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Results for “immune modulation”

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PubMed1994

Modulation of immune response to Lol p I by pretreatment with anti-idiotypic antibody is not restricted to the idiotypic expression.

To study the role of anti-idiotypic antibodies in the regulation of the immune response to Lol p I (the major allergenic component of rye grass pollen), we have recently generated a panel of three MoAbs directed against distinct epitopes of Lolp I and an anti-idiotypic MoAb directed against the idiotype borne by one of the anti-Lol p I MoAbs (290A-167). The effects of pretreatment with this anti-idiotypic MoAb in BALB/c mice before immunization with the antigen have been examined. The anti-idiotypic MoAb or unrelated MoAb were given weekly for 8 weeks intraperitoneally. Mice then received the antigen (2 micrograms) adsorbed with alum (2 mg) at weeks 9, 11 and 13. Serum anti-Lol p I antibodies (IgG or IgE) and specific idiotypic responses were measured. Anti-Lol p I IgG antibodies could be detected before immunization with Lol p I only in mice pretreated with anti-idiotypic MoAb. Immunization with Lol p I induced an anti-Lol p I IgG response in both groups, but this response was higher in mice that received anti-idiotypic MoAb. Similar profiles were seen for specific IgE antibodies and idiotypic responses. Surprisingly, idiotypes borne by other anti-Lol p I MoAbs (539A-6 and 348A-6) had also been enhanced after pretreatment with the anti-290A-167 MoAb. These observations suggested that the pretreatment with this anti-idiotypic MoAb modulates not only the expression of the respective idiotype, but also affects other idiotype responses.

Allergens↗

PubMed1993

[The immune system and physical training].

The effects on the immune system of sudden physical exercise and degree of training are reviewed. During moderate as well as strenuous physical exercise natural killer (NK) cells especially, but also T and B cells are released into the blood. A few hours after moderate physical exercise the immune system is back to the pre-exercise state, but following strenuous exercise the lymphocyte concentration and the NK and B cell functions are suppressed. The immune suppression following strenuous exercise is at least partly due to release of prostaglandins from an elevated number of monocytes in the circulation. The importance of stress hormones for mediating the immune modulation is discussed. Examination of trained persons at rest show that these have elevated NK cell activity when compared to matched controls. There are sporadic reports in the literature, showing that persons who train moderately have fewer infections, while persons who train very hard have increased risk of upper respiratory diseases. These findings are in accordance with the observed immune modulation on moderate versus strenuous exercise. The effects of physical training in relation to acute and chronic diseases are evaluated.

Endorphins↗

PubMed2005

Milk-derived GM(3) and GD(3) differentially inhibit dendritic cell maturation and effector functionalities.

Gangliosides are complex glycosphingolipids, which exert immune-modulating effects on various cell types. Ganglioside GD(3) and GM(3) are the predominant gangliosides of human breast milk but during the early phase of lactation, the content of GD(3) decreases while GM(3) increases. The biological value of gangliosides in breast milk has yet to be elucidated but when milk is ingested, dietary gangliosides might conceptually affect immune cells, such as dendritic cells (DCs). In this study, we address the in vitro effect of GD(3) and GM(3) on DC effector functionalities. Treatment of bone marrow-derived DCs with GD(3) before lipopolysaccharide-induced maturation decreased the production of interleukin-6 (IL-6), IL-10, IL-12 and tumor necrosis factor-alpha as well as reduced the alloreactivity in mixed leucocyte reaction (MLR). In contrast, only IL-10 and IL-12 productions were significantly inhibited by GM(3,) and the potency of DCs to activate CD4(+) cells in MLR was unaffected by GM(3). However, both gangliosides suppressed expression of CD40, CD80, CD86 and major histocompatibility complex class II on DCs. Because GD(3) overall inhibits DC functionalities more than GM(3), the immune modulating effect of the ganglioside fraction of breast milk might be more prominent in the commencement of lactation during which the milk contains the most GD(3).

