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PubMed1998

Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations.

Dental amalgam restorations are a significant source of mercury exposure in the human population, but their potential to cause systemic health effects is highly disputed. We examined effects on the immune system by giving genetically mercury-susceptible Brown Norway (BN) rats and mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars of the upper jaw, causing a body burden similar to that described in human amalgam-bearers (from 250 to 375 mg amalgam/kg body weight). BN rats with amalgam restorations, compared with control rats given composite resinous restorations, developed a rapid activation of the immune system, with a maximum 12-fold increase of the plasma IgE concentration after 3 wks (p < 0.001; Mann-Whitney's test). LE rats receiving amalgam restorations showed no significant increase of plasma IgE (p > 0.05). After 12 wks, BN rats with amalgam restorations showed significantly increased (p < 0.05) titers of immune-complex (IC) deposits in the renal glomeruli and in the vessel walls of internal organs. These rats also showed a significant (p < 0.05), from six- to 130-fold, increase in tissue mercury concentration in the concentration order kidney > spleen > cerebrum occipital lobe > cerebellum > liver > thymus, and the tissue silver concentration was significantly (p < 0.05) increased from three- to 11-fold. Amalgam-implanted BN rats showed a significant (p < 0.05) increase in copper concentration in the kidney and spleen, and in kidney selenium concentration. We conclude that dental amalgam restorations release substantial amounts of their elements, which accumulate in the organs and which, in genetically susceptible rats, give rise to activation of the immune system and systemic IC deposits.

Analysis of Variance↗
PubMed2006

Protective and destructive immunity in the periodontium: Part 2--T-cell-mediated immunity in the periodontium.

Based on the results of recent research in the field and Part 1 of this article (in this issue), the present paper will discuss the protective and destructive aspects of the T-cell-mediated adaptive immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) osteoimmunology and periodontal disease; (ii) some molecular techniques developed and applied to identify critical microbial virulence factors or antigens associated with host immunity (with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species); and (iii) summarizing the identified virulence factors/antigens associated with periodontal immunity. Thus, further understanding of the molecular mechanisms of the host's T-cell-mediated immune responses and the critical microbial antigens related to disease pathogenesis will facilitate the development of novel therapeutics or protocols for future periodontal treatments.

Aggregatibacter actinomycetemcomitans↗
PubMed1990

Experimental model of immune-mediated hearing loss using cross-species immunization.

The presence of immune-mediated hearing loss was investigated in an animal model. Eight guinea pigs and four mice underwent immunizations with a preparation of chick or guinea pig cochlear tissue and Freund's adjuvant. Hearing thresholds were monitored by auditory brainstem response (ABR) testing over a 5-week period after immunization. The serum and temporal bones of test and control animals were then examined using an enzyme-linked immunosorbent assay (ELISA), immunocytochemical, and histological techniques. Hearing loss of 20 dB or greater occurred in eight animals. ELISA demonstrated antibodies to cochlear antigens in the sera of all test animals. Immunocytochemistry revealed immunostaining of hair cell stereocilia in the organ of Corti and saccule. Endolymphatic hydrops, and organ of Corti degeneration was observed in the temporal bones of three animals. This study provides evidence to suggest that cross-species immunization with cochlear antigens might produce a humoral response that can be associated with inner ear pathologic change and sensorineural hearing loss.

Animals↗
PubMed2006

Innate immune defenses in HIV-1 infection: prospects for a novel immune therapy.

HIV-1 infection leads to a severe decrease of CD4(+) T lymphocytes, dysregulation of several leukocyte subpopulations and generalized immune activation, with the subsequent development of opportunistic infections and malignancies. Administration of highly active antiretroviral therapy (HAART) has been successful in reducing HIV-1 plasma viremia; however, the ability of HAART to restore immunocompetence appears incomplete, particularly in patients with chronic and advanced disease. Several components of the innate immune system have direct anti-HIV-1 effects, and studies to analyze the benefits of enhancing the function of the innate response during HIV-1 infection are increasing. Development of any complementary therapeutic approaches to HIV-1 infection, particularly those able to compensate for the limitations of HAART, and enhance the anti-HIV-1 innate immune activity would be of interest. The stimulation of innate immune responses using Toll-like receptor agonists, such as monophosphoryl lipid A and oligodeoxynucleotides with CpG motifs, are currently being investigated and their benefit in HIV-1-infected patients are under evaluation.

Anti-HIV Agents↗
PubMed2003

Effect of passive immunity on the development of a protective immune response against bovine viral diarrhea virus in calves.

