developmental abnormalities in a subset of children with these disorders.

Antibodies, Antinuclear↗
PubMed2006

Age- and breed-dependent adapted immune responsiveness of poultry to intratracheal-administered, pathogen-associated molecular patterns.

Immune modulation of poultry by airborne pathogen-associated molecular patterns (PAMP) was studied. White and Brown layer chicks were exposed intratracheally during 5 consecutive days at 7 wk of age with Escherichia coli-derived lipopolysaccharide (LPS), Saccharomyces cerevisiae-derived 1,3 beta-glucan (BGL), a combination of both, or PBS as a control. Six weeks later, birds received similar or crossover PAMP treatments. Body weight (gain), feed conversion, (primary and secondary) specific antibody responses to model antigens, and natural antibody levels were measured. In general, BGL enhanced but LPS exposure decreased primary immune responses at 7 wk of age, whereas both PAMP-enhanced secondary immune responses but decreased primary immune responses at 13 wk of age. Body weight gain and feed conversion at both ages were negatively affected by LPS, especially in White birds, but not by BGL. Pathogen-associated molecular patterns exposure at 7 wk of age also affected Ab responses at 13 wk of age. Birds exposed to a combination of LPS + BGL at 7 wk of age had significantly lower secondary total and IgG Ab responses at 13 wk of age. Birds from both breeds showed enhanced BW gain after exposure to LPS at 13 wk of age, when initially challenged at 7 wk of age with LPS, BGL, or a combined challenge with both. Pathogen-associated molecular patterns exposure at 7 wk of age affected humoral immunity and BW gain at 13 wk of age in a positive (BGL) or negative (LPS) fashion. Repeated exposure to PAMP did not affect Ab responses, but crossover exposure to PAMP in general enhanced Ab responses. Body weight gain was positively affected by repeated exposure but not by crossover exposure, suggesting adaptation of the birds to early PAMP exposure. Our findings suggest that sensitivity of poultry for immune modulation by airborne PAMP differs between ages, is breed-dependent, and is not irreversible of nature. In addition, our data suggest different adaptation to hygienic conditions, both with respect to immune reactivity and BW gain.

Aging↗