Animals↗

PubMed2005

Severe acute respiratory syndrome and the innate immune responses: modulation of effector cell function without productive infection.

Severe acute respiratory syndrome (SARS) caused by a novel human coronavirus (CoV), designated SARS-CoV, is a highly contagious respiratory disease with the lungs as a major target. Although the exact mechanism of SARS-CoV pathogenesis remains unknown, an intense, ill-regulated local inflammatory response has been suggested as partially responsible for the devastating lung pathology. We investigated the interaction of SARS-CoV with human macrophages (Mphi) and dendritic cells (DC), two key innate immune cells of the host immune system, by focusing on their susceptibility to viral infection and subsequent responses (e.g., phenotypic maturation, T cell-priming activity, phagocytosis, and cytokine production). We found neither cell to be permissive for SARS-CoV replication. However, incubation of Mphi and DC with live, but not gamma irradiation-inactivated, viruses appeared to better sustain their viability. Also, exposure to infectious SARS-CoV led to the phenotypic and functional maturation of DC, with regard to MHC class II and costimulatory molecule expression, T cell-stimulatory capacity, and cytokine production, respectively. Cytokine production was also observed for Mphi, which were refractory to cell surface phenotypic changes. Strikingly, live SARS-CoV could further prime cell types to respond to a suboptimal dose of bacterial LPS (100 ng/ml), resulting in massive release of IL-6 and IL-12. However, the endocytic capacity (e.g., Ag capture) of Mphi was significantly compromised upon exposure to infectious SARS-CoV. This study is the first demonstration that although SARS-CoV does not productively infect human Mphi or DC, it appears to exert differential effects on Mphi and DC maturation and functions, which might contribute to SARS pathogenesis.

Cell Death↗

PubMed1994

The relationship of clinical-pathologic status and adjuvant treatment with natural killer cell activity in stage I and II endometrial carcinoma.

OBJECTIVE: The aim of our study was to evaluate the basal immune reactivity in patients with locally advanced endometrial carcinoma, and the immune modulating effect of adjuvant treatment in cancer population randomized to endocrine or radiation therapy. MATERIAL AND METHODS: Forty-three patients with FIGO stage I and II endometrial carcinoma, treated with primary radical surgery, were randomly selected to receive endocrine (medroxy-progesterone acetate 30 mg weekly and Tamoxifen 300 mg weekly, given consecutively) or radiation adjuvant treatment (external beam photon treatment of the whole pelvis, with an average total dose of 3680 cGy rad). The immune assay included the evaluation of natural killer cell activity by target cell retention of the fluorescent dye carboxyfluoresceyn diacetate, using sensitive cell line K 562. The immunological monitoring was performed before surgery, and then before, during, and after adjuvant treatment. Nine patients, who refused any adjuvant treatment, were recruited as controls. RESULTS: Patients, matched for age and demographic characteristics, with locally advanced endometrial carcinoma had significantly lower mean values of natural killer activity than in healthy controls; the decrease of natural cytotoxicity was significantly related to the depth of myometrial invasion. The adjuvant treatment was associated with a significant immune modulation: patients in endocrine therapeutic regimen showed an increase of natural killer activity, while patients in radiation therapy had a reduction; in the control group there was no significant modification of natural cytotoxicity during negative follow up. CONCLUSIONS: Natural killer cell activity of peripheral blood is significantly reduced in local advanced endometrial carcinoma patients. The natural cytotoxicity evaluation, as a function of therapeutic modality, may be useful in establishing a relationship between adjuvant treatment and immune status in endometrial carcinoma.

Adenocarcinoma↗

PubMed2005

Neurobiology of the stress response: contribution of the sympathetic nervous system to the neuroimmune axis in traumatic injury.

Acute injury produces an immediate activation of neuroendocrine mechanisms aimed at restoring hemodynamic and metabolic counter-regulatory responses. These counter-regulatory responses are mediated by the systemic and tissue-localized release of neuroendocrine-signaling molecules known to affect immune function. This has led to the recognition of the importance of neuroendocrine-immune modulation during acute injury as well as throughout the recovery period. The period immediately after acute injury is characterized by upregulation of proinflammatory cytokine expression leading to a later period of generalized immunosuppression. The course and progression of the host recovery from traumatic injury and the integrity of its response to a secondary challenge is directly related to the effective control of the immediate proinflammatory responses to the initial insult. Among the neuroendocrine mechanisms involved in restoring homeostasis, the sympathetic nervous system plays a central role in mediating acute counter-regulatory stress responses to injury. In addition to its recognized cardiovascular, hemodynamic, and metabolic effects, the neurotransmitters released by the sympathetic nervous system have been shown to affect immune function through specific adrenergic receptor-mediated pathways. In turn, cells of the immune system and their products have been shown to influence peripheral and central neurotransmission, leading to the conceptualization of a bidirectional neuroimmune communication system. The reflex activation of this bidirectional neuroimmune pathway in response to injury, integrated with the parasympathetic nervous system, and opioid and glucocorticoid pathways responsible for orchestrating the counterregulatory stress response, results in dynamic regulation of host defense mechanisms vital for immune competence and tissue repair. This review provides the biological framework for the integration of our understanding of the neuroendocrine mechanisms involved in mediating the stress response and their role in modulating immune function during and after traumatic injury.

Humans↗

PubMed1995

Roles of cytokines in the neural-immune interactions: modulation of NMDA responses by IFN-alpha.

Several lines of evidence have indicated that interferon-alpha (IFN-alpha) induces a variety of central actions; e.g., fever anorexia, slow wave sleep and depression. However, little is known about the cellular mechanisms by which IFN-alpha affects neuronal activity. In the present article, the effects of recombinant human IFN-alpha on N-methyl-D-aspartate (NMDA)-induced responses of rat medial preoptic (MPO) neurons were examined by means of slice patch method as an in vitro model of neural-immune interactions. The results suggest that IFN-alpha suppresses the NMDA responses through its action on opioid receptors and the production of free radicals such as hydroxyl radicals and nitric oxide (NO) due to the neuron-glial cell interactions.

Animals↗

PubMed2004

Ginseng modulates the immune response by induction of interleukin-12 production.

In infections with intracellular microorganisms such as mycobacteria and Leishmania parasites as well as certain extracellular chronic infections such as Pseudomonas aeruginosa a Th1 response with activation of macrophages is desirable. Several studies indicate that such a response is associated with better recovery from infection, improved course of the chronic infection, and higher survival rate. In Th1 responses there is increased interferon-gamma (IFN-gamma) and interleukin-12 (IL-12) production, whereas that of interleukin-10 (IL-10) is decreased. The present study indicated that Ginseng modulation of stimulated peripheral blood mononuclear cells (PBMC) results in a higher IL-12 production. The enhanced IL-12 production could induce a stronger Th1 response, resulting in better protection against infection with a variety of pathogens.

Adult↗

PubMed1993

Prostaglandin E1 analogues misoprostol and enisoprost decrease microbial translocation and modulate the immune response.

The aim of this study was to investigate the ability of two prostaglandin E1 (PGE1) analogues, misoprostol and enisoprost, to alter bacterial translocation following burn injury. Balb/c mice were treated with misoprostol (n = 36) or enisoprost (n = 36) for 3 days with different doses (20 or 200 micrograms/kg/day) prior to receiving a 20% full-thickness burn and simultaneous gavage with 1 x 10(10) 14C-Escherichia coli. Animals were sacrificed 4 and 24 hr postburn, and blood, peritoneal fluid, mesenteric lymph nodes, spleen, liver, and lungs were harvested aseptically. Radionuclide counts, number of viable bacteria, and percentage of translocating bacteria remaining alive in each tissue suggested that the high doses of misoprostol or enisoprost decreased the magnitude of 14C-E. coli translocation, while the low dose of both drugs enhanced bacterial clearance. Therefore, both misoprostol and enisoprost reduce bacterial translocation, and modulate bacterial clearance in a dose-dependent manner.

Alprostadil↗

PubMed2005

Phosphatidylinositol-specific phospholipase C of Bacillus anthracis down-modulates the immune response.

Phosphatidylinositol-specific phospholipases (PI-PLCs) are virulence factors produced by many pathogenic bacteria, including Bacillus anthracis and Listeria monocytogenes. Bacillus PI-PLC differs from Listeria PI-PLC in that it has strong activity for cleaving GPI-anchored proteins. Treatment of murine DCs with Bacillus, but not Listeria, PI-PLC inhibited dendritic cell (DC) activation by TLR ligands. Infection of mice with Listeria expressing B. anthracis PI-PLC resulted in a reduced Ag-specific CD4 T cell response. These data indicate that B. anthracis PI-PLC down-modulates DC function and T cell responses, possibly by cleaving GPI-anchored proteins important for TLR-mediated DC activation.

Animals↗

PubMed2002

Modulatory effects of compound polysaccharide erweikang on the immune function of mice.

In order to study the modulatory effects of compound polysaccharide Erweikang on the immune function of the immunosuppressive mice, the positive immune modulation of Erweikang at different doses and different time points was compared when normal saline and cyclophosphamide served as controls. The results showed that different doses of Erweikang could effectively reverse the decreased induction levels of NK, IL-2, gamma-IFN and the contents of TNF and IgF of the immunosuppressive mice after administration of Erweikang for 7 to 14 days. It was suggested that compound polysaccharide Erweikang presents positive immune modulation in dose- and time-dependent manners.

Adjuvants, Immunologic↗

PubMed1997

Clostridial gas gangrene: evidence that alpha and theta toxins differentially modulate the immune response and induce acute tissue necrosis.

The rapid extension of necrosis and an absence of polymorphonuclear leukocytes (PMNL) at the site of infection are two hallmarks of Clostridium perfringens gas gangrene. While both alpha and theta toxins profoundly affect PMNL function and viability in vitro, their roles in muscle destruction and impairment of the inflammatory response in vivo have not been investigated. Comparative histopathologic examinations were performed on animals infected with either wild-type C. perfringens, or isogenic, toxin-deficient mutants of C. perfringens. Tissue destruction was modest in animals infected with the alpha toxin-deficient mutant; destruction was more pronounced in tissues infected with the theta toxin-deficient mutant or the wild-type strain. alpha and theta toxins also displayed differing abilities to modulate the inflammatory response. Histopathologic studies in which recombinant toxins were injected together with killed, washed C. perfringens further substantiated these tissue-destructive and differential antiinflammatory effects.

Animals↗

PubMed2007

Fecal water from ileostomic patients consuming oat beta-glucan enhances immune responses in enterocytes.

Yeast, fungal, and dietary beta-glucans have immune-modulating effects in vitro and in vivo, as thought, mainly by affecting leukocytes; however, effects of oat beta-glucan on enterocytes have never been studied. As recognized, supplying oat beta-glucans as such to cells in culture directly is difficult because of solubility problems. Therefore, six ileostomic patients consumed, in random order, a control diet or an oat beta-glucan enriched diet (5 g) and from the collected ileostomic content, fecal water was prepared and added to two small intestinal cell lines (INT407, Caco-2) and two colon cell lines (HT29, T84) together with a cytokine cocktail (IL-1beta + INFgamma + TNFalpha). Several parameters reflecting immune-modulation were measured. As compared to placebo fecal water, beta-glucan enriched fecal water significantly increased IL-8 production in HT29 (5.0%; p = 0.046) and INT407 cells (22.0%; p = 0.028). Intercellular adhesion molecule (ICAM)-1 expression increased in T84 (11.0%; p = 0.028) and Caco-2 cells (20.4%; p = 0.075). These immune-stimulating effects were confirmed by enhancement of inflammatory expression profiles, as determined with an antibody array. Our findings show immune enhancement by fecal water from ileostomic patients consuming oat beta-glucan both in small intestinal and colon cell lines after stimulation, which is in agreement with documented effects in leukocytes. Whether these immune-stimulating effects on enterocytes contribute to the enhanced protection of the host against invading pathogens as observed both in animals and in humans, as well as the underlying mechanism, needs further evaluation.

Adjuvants, Immunologic↗

PubMed2005

Immune activation modulates hematopoiesis through interactions between CD27 and CD70.

The differentiation of hematopoietic stem cells into mature blood cell lineages is tightly regulated. Here we report that CD27, which is expressed on stem and early progenitor cells in bone marrow, can be important in this process. Deletion of CD27 increased the myeloid colony-forming potential of stem and early progenitor cells and enhanced B lymphoid reconstitutive capacity in competitive transplantation experiments. Conversely, stimulation of CD27(+) progenitor cells with CD70, the unique ligand for CD27, inhibited colony-forming potential in vitro and lymphocyte outgrowth in vivo. As CD70 is expressed only on activated immune cells, we suggest that CD27 triggering on early progenitor cells provides a negative feedback signal to leukocyte differentiation during immune activation.

Animals↗

PubMed2003

Testosterone as a protective factor against atherosclerosis--immunomodulation and influence upon plaque development and stability.

Inflammation plays a central pathogenic role in the initiation and progression of coronary atheroma and its clinical consequences. Cytokines are the mediators of cellular inflammation and promote local inflammation in the arterial wall, which may lead to vascular smooth muscle apoptosis, degradation of the fibrin cap and plaque rupture. Platelet adhesion and thrombus formation then occur, resulting clinically in unstable angina or myocardial infarction. Recent studies have suggested that cytokines are pathogenic, contributing directly to the disease process. 'Anti-cytokine' therapy may, therefore, be of benefit in preventing or slowing the progression of cardiovascular disease. Both oestrogens and testosterone have been shown to have immune-modulating effects; testosterone in particular appears to suppress activation of pro-inflammatory cytokines. Men with low testosterone levels are at increased risk of coronary artery disease. An anti-inflammatory effect of normal physiological levels of sex hormones may, therefore, be important in atheroprotection. In this Article, we discuss some of the mechanisms involved in atherosclerotic coronary artery disease and the putative link between testosterone deficiency and atheroma formation. We present the hypothesis that the immune-modulating properties of testosterone may be important in inhibiting atheroma formation and progression to acute coronary syndrome.

Apoptosis↗

PubMed1989

A phase I clinical trial of recombinant interleukin-2 by periodic 24-hour intravenous infusions.

Recombinant interleukin-2 (rIL-2) (NSC# 600664; Hoffmann-La Roche, Inc., Nutley, NJ) was studied in a phase I clinical trial in 33 patients with advanced, measureable cancer of the colon or malignant melanoma, Eastern Cooperative Oncology Group (ECOG) performance status O-1, and no prior chemotherapy or radiotherapy. The goal of the study was to identify a dose and schedule of IL-2 to generate maximal immune modulation with tolerable toxicity. Such a regimen might allow the addition of other treatment modalities and/or prolonged treatment duration in later trials. Each patient received IL-2 as a continuous 24-hour infusion once weekly for 4 weeks and then twice weekly for 4 weeks. Five treatment groups received from 10(3) U/m2 to 3 x 10(7) U/m2 per 24-hour infusion. The maximal tolerated dose was 3 x 10(7) U/m2/d twice weekly. Patients treated twice weekly at 1 x 10(7) and 3 x 10(7) U/m2/d had immune modulation in terms of lymphocytosis, eosinophilia, increased natural killer (NK) activity, and elevated numbers of peripheral blood mononuclear cells expressing CD16, OKT10/Leu-17, and Leu-19 surface markers. Endogenous generation of peripheral blood lymphokine-activated killer (LAK) activity was demonstrated by lysis of NK-resistant Daudi targets, in patients treated at 3 x 10(7) U/m2/d. Biochemical and hematological abnormalities were moderate and reversible. Clinical toxicity included hypotension, myalgia, arthralgia, stomatitis, fever, fatigue, nausea, headache, chills, diarrhea, and oliguria at high doses. Cardiovascular toxicity was tolerable for most patients and reversed after IL-2 was stopped. Two of six melanoma patients at 3 x 10(7) U/m2/d achieved partial responses by the end of the eighth week. This IL-2 schedule appears to produce potentially clinically useful immune enhancement with tolerable toxicity.

Adolescent↗

PubMed1993

[Immunomodulating treatment of severe aplastic anemia in adults].

Immune modulating therapy has greatly improved the prognosis in aplastic anaemia, but the response to treatment varies considerably. We describe eight patients who were treated for severe aplastic anaemia. Antithymocyte globulin was given as first line treatment, followed by cyklosporine A if the patient failed to respond. Seven patients entered complete remission, but two of these relapsed later. Both developed paroxysmal nocturnal haemoglobinuria. One patient failed to respond to therapy. She died of bone marrow failure and haemochromatosis 12 months after start of therapy. Immune modulating therapy is discussed in relation to bone marrow transplantation, which is the alternative therapy for younger patients.

Adolescent↗

PubMed2004

Is chronic fatigue syndrome an autoimmune disorder of endogenous neuropeptides, exogenous infection and molecular mimicry?

Chronic fatigue syndrome is a disorder characterised by prolonged fatigue and debility and is mostly associated with post-infection sequelae although ongoing infection is unproven. Immunological aberration is likely and this may prove to be associated with an expanding group of vasoactive neuropeptides in the context of molecular mimicry and inappropriate immunological memory. Vasoactive neuropeptides including vasoactive intestinal peptide (VIP) and pituitary adenylate activating polypeptide (PACAP) belong to the secretin/glucagon superfamily and act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to smaller peptide fragments by antibody hydrolysis. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions. Vasoactive neuropeptides are widely distributed in the body particularly in the central, autonomic and peripheral nervous systems and have been identified in the gut, adrenal gland, reproductive organs, vasculature, blood cells and other tissues. They have a vital role in maintaining vascular flow in organs, and in thermoregulation, memory and concentration. They are co-transmitters for acetylcholine, nitric oxide, endogenous opioids and insulin, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system to toxic assault, promotion of neural development and the maintenance of homeostasis. This paper describes a biologically plausible mechanism for the development of CFS based on loss of immunological tolerance to the vasoactive neuropeptides following infection, significant physical exercise or de novo. It is proposed that release of these substances is accompanied by a loss of tolerance either to them or their receptor binding sites in CFS. Such an occurrence would have predictably serious consequences resulting from compromised function of the key roles these substances perform. All documented symptoms of CFS are explained by vasoactive neuropeptide compromise, namely fatigue and nervous system dysfunction through impaired acetylcholine activity, myalgia through nitric oxide and endogenous opioid dysfunction, chemical sensitivity through peroxynitrite and adenosine dysfunction, and immunological disturbance through changes in immune modulation. Perverse immunological memory established against these substances or their receptors may be the reason for the protracted nature of this condition. The novel status of these substances together with their extremely small concentrations in blood and tissues means that clinical research into them is still in its infancy. A biologically plausible theory of CFS causation associated with vasoactive neuropeptide dysfunction would promote a coherent and systematic approach to research into this and other possibly associated disabling conditions.

Autoimmune Diseases↗