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PubMed1998

Inhibition of the cAMP signaling cascade via cannabinoid receptors: a putative mechanism of immune modulation by cannabinoid compounds.

Immune modulation by cannabinoids has been widely established over the past three decades. In spite of this, the mechanism of action responsible for immune modulation and other well described biological effects attributed to cannabinoid compounds has been elusive. The identification and cloning of two novel G protein coupled receptors, CB1 and CB2, both of which bind cannabimimetic agents has served as the basis for a putative mechanism of action. CB1, which is also referred to as the central cannabinoid receptor is the primary form expressed within the central nervous system (CNS). Conversely, the peripheral cannabinoid receptor, CB2, does not appear to be expressed within the CNS but is the predominant form of the receptor expressed within the immune system. Both CB1 and CB2 negatively regulate adenylate cyclase activity through a pertussis toxin sensitive GTP-binding protein. Recent investigations addressing the mechanism by which cannabinoids disrupt leukocyte function have demonstrated that in the presence of cannabinoids the cAMP signaling cascade is markedly inhibited as evidenced by decreased adenylate cyclase and protein kinase A activity and decreased DNA binding by cAMP response element binding proteins. The focus of this discussion will be on the effects cannabinoids elicit on events within the cAMP cascade and related signaling pathways critical to the regulation of cytokine genes.

Animals↗
PubMed2005

Biologic effects and basic science of a novel immune-modulation therapy.

The immune system is a system of dynamic equilibrium, with inflammatory responses (mediated by T helper type 1 cells, interleukin [IL]-1beta, interferon-gamma, and tumor necrosis factor-alpha [TNF-alpha]) being balanced by anti-inflammatory responses (mediated by T regulatory type 1 cell, T helper type 3 cells, IL-4, IL-10, and transforming growth factor-beta). Therefore, neutralization of inappropriate inflammatory cytokines is a therapeutic strategy that has been attempted in many chronic inflammatory conditions, mostly targeting TNF-alpha, using either monoclonal antibodies or modified receptor proteins (etanercept). There is functional redundancy among the inflammatory cytokines. For example, in addition to TNF-alpha, both IL-1beta and IL-6 are elevated in patients with chronic heart failure (CHF); thus neutralizing the activity of TNF-alpha alone may be an inadequate approach in this patient group. Immune-modulation therapy (IMT) results in downregulation of proinflammatory cytokine levels and upregulation of anti-inflammatory cytokines. This alteration in the balance between proinflammatory and anti-inflammatory cytokines may be more appropriate than neutralizing the activity of a single cytokine in the treatment of conditions such as CHF. Several animal studies investigating the effect of IMT in inflammatory conditions including allergic contact hypersensitivity, ischemia reperfusion injury, and atherogenesis are reviewed.

Animals↗
PubMed2003

Synthetic analogues of the bacterial signal (quorum sensing) molecule N-(3-oxododecanoyl)-L-homoserine lactone as immune modulators.

Comparative immune modulatory activity for a range of synthetic analogues of a Pseudomonas aeruginosa signal molecule, N-(3-oxododecanoyl)-l-homoserine lactone (3O, C(12)-HSL), is described. Twenty-four single or combination systematic alterations of the structural components of 3O, C(12)-HSL were introduced as described. Given the already defined immunological profile of the parent compound, 3O, C(12)-HSL, these compounds were assayed for their ability to inhibit murine and human leucocyte proliferation and TNF-alpha secretion by lipopolysaccharide (LPS) stimulated human leucocytes in order to provide an initial structure-activity profile. From IC(50) values obtained with a murine splenocyte proliferation assay, it is apparent that acylated l-homoserine lactones with an 11-13 C side chain containing either a 3-oxo or a 3-hydroxy group are optimal structures for immune suppressive activity. These derivatives of 3O, C(12)-HSL with monounsaturation and/or a terminal nonpolar substituent on the side chain were also potent immune suppressive agents. However, structures lacking the homoserine lactone ring, structures lacking the l-configuration at the chiral center, and those with polar substituents were essentially devoid of activity. The ability of compounds selected from the optimal activity range to modulate mitogen-driven human peripheral blood mononuclear cell proliferation and LPS-induced TNF-alpha secretion indicates the suitability of these compounds for further investigation in relation to their molecular mechanisms of action in TNF-alpha driven immunological diseases, particularly autoimmune diseases such as psoriasis, rheumatoid arthritis, and type 1 (autoimmune) diabetes.

Adjuvants, Immunologic↗
PubMed2005

Commensal gut bacteria: mechanisms of immune modulation.

Mucosal immune responses to pathogenic gut bacteria and the mechanisms that govern disease progression and outcome have been researched intensely for decades. More recently, the influence of the resident non-pathogenic or 'commensal' microflora on mucosal immune function and gut health has emerged as an area of scientific and clinical importance. Major differences occur in the mucosal immune response to pathogens and commensals. In part, this functional dichotomy is explained by the presence of virulence factors in pathogenic species, which are generally absent in commensals. Additionally, immunological 'unresponsiveness' towards the resident commensal microflora is thought to permit their successful colonisation and co-existence within the host gut. However, evidence of an active dialogue between members of the commensal microflora and the host mucosal immune system is rapidly unfolding. This crosstalk is likely to affect immunological tolerance and homeostasis within the gut and to explain some of the differential host responses to commensal and pathogenic bacteria.

Animals↗
PubMed2004

Immune modulation of HIV replication: relevance to HIV immuno- and neuro-pathogenesis.

Much attention has been focused on CD4+ memory/primed T cells and monocytes/macrophages as the predominant targets of HIV infection. Considerable evidence, however, indicates that cell types that are classically not permissive to HIV infection, can be a potent source of productive virus replication in response to immune modulation. This immune modulation can be in the form of cytokine stimulation pre- or post-infection or by activating these "non-conventional" targets. In this review, we will provide evidence for immune modulation of HIV infection with special emphasis on immune modulation of HIV replication in classically non-HIV permissive primary cells of both lymphoid and non-lymphoid origins. We will also examine the impact of HIV infection of these non-conventional targets as they pertain to both HIV immuno- and neuro-pathogenesis.

AIDS Dementia Complex↗
PubMed1987

Immune modulators as antiviral agents.

Immune modulators have exhibited some limited efficacy in the prevention or treatment of viral infection. Such agents have included transfer factor, thymosin, thymic humoral factors, levamisole, isoprinosine, immune RNA, young lymphocytes, vitamin C, and BCG. This article focuses on data that have examined clinical application of immune adjuvant therapy.

Adjuvants, Immunologic↗
PubMed1983

Immune mechanisms in C57Bl mice genetically resistant to Trypanosoma congolense infection. I. Effects of immune modulation.

The effect of immune modulation on the pattern and course of infection with T. congolense was investigated in a strain of mice (C57Bl) which is known to possess a significant degree of trypanotolerance, and a susceptible strain (CFLP) which rapidly succumbs to infection. Immunosuppression of C57Bl mice by splenectomy, cyclophosphamide treatment or gamma irradiation reduced their survival to near that of susceptible strains of mice. In contrast, attempts to enhance the immune response of susceptible CFLP mice using either a variety of immunostimulants, simultaneous vaccination with irradiated parasites at the time of infection, passive immunization or reducing the number of parasites used for infection, failed to confer a level of protection comparable to that of C57Bl mice. It was concluded that the basis of trypanotolerance, although immunological in nature, is associated with, as yet, undetermined factors.

Adjuvants, Immunologic↗
PubMed2006

Nutrients with immune-modulating effects: what role should they play in the intensive care unit?

PURPOSE OF REVIEW: This review will summarize recent clinical and experimental data on the use of immune-modulating nutrients in critical illness. It will present the concept of these nutrients as pharmacologic agents or 'nutraceuticals' administered in addition to protein, calorie, vitamin, and trace element sources. RECENT FINDINGS: Studies have defined the physiologic roles of arginine in critical illness, such as its role as a precursor for the production of nitric oxide. Investigations have determined that, in critical illness, glutamine levels decrease and severe glutamine deficiency is associated with increased mortality. Experimental studies have revealed that glutamine attenuates proinflammatory cytokine responses, improves gut barrier and immune cell functions, increases the ability to mount a stress response, and decreases mortality. Clinical trials and meta-analyses of studies testing immune-modulating nutritional formulations have reported numerous benefits but also some conflicting results. Dose and route of administration are key factors that influence the benefit, or lack thereof, of these nutraceuticals. SUMMARY: Cumulative studies of enteral immune-modulating nutritional formulations report benefits in surgical critically ill patients such as burn, trauma, or gastrointestinal surgery populations. Conflicting data in patients with sepsis warrant concern and further evaluation; in particular, controversy seems to stem around the use of arginine. Glutamine is beneficial when given in high doses or via the parenteral route (>0.20-0.30 g/kg per day or >or=30 g/day). Providing both omega-3 and omega-6 polyunsaturated fatty acids is important in immune modulation. The best doses and combinations of immune-modulating components remain unclear.

Arginine↗
PubMed2002

Poxvirus immune modulators: functional insights from animal models.

Poxviruses express several different classes of immune modulators that suppress the host response to infection, including soluble cytokine binding proteins, serpins, chemokine binding proteins, a complement control protein, and members of the semaphorin and Toll/IL-1 receptor families. Biochemical activity of these proteins has been demonstrated by many in vitro studies. Conservation in evolution of poxvirus immune modulators implies that these genes are functional in vivo, but the results of infecting animals with knockout viruses have not always been clear cut. Studies involving different animal models are reviewed, and the criteria for suitable models are discussed. Challenges include finding an appropriate animal host, and using an inoculation route that resembles the process of natural infection. The fact that multiple immune modulators can target the same pathway at different steps may explain why single knockout mutants are not always attenuated in animals.

Adjuvants, Immunologic↗
PubMed2006

Early postoperative jejunostomy feeding with an immune modulating diet in patients undergoing resectional surgery for upper gastrointestinal cancer: a prospective, randomized, controlled, double-blind study.

BACKGROUND: The provision of perioperative immune modulating enteral feeds after major surgery may result in reduced infective complications, but meta-analyses have not demonstrated a survival advantage. The aim of this study was to determine whether early postoperative immune modulating jejunostomy feeding results in reduced infective complications in patients undergoing resectional surgery for upper gastrointestinal cancer. METHODS: A total of 120 patients undergoing resection for cancers of the pancreas, oesophagus and stomach were randomized in a double-blind manner to receive jejunostomy feeding with an immune modulating diet (Stresson-Group A) or an isonitrogenous, isocaloric feed (1250 Calories and 75 g protein/l--Nutrison High Protein-Group B) for 10-15 days. Feeding was commenced 4h postoperatively and continued for 20 h/day. The target volume (ml/h) was 25 on day 0, 50 on day 1, and 75 thereafter. Outcome measures included complications, hospital stay and mortality. RESULTS: A total of 108 patients (54 in each group) were analysed. Feed delivery, although less than targeted, was similar in both groups. There were 6 (11%) deaths in each group. Median (IQR) postoperative hospital stay was 14.5 (12-23) days in Group A and 17.5 (13-23) days in Group B (P=0.48). A total of 24 (44%) patients in each group had infective complications (P=1.0). A total of 21 (39%) patients in Group A and 28 (52%) in Group B had non-infective complications (P=0.18). Jejunostomy-related complications occurred in 26 (48%) patients in Group A and 30 (56%) in Group B (P=0.3). CONCLUSION: Early postoperative feeding with an immune modulating diet conferred no outcome advantage when compared with a standard feed.

Adjuvants, Immunologic↗
PubMed2006

Immune modulation by cadmium and lead in the acute reporter antigen-popliteal lymph node assay.

Immune modulation by heavy metals may cause serious adverse health effects in humans, although the mechanisms involved are not well understood. Both cadmium and lead are important environmental and occupational toxins. Therefore, in the current study, the costimulatory/adjuvant effects and the T-cell-activating potential of these metals (i.e., CdCl2 and PbCl2), are examined. These immune-modulating properties are critical in the development of conditions such as allergy, hypersensitivity, and autoimmunity. Using the direct popliteal lymph node assay (PLNA) and reporter antigen-popliteal lymph node assay (RA-PLNA) both metals were examined individually for immunotoxicity. Mercury (i.e., HgCl2) was included for comparative purposes as its effects in the RA-PLNA are well documented. Seven days following a single footpad injection containing metal and/or RA (trinitrophenyl-ovalbumin [TNP-OVA] or TNP-Ficoll), BALB/c mice were sacrificed and the popliteal lymph nodes (PLNs) removed. PLN cellularity, TNP-specific antibody-secreting cells (ASCs), and lymphocyte subsets were assessed. All three metals strongly stimulated T- and B-cell proliferation and ASC production following coinjection with the RA TNP-OVA. In each case, ASC production was skewed towards the IgG1 isotype. In addition, all three metals induced IgG production to TNP-Ficoll (although relatively weakly in the case of Cd). These results show that each of these metals can provide adjuvant signals to promote lymphocyte proliferation and enhance adaptive immune responses to unrelated antigens. Skewing of immune responses towards T helper type 2 responses suggests that each of these metals can enhance allergic and hypersensitivity reactions to environmental antigens. Furthermore, the induction of IgG responses to TNP-Ficoll, a T-cell-independent antigen, indicates that each of these metals can activate neoantigen-specific T cells. T-cell activation by metals can lead to metal hypersensitivity and has been implicated in the development of autoimmunity. This is the first report of immune modulation by CdCl2 and PbCl2 in the RA-PLNA.

Animals↗
PubMed2001

The value of immune modulating parameters in predicting the progression from peritonitis to septic shock.

Intra-abdominal infection is one of the major causes of septic shock and multiple organ failure. To date, what causes the disease's progression remains unclear and therefore the relevance of immune modulating therapies remains speculative. The primary outcome measure of this study was to investigate immune modulating mediators at the onset of peritonitis before the development of subsequent septic shock. The secondary outcome measure was to investigate the usefulness of these immune parameters in predicting progression from peritonitis to septic shock. Fifty-eight peritonitis patients were included in this study: 14 patients subsequently developed septic shock. All patients were examined on "diagnosis of peritonitis" (<4 h within establishment of diagnosis), during "early septic shock" (<12 h following the onset of septic shock), and once again during "late septic shock" (within 72-98 h following the onset of septic shock). The immune modulating parameters tumor necrosis factor-alpha (TNF-alpha), the soluble TNF-alpha receptors I and II (sTNF-alpha RI and sTNF-alpha RII), interleukines (IL) -1beta, -6, -8, and -10, and the adhesions molecules endothelial-leukocyte-adhesion-molecule (E-Selectin), intercellular-adhesion-molecule-1 (ICAM-1), and vascular-adhesion-molecule-1 (VCAM-1), in addition to nitrate and nitrite, were determined. In the peritonitis group with subsequent septic shock, TNF-alpha, sTNF-alpha RI + RII IL-1beta, IL-8, IL-10, and nitrate were significantly increased before the onset of septic shock. TNF-alpha had an area under the receiver operating characteristics curve (AUC) of 0.84 and was reliable in predicting the progression from peritonitis to septic shock. The AUC of the other immune modulating parameters, despite being significantly elevated, ranged from 0.71 to 0.76. The AUC of the conventional laboratory markers such as leukocytes and C-reactive protein ranged from 0.64 to 0.68. In peritonitis that progressed to septic shock, an early immune response had already occurred before the onset of septic shock. The progression was best predicted by TNF-alpha. Therefore, mediator therapy might be considered in high-risk peritonitis patients who show an exaggerated immune response before the progression to septic shock.

Adult↗
PubMed2002

Antigen-based immune modulation: DNA vectors and beyond.

The ultimate goal for autoimmune immunotherapy is to achieve a specific downregulation or modification of autoaggressive immune responses while leaving in place the normal repertoire, capable of mediating antimicrobial responses. A multitude of preclinical studies, particularly during the last 15 years, raised hopes that self-antigens could be used to achieve the goal of specific immune modulation. Difficulties associated with the translation of this concept to the clinic revealed inherent limitations of antigen-based immune modulation. To increase the efficiency of antigen-dependent immune modulation, researchers started to investigate novel vectors for antigen delivery. Plasmid vectors, as opposed to protein antigens or peptides, have the ability to trigger prolonged production of limited amounts of antigen in the periphery. However, one complicating factor may be the inherent "danger" signal stimulated by the nature of the unmethylated CpG motifs on bacterial plasmid. Currently, various approaches are being explored to improve the efficacy of response while ameliorating the safety concerns of plasmids as immunotherapeutic tools. This manuscript offers a perspective on such efforts and outlines how the knowledge accumulated in the process will help scientists advance to the next generation of immunotherapeutics.

Adjuvants, Immunologic↗
PubMed2000

Effects of mixed chimerism and immune modulation on GVHD, disease recurrence and survival after HLA-identical marrow transplantation for hematologic malignancies.

BACKGROUND: The success of allogeneic bone marrow transplantation(allo-BMT) is affected by underlying disease relapse. Although mixed chimerism(MC) is not necessarily a poor prognostic factor, several groups have suggested that MC is associated with an increased risk of disease relapse. There is evidence that patients with MC benefit from additional immunotherapy if the treatment is started in minimal residual disease status(mixed chimerism status), not in frank hematological relapse. The purposes of this study are to evaluate 1) the risk for relapse or graft rejection in correlation to persistent MC status after allo-BMT, and 2) the possibility of preventing relapse by immune modulation treatments (withdrawal or rapid taper-off of post-transplant immuno-suppression, additional interferon treatment, or the administration of donor lymphocytes) in hematologic malignancies. PATIENTS AND METHODS: Of 337 allogeneic donor-recipient pairs between March 1996 and August 1998, 12 patients who showed persistent or progressive MC and who received immune modulation treatments were evaluated. Twelve patients, median age 31 years(range 9 to 39 years), received an allo-BMT for: acute myelogenous leukemia(AML, n = 5), chronic myelogenous leukemia(CML, n = 4), acute lymphocytic leukemia(ALL, n = 3). Serial polymerase chain reaction(PCR) analysis of YNZ 22-, 33.6-minisatellites or Y chromosome-specific PCR analysis at short term intervals(pre- and post-transplant 1, 3, 6, 9, ... months) was performed. Once MC was detected, immune modulation treatments on the basis of increasing MC in an early phase of recurrence of underlying disease were started. RESULTS: Nine of 12 patients converted to complete chimerism(CC) (AML 5/5, CML 3/4, ALL 1/3). Four of 9 CC patients developed graft-versus-host disease(GVHD) grade < or = 2 during immune modulation. All were treated successfully with steroids. Three patients who were not converted to CC showed relapse of underlying diseases or graft failure. CONCLUSION: The results demonstrate that, in patients with hematologic malignancies after allo-BMT, persistent MC is associated with relapse of underlying diseases or graft failure. Furthermore, when patients receive early immune modulation treatment, MC can be changed to complete donor pattern chimerism and ultimately prevent relapse.

Adolescent↗
PubMed2003

A C-terminal EGF-like domain governs BAD1 localization to the yeast surface and fungal adherence to phagocytes, but is dispensable in immune modulation and pathogenicity of Blastomyces dermatitidis.

BAD1, an adhesin and immune modulator of Blastomyces dermatitidis, is an essential virulence factor that is released extracellularly before association with the yeast surface. Here, deletion of the C-terminal EGF-like domain profoundly affected BAD1 function, leading to non-association with yeast, extracellular accumulation and impaired yeast adherence to macrophages. In equilibrium binding assays, DeltaC-term BAD1, lacking an EGF-like domain, bound poorly to BAD1 null yeast, yielding a low affinity (Kd, 3 x 10(-7) M versus 5 x 10(-8) M) and Bmax (1.9 x 10(5) versus 7.9 x 10(5)) compared with BAD1. Similar protein binding profiles were observed using chitin particles, reinforcing the notion that chitin fibrils are a receptor for BAD1, and that the EGF-like domain is critical for BAD1 interactions with chitin on yeast. DeltaC-term strains bound poorly to macrophages, compared with parental or BAD1-reconstituted null strains. However, DeltaC-term strains and the purified protein itself sharply suppressed tumour necrosis factor (TNF)-alpha release by phagocytes in vitro and in lung in vivo, and the strains retained pathogenicity in a murine model of blastomycosis. Our results illustrate the previously undefined role of the EGF-like domain for BAD1 localization to yeast surfaces during cell wall biogenesis. They also demonstrate that the requirements for host cell binding and immune modulation by BAD1 can be dissociated from one another, and that the former is unexpectedly dispensable in the requisite role of BAD1 in pathogenesis.

Amino Acid Sequence↗
PubMed2004

[Experimental study on xiaoliu decoction in treating tumor and modulating immune function].

OBJECTIVE: To study the anti-tumor effect and immune function modulation of Xiaoliu decoction (XLD) and to explore the possible mechanism. METHODS: S180 tumor bearing mice were treated with large or small dose of XLD and cyclophosphamide (CTX) to observe the tumor suppressive rate, lymphocyte transformation rate, natural killer cell (NK) activity, tumor necrosis factor alpha (TNFalpha) level in the mice, as well as the tumor cell apoptosis in vitro. RESULTS: The tumor suppressive rate of XLD on tumor bearing mice was over 30%. XLD showed obvious trend in enhancing the tumor suppressing rate of chemotherapy, could increase the lymphocyte transformation rate, NK activity, and TNFalpha level. It also could accelerate the tumor cell apoptosis in vitro. CONCLUSION: XLD has significant anti-tumor effect, it could elevate the immune function or organism and alleviate the chemotherapy induced lowering of immune function.

Adjuvants, Immunologic↗
PubMed2000

Cytomegalovirus immune globulin intravenous (human) administration modulates immune response to alloantigens in sensitized renal transplant candidates.

One of the important parameters for prolonged waiting time for potential renal transplant recipients is the presence of preformed antibodies to human leucocyte antigen (HLA) antigens, which is often caused by previous transplants, pregnancy or transfusions. In vivo administration of specific and unselected polyclonal intravenous immunoglobulin (IVIGs) preparations have been shown to inhibit anti-HLA alloantibodies in highly sensitized patients. We sought to determine whether Cytogam (Medimmune Inc., Gaithersburg, MD, USA), a hyperimmune anticytomegalovirus immunoglobulin would (1) effect either in vitro or in vivo alloreactivity, and (2) whether Cytogam therapy could reduce the titre of preformed anti-HLA antibodies in highly sensitized patients. Alloreactivity was assessed by mixed lymphocyte reaction (MLR) and cytotoxic T lymphocyte (CTL) assay. A complement dependent microlymphocytotoxicity assay was done to assess for panel reactive antibody (PRA) status and the presence of anti-idiotypic antibodies in the Cytogam preparation. The MLR was inhibited by Cytogam in vitro in a dose-dependent fashion ranging from 31-92%. Significant inhibition of the MLR responses was not observed in recipients who received Cytogam in vivo (50 mg/kg). This could be a result of adminstration of a low dose of IVIG. However, CTL activity against the alloantigens in all individuals assessed was significantly inhibited after in vivo administration of Cytogam. Three of five individuals experienced a decrease of 5-32% in the PRA status at 4 weeks post administration of Cytogam. Cytogam also blocked the anti-HLA antibody titres in a microlymphocytotoxicity assay, suggesting the presence of anti-idiotypic antibodies. Our study was based on a single prophylactic dose of Cytogam (50 mg/kg), however, higher dose administration could be feasible by removing more fluid at dialysis, but should be given intradialytically to avoid volume overload. Overall, our results suggest that Cytogam can modulate the in vivo and in vitro T cell responses against the alloantigens.

Adult↗
PubMed1998

Effects of an anti-IL-10 monoclonal antibody on rIFNbeta-1b-mediated immune modulation. Relevance to multiple sclerosis.

The mechanism of action of recombinant IFNbeta1b (IFNbeta-1b), as a therapy for multiple sclerosis (MS), is still unknown but may result from the enhancement of ConA-induced suppressor cell function and the inhibition of IFNgamma secretion by lymphocytes. We previously demonstrated that IFNbeta-1b stimulated modest amounts of IL-10 secretion by monocytes and IL-10 activity, as cytokine synthesis inhibitory factor, was normal in MS. To determine whether IL-10 plays a role in IFNbeta-1b modulation of immune function in MS, we studied ConA-induced suppressor cell function and IFNgamma production in presence of IFNbeta-1b and an anti-IL-10 monoclonal antibody (mAb). Anti-IL-10 mAb significantly reduced the effect of IFNbeta-1b on ConA-induced suppressor cell function and IFNgamma production in healthy subjects; MS patients showed a trend of inhibition. We hypothesized that IL-10 may play a role in mediating the effects of IFNbeta-1b on suppressor cell function and IFNgamma production but suppressor molecules other than IL-10 could be also involved.

Adult↗