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PubMed2004

[Immunonutrition].

Several specific nutritional substrates have been shown to augment and/or modulate host immune function. Some enteral formulas enriched with specific immune-modulating nutrients are presently available for clinical use in Japan. Such nutrients include n-3 fatty acids, arginine, glutamine and nucleotides. Recent meta-analyses of clinical trials showed risk of infection, length of hospital stay and medical costs to be reduced by immunonutrition. The benefits of enteral immunonutrition to be most pronounced in GI surgical patients. However, in critical illness, it is difficult to draw any conclusion on the effect of immunonutrition because of the heterogeneity of the critically ill patients and few clinical trials Further clinical trials to determine which groups of patients are indicated for immunonutrition, as well as what is the optimal combinations of specific nutrients, are needed. Studies are also required to determine the safety of immunonutrition.

Adjuvants, Immunologic↗

PubMed2004

[Pathogenesis of autoimmune hepatitis].

OBJECTIVES: The aim of the study was to review the pathogenic mechanisms of auto-immune hepatitis. METHODS: The study was based on a review of all relevant articles from literature on the mechanisms of auto-immunity in auto-immune hepatitis. RESULTS: The precise mechanisms through which liver damage occurs are not fully understood. Auto-immune hepatitis seems to be a consequence of auto-antigen exposure, genetic predisposition and defective immuregulatory mechanisms. Auto-antigen is presented by class II molecules of the major histocompatibility complex. Cytokines and non specific auto-immune promotors modulate immune reactivity. Cell-mediated and antibody-dependent forms of cytotoxicity are probably interactive pathogenic mechanisms. CONCLUSION: Disturbance in the tight balance between auto-aggression and self-tolerance, affected by several internal and external factors are likely in auto-immune hepatitis.

Age Factors↗

PubMedDate not supplied

Novel therapies for heart failure: focus on anti-inflammatory strategies.

The understanding of the pathomechanisms leading to heart failure has evolved from the simplistic pump-failure concept to the more complex syndrome involving neurohormonal and inflammatory systems. Anti-inflammatory therapy targeting specific cytokines, however, such as tumor necrosis factor-alpha, has failed to show clinical benefit. As a result, the focus has turned toward more broad-spectrum anti-inflammatory strategies. This review examines the various broad-spectrum anti-inflammatory modalities that have been used in heart failure: IV immunoglobulin administration, immune modulation therapy, immune adsorption, and plasmapheresis.

Anti-Inflammatory Agents↗

PubMed1978

[Biochemical and pharmacological properties of new 2-substituted aziridines. Contribution to experimental tumor research].

A new class of compounds, the 2-cyanaziridines, has immune-modulating properties. This immune-modulation was proved by the influence on the delayed type hypersensitivity reaction, the increase of the lymphocyte transformation by T-cell-specific mitogens ConA and PHA, the increase of phagocytosis of macrophages, the increase of resistance against bacterial, fungal and virus infections and by the influence on various transplantation tumors in mice and rats.

Animals↗

PubMed1995

Pathophysiology of pneumonia.

The care and management of the pneumonia patient are formidable challenges to the physician. As long as the basic underlying host defense defects in these patients remain elusive, the clinician's approach will remain symptomatic and empirical. Further knowledge of the underlying pathophysiology of pneumonia will undoubtedly provide innovative approaches to both the prevention and the early and effective treatment of this infection. Clearly, the development of a multimodal approach, including components of immune modulation and immune restoration, is needed to improve the multiple defects in the host defense system; however, the normal host defense system operates in a delicate balance. Efforts to stimulate the immune system nonselectively may prove to be as deleterious to the patient as are the negative effects of their immunocompromised state.

Antibody Formation↗

PubMed2005

Modulation of immune response following dietary genistein exposure in F0 and F1 generations of C57BL/6 mice: evidence of thymic regulation.