OBJECTIVE: To determine whether passively acquired antibodies prevent development of a protective immune response to live virus in calves. ANIMALS: 18 calves. PROCEDURES: Calves were caught immediately after birth and tested free of bovine viral diarrhea virus (BVDV) and serum antibodies against BVDV. Within 48 hours, 12 calves were fed colostrum that contained antibodies against BVDV and 6 calves received BVDV antibody free milk replacer. Three milk replacer fed and 6 colostrum fed calves were exposed to virulent BVDV2-1373 at 2 to 5 weeks of life when passively acquired serum antibody titers were high. After serum antibody titers against BVDV had decayed to undetectable concentrations (at 7 to 9 months of age), the 3 remaining milk replacer fed calves, 6 colostrum fed calves previously exposed to BVDV2-1373, and 6 colostrum fed calves that had not been exposed to the virus were inoculated with BVDV2-1373. RESULTS: Passively acquired antibodies prevented clinical disease in inoculated colostrum fed calves at 2 to 5 weeks of life. Serum antibody titers did not increase in these calves following virus inoculation, and serum antibody titers decayed at the same rate as in noninoculated colostrum fed calves. Inoculated colostrum fed calves were still protected from clinical disease after serum antibody titers had decayed to nondetectable concentrations. Same age colostrum fed calves that had not been previously exposed to the virus were not protected. CONCLUSIONS AND CLINICAL RELEVANCE: A protective immune response was mounted in calves with passive immunity, but was not reflected by serum antibodies titers. This finding has implications for evaluating vaccine efficacy and immune status.

Animals↗
PubMed1983

Pulmonary immune effector cells in guinea pigs with immune complex disease. I. Changes in T- and B-lymphocyte populations after exposure to antigen.

Changes in immunologic effector cell populations in lung tissue, bronchoalveolar spaces, tracheobronchial lymph nodes, spleen, and peripheral blood were evaluated during the course of a pulmonary immune complex disease in guinea pigs. The number of macrophages, lymphocytes, and neutrophils present in each cell population were determined. T and B lymphocytes were identified by E and EAC rosette formation, respectively. An increase in the total number of lymphocytes in tracheobronchial lymph nodes and a greater proportion of B cells in these lymphocyte populations were observed at 12 and 24 hr postchallenge. The total number of macrophages, lymphocytes, and neutrophils recovered from the bronchoalveolar spaces also increased, as did the proportion of lymphocytes and neutrophils. A similar proportional increase of lymphocytes obtained from lung tissue also occurred. The proportion of B cells in the lymphocyte populations of the bronchoalveolar spaces and lung tissue increased to a maximum at 24-48 hr postchallenge. Cell populations from peripheral blood or spleen remained stable, by all parameters examined, during the disease process. Thus, there appears to be a localization of the immune inflammatory response in the lungs during the course of this pulmonary immune complex disease. In addition, this study provides evidence that immune effector cells obtained by bronchial lavage accurately reflect the cellular changes associated with the acute inflammatory response in lung tissue and pulmonary lymph nodes.

Animals↗
PubMed1993

The endocrine function of the immune cells in the initiation of humoral immunity.

The endocrine functions of different hormones are well documented. Recently, however, evidence of the immune function of several hormones has been accumulated. These findings raised the possibility that immune cells might secrete hormones and in turn self-regulate different immune functions. Indeed, immune cells have been found to secrete different peptide and protein hormones. Adrenocorticotropin hormone (ACTH) is the most studied and was found to be secreted by lymphocytes. In the present authors' laboratory, it was found that not only do lymphocytes secrete ACTH but also that circulating concentrations of corticosterone increased following antigen challenge. It was also observed that at the time of the increased corticosterone, there was a redistribution of different lymphocyte subpopulations from the blood to spleen, the site of antigen presentation and antibody production. It was concluded that the endocrine function of lymphocytes might be important in the initiation of antibody production in chickens.

Adrenocorticotropic Hormone↗
PubMed2001

Mediators of innate immunity that target immature, but not mature, dendritic cells induce antitumor immunity when genetically fused with nonimmunogenic tumor antigens.

Chemokine receptors are differentially expressed on immature and mature dendritic cells (DC). Herein, we demonstrate for the first time that murine antimicrobial peptides beta-defensins 2 and 3 bind murine CCR6, similarly to inflammatory chemokine macrophage-inflammatory protein 3alpha, and they chemoattract bone marrow-derived immature, but not mature DC. Using various chemokines or defensins fused with nonimmunogenic tumor Ags, we studied their capacity to delivery Ags to subsets of immune cells to elicit antitumor immunity. We demonstrate that DNA immunizations with fusion constructs with beta-defensin 2 or inflammatory chemokines that target immature DC, but not homeostatic chemokines secondary lymphoid tissue chemokine, CCL21, or stromal cell-derived factor 1, CXCL12, which chemoattract mature DC, elicit humoral, protective, and therapeutic immunity against two different syngeneic lymphomas.

Animals↗
PubMed2005

Immunization with lentiviral vector-transduced dendritic cells induces strong and long-lasting T cell