To further determine whether genistein (GEN) modulation of the immune responses was related to its endocrine-disrupting properties and time of exposure, pregnant C57BL/6 mice were exposed to GEN at 0-1250 ppm in feed starting on day 14 of gestation. The C57BL/6 offspring were exposed to GEN in utero and lactationally, and through feed after weaning until postnatal day 42. In dams, exposure to GEN increased the terminal body weight (250 and 1250 ppm), the number of splenic T cells and NK cells (250 ppm), and the activity of NK cells (250 ppm). In F(1) males, GEN increased the terminal body and spleen weights (25 and 250 ppm), the number of CD4(+)CD8(+) and CD4(-)CD8(+) thymocytes (25 ppm), and the number of splenic T cell subsets and NK cells (25 and 250 ppm). Moreover, splenic NK cell activity and anti-CD3-mediated splenocyte proliferation were increased in all treatment groups. In F(1) females, the percentages of CD4(-)CD8(+) and CD4(-)CD8(-) thymocytes (25 and 250 ppm), and CD4(+)CD8(-) and CD4(+)CD8(+) splenocytes (25 and 250 ppm) were increased. In contrast, the percentage and number of CD4(+)CD8(+) thymocytes were decreased (250 ppm). Exposure to GEN decreased the percentages of splenic NK cells in all treatment groups, and decreased the activity of splenic NK cells at the 25 ppm concentration. Additionally, evaluation of CD25(+) and CD44(+) expression by thymocytes indicated that the decrease in the percentage of CD44(+)CD25(+) thymocytes was at least partially responsible for the decrease in the percentage of CD4(-)CD8(-) thymocytes in F(1) male mice. Overall, the results demonstrate that GEN can modulate the immune system in both adult and developing C57BL/6 mice in a dose-specific manner. The gender-specific effects of GEN on the immune responses in F(1) mice suggest that GEN may modulate the immune system by functioning as either an estrogen agonist or antagonist. The differential effects of GEN on thymocytes in F(1) male and female mice indicate that GEN immunomodulation might be related to its effect on thymus.

Animals↗

PubMed1988

Comparable modulation of human monocyte functions by commercial factor VIII concentrates of varying purity.

Our previous observation on immune modulation induced by a given factor VIII (F VIII) concentrate preparation was extended by showing that the immune-modulating capacity is a more general feature of F VIII products and is independent of product purity. Interaction of human monocytes with therapeutic concentrations of various F VIII concentrates (0.2 to 2 IU F VIII/mL, six different F VIII concentrates from four manufacturers) led to a significant reduction in the expression of IgG Fc receptors in the membrane of these cells (F VIII concentrate-induced downmodulation of the receptor). This Fc receptor downmodulation was achieved by a short (1-hour) incubation of human monocytes with F VIII concentrates 16 hours prior to the Fc receptor assay and did not correlate with the respective product's IgG content. Although the IgG concentrations of the different products varied greatly (from 1.0 to 177.3 mg/1,000 IU F VIII), all products behaved comparably with respect to Fc receptor downmodulation (F VIII-treated monocytes: 34% +/- 7% to 44% +/- 4% rosette-forming cells; controls in the absence of F VIII: 83% +/- 5%). Furthermore, we also were able to demonstrate that heat treatment of F VIII, now used by virtually every manufacturer to eliminate contaminating viruses, had no effect on the respective products' Fc receptor-modulating capacity. The immune-modulating component was characterized as being a high-molecular-range compound containing IgG, IgM, F VIII, and blood group substances (most likely a combination of immune complexes and immunoglobulin aggregates). This compound is present in comparable amounts in both high-purity and intermediate-purity products and apparently copurifies with F VIII during the manufacturing process.

Antigen-Antibody Complex↗

PubMed2003

Anthrax-protective effects of yeast beta 1,3 glucans.

CONTEXT: The recent events increasing the threat of bioterrorism have prompted a widespread search for defenses against this peril. OBJECTIVE: To evaluate the anthrax-protective effect of beta1,3-glucan immune modulators (PGG-glucan and WGP beta glucan) in an experimental animal model. DESIGN: Beta1,3-glucan immune modulators were administered by subcutaneous injection to Balb/c mice 2 days prior to anthrax challenge. WGP beta glucan was administered by daily oral gavage for 7 days prior to challenge, or in drinking water for 10 days postchallenge with a lethal dose of Bacillus anthracis spores. Survival, survival time, and microbial bioburden relative to an infected, untreated control group were assessed. RESULTS: A single injected dose of PGG-glucan or WGP beta glucan immune modulators given 2 days before challenge significantly: (a) increased the survival rate of infected mice (2.5-fold), (b) diminished the bacterial load in the lungs of infected mice (4-8-fold), and (c) increased the proportion of bacteria-free animals 10 days after challenge (2-fold). In mice prophylactically administered oral WGP beta glucan for 1 week prior to infection, survival increased from 50% to 100%; therapeutic administration of oral WGP beta glucan for 10 days postinfection increased survival from 30% up to 90% in treatment groups. CONCLUSIONS: These results demonstrate the potential for beta1,3-glucan immune modulators to provide a significant degree of protection against anthrax, a potential biological warfare (BW) agent in a mouse model of anthrax infection. Further studies are needed to optimize protection, evaluate activity in combination with other treatment options, demonstrate activity in a validated primate model of infection, and determine if protection is effective against other potential BW agents.

Adjuvants, Immunologic↗

PubMed1978

Modulation of immune responses by suppressor T cells.

The activity of suppressor T cells has been demonstrated in almost every phase of the immune response. These regulatory cells modulate both humoral and cell-mediated immunity utilizing antigen-specific and nonspecific mechanisms. For comparative purposes two murine models are described, the nonspecific suppressor T cell stimulated by the mitogen concanavalin A and the antigen-specific suppressor T cell stimulated by injection of the synthetic terpolymer acid 60-L-alanine30-L-tyrosine10 (GAT) in nonresponder mice. These two T cells are similar to expression of Ly alloantigens, ability to inhibit antibody responses, and the mediation of suppression, at least in part, by soluble products. However, differences in radio-resistance and antigenic specificity of the suppressor T cells, as well as differences in molecular characteristics of the soluble factors and their targets suggest that these T cells regulate the immune response by different mechanisms. The relationship of these two suppressor T cells to other nonspecific and antigen-specific suppressor T cells is discussed.

Alanine↗

PubMed2005

[Ginseng modulates the immune response via its effect on cytokine production--secondary publication].

Ginseng has been shown to modulate the immune system. In this study, ginseng"s effects against chronic P. aeruginosa lung infection in animal models and its cytokine-modulating effects on leukocytes were investigated. Leukocytes cultured with ginseng produced more interleukin-12. Animal models treated with ginseng s.c. showed a much faster bacterial clearance, milder lung pathology, activation of phagocytes and a Th1 immune response. These results suggest that ginseng treatment induced a Th1-like immune response, which improved the pathologic course in our animal models.

Animals↗

PubMed2004

Modulation of immune and inflammatory responses by dietary lipids.

PURPOSE OF REVIEW: There continues to be considerable interest in the modulating effect of dietary lipids on immune and inflammatory responses. Although controversy still exists in research in this area, new concepts and approaches have emerged providing useful suggestions. Analysis of the recent findings will help in understanding certain paradoxical findings as well as introducing new strategies to guide future studies. RECENT FINDINGS: The tissue polyunsaturated fatty acid composition was found to be correlated with changes in certain indices of immune function in individuals consuming habitual diets. It seems that individuals or animals with disordered immune systems are more reactive to polyunsaturated fatty acid supplementation, and genetic variation is also a determinant. N-3 polyunsaturated fatty acids were shown to reduce both resistance to bacterial infection and host survival. The studies on other non-classic fatty acids also demonstrated interesting findings. A proposed immuno-enhancing effect of conjugated linoleic acid has not been confirmed by studies and even an adverse effect has been implied. Trans fatty acids have been shown to increase the production of inflammatory cytokines, which may contribute to their pro-atherogenic property. SUMMARY: Current data suggest that the intake of polyunsaturated fatty acids, particularly n-3 polyunsaturated fatty acids, can modulate immune and inflammatory responses, although a discrepancy is still present. Some recent studies have provided useful information explaining possible underlying reasons. Factors such as genetic variation, health status, disease, immune response stage, stimulation type, and possibly age, all contribute to the responsiveness to polyunsaturated fatty acid supplementation in terms of immune function.

Animals↗

PubMed2004

Effect of L-arginine on restraint stress induced modulation of immune responses in rats and mice.

The present study investigates the role of nitric oxide (NO) on restraint stress (RS)-induced modulation of humoral and cell-mediated immune responses in rats and mice. RS produced suppression of humoral immune response, i.e., anti-SRBC antibody titre ( 7.38 +/- 0.32 versus 4.13 +/- 0.30; mean +/- S.E.M., P < 0.001). In case of cell-mediated immunity, in delayed type hypersensitivity (DTH) response the change in paw volume decreased from 0.069 +/- 0.003 mm (mean +/- S.E.M.) in control non-stressed group to 0.038 +/- 0.002 mm in the stressed group (P < 0.001) while percentage leucocyte migration inhibition (% LMI) decreased from 39.7 +/- 1.95 in control non-stressed animals to 15.2 +/- 1.07 in animals subjected to stress (P < 0.01). Pretreating the animals with an NO precursor, L-arginine (1000 mg kg-1, i.p.) antagonized the effect of RS on humoral (anti-SRBC antibody titre 6.50 +/- 0.27 versus 4.13 +/- 0.30, P < 0.001 ) and cell-mediated (DTH response 0.066 +/- 0.002 mm versus 0.038 +/- 0.002 mm, P < 0.001; % LMI 41.5 +/- 1.46 versus 15.2 +/- 1.07, P < 0.01) immune responses. Administration of 7-nitroindazole (7-NI, 50 mg kg-1, i.p.), an inhibitor of neuronal NO synthase, alone further enhanced the immunosuppressive effect of RS (anti-SRBC antibody titre 2.75 +/- 0.25 versus 4.13 +/- 0.30, P < 0.001; DTH response 0.019 +/- 0.002 mm versus 0.038 +/- 0.002 mm, P < 0.001; % LMI 5.0 +/- 1.08 versus 15.2 +/- 1.07, P < 0.01). However, when given before L-arginine treatment, 7-NI reversed the effect of the latter drug on stress-induced immunomodulation (anti-SRBC antibody titre 3.00 +/- 0.27 versus 6.5 +/- 0.27, P < 0.001; DTH response 0.043 +/- 0.003 mm versus 0.066 +/- 0.002 mm, P < 0.001; % LMI 12.0 +/- 0.93 versus 41.5 +/- 1.46, P < 0.01). Unlike its effect on RS-induced immune responsiveness, L-arginine (250, 500, 1000 mg kg-1) when given for 5-7 days to naive non-stressed animals produced dose dependent suppression of both humoral (anti-SRBC antibody titre 6.4 +/- 0.32 versus 5.4 +/- 0.32, 4.0 +/- 0.27, 3.1 +/- 0.30, respectively) and cell-mediated (DTH 0.065 +/- 0.003 mm versus 0.064 +/- 0.004 mm, 0.039 +/- 0.003 mm, 0.020 +/- 0.002 mm, respectively and % LMI 37.52 +/- 1.58 versus 30.48 +/- 1.07, 28.18 +/- 1.22, 19.76 +/- 0.83, respectively) immune responses. 7-NI significantly blocked these immunosuppressive effects of L-arginine (anti-SRBC antibody titre 6.0 +/- 0.38 versus 3.1 +/- 0.030, P < 0.01; DTH response 0.056 +/- 0.004 mm versus 0.020 +/- 0.002 mm, P < 0.001; % LMI 34.76 +/- 1.31 versus 19.76 +/- 0.83, P < 0.01). However, 7-NI when given to non-stressed animals failed to modulate immune responsiveness. Thus, NO appears to play an important role in RS-induced immunomodulation and these effects are different from its effect on immune responsiveness in non-stressed animals.

Animals↗

PubMed1988

Neuroendocrine modulation of the immune system. Possible implications for inflammatory bowel disease.

Evidence for neuroendocrine regulation of the immune system is reviewed. This includes human clinical studies of the influence of psychological stress on immune function, direct experimentation in animals, including classical Pavlovian conditioning of the immune response, modulation of immune function in vitro by chemical messengers such as neuropeptides, the finding of receptors for neuropeptides on immunocytes, and the demonstration that lymphoid tissue is directly innervated. Secretory products of the immune system, which include interleukins and neuropeptides, may also influence the neuroendocrine system. Communication between the two systems is therefore bidirectional. The potential importance of the neuropeptide-immunocyte interaction within the intestinal mucosal immune system is emphasized, and its possible relevance in inflammatory disorders is discussed. This aspect of the "gut-brain" interaction deserves further study.

Animals↗

PubMed1987

Anti-idiotype immunization of cancer patients: modulation of the immune response.

Thirty patients with advanced colorectal carcinoma (CRC) were treated with alum-precipitated polyclonal goat anti-idiotypic antibodies (Ab2) to monoclonal anti-CRC antibody CO17-1A (Ab1) in doses between 0.5 and 4 mg per injection. All patients developed anti-anti-idiotypic antibodies (Ab3) with binding specificities on the surfaces of cultured tumor cells similar to the specificity of Ab1. Furthermore, the Ab3 competed with Ab1 for binding to CRC cells. Fractions of Ab3-containing sera obtained after elution of the serum immunoglobulins from CRC cells bound to purified tumor antigen and inhibited binding of Ab2 to Ab1. The Ab3, therefore, may share idiotopes with Ab1. Six patients showed partial clinical remission and seven patients showed arrest of metastases following immunotherapy. Four of the thirteen patients with measurable clinical responses had received Ab2 alone, whereas 9 patients had also received chemotherapy.

Antibodies, Anti-Idiotypic↗

PubMed2001

Immune induction and modulation in mice following immunization with DNA encoding F protein of respiratory syncytial virus.

Respiratory syncytial virus (RSV) is one of the principal agents of bronchiolitis and pneumonia in young children. Thus, there is a strong need to make a safe and effective vaccine against the RSV infection. DNA immunization is very effective at inducing both cellular and humoral immune responses. In this study, we inserted the RSV-F gene into expression vectors, pcDNA3.1 and pQE. These constructs were transformed into C2C12 and E. coli M15 cells, respectively. The expression of the RSV-F protein was confirmed by SDS-PAGE, followed by Western blot analyses. The immunization of pcDNA3.1-RSV-F elicited both anti-RSV-F titer in mouse sera and CTL activities with mouse splenocytes. Especially, the co-administration of IL-4, or the GM-CSF gene with the RSV-F gene construct, enhanced the production of anti-RSV-F Ab. However, this enhancement disappeared by the simultaneous injection of the Th1 and Th2 type cytokine genes. The CTL activities were affected by the co-delivery of the IFN-gamma gene, but not by Th2-type cytokines.

Aged↗

PubMed2003

Mechanisms of stress-induced modulation of immunity.

The purpose of this chapter is to discuss the wealth of animal studies of stress-induced modulation of immunity, and to relate our understanding of stress and immunity to clinical populations, particularly cancer patients.

Animals↗

PubMed2004

The modulator role of the hypothalamic paraventricular nucleus on immune responsiveness.

Role of the paraventricular nucleus of the hypothalamus (PVH) upon immune modulation was studied by either mechanically destroying the PVH (PVHL) or by isolating the PVH (PVHI) with a knife-cut. PVHL or PVHI manipulations induced significant leukopenia characterized by a decrease in the number of neutrophils and lymphocytes two weeks post surgery. The numbers of circulating monocytes and eosinophils were not affected by PVH interventions. In addition, PVHL and PVHI were also associated with a reduction, relative to controls, in the phagocytosis by neutrophils and an increase in blastic transformation of T lymphocytes induced by phytohemagglutinin-M (PHA-M). Antibody titers rose against sheep red blood cells (SRBC) after either PVHL or PVHI were reduced. The magnitude of the SRBC antibody reduction after PVH manipulations was similar to that observed in rats that received a peripheral chemical sympathectomy two hrs prior immunization. Comparison of thyroid hormones blood levels two weeks after PVHL or PVHI revealed significant reductions in comparison with sham-operated group (SO), whereas blood corticosterone was not significantly altered. In summary, we provide evidence that lesion or isolation of the PVH selectively reduces circulating white blood cells and the primary immune response, while it enhances the cell-mediated immune function. Taken together our data showed that PVH modulates immune functions by altering both the peripheral sympathetic tone and thyroid hormone secretion.

Animals↗

PubMed1998

Centrally-mediated opioid-induced immunosuppression. Elucidation of sympathetic nervous system involvement.

Opioid-induced modulation of the immune system is a complex phenomenon involving opioid receptors, central and sympathetic neural pathways, catecholamine receptors, and other regulatory mechanisms. The precise neural pathways involved in centrally-mediated immune modulation are not currently defined. In addition, the physiological purpose for endogenous opioid modulation of the immune system is not well understood. Perhaps this modulation phenomenon represents an integral feedback loop within a much larger homeostatic control system. Indeed, the role of the HPA axis in immune regulation can not be discarded, and in fact, probably serves to balance immune function, in concert with multiple feedback systems, around some undiscovered parameter of efficiency. Perhaps the physiological role of endogenous opioid control is to act as a monitor poised to subvert chronic inflammatory processes and autoimmune disorders. Regardless of the evolutionary heritage of this and despite the overwhelming complexity of immune regulation, important work substantiating a bidirectional communication link between the brain and the immune system has created a foundation for further elucidation of the intricacies of immunoregulation.

Animals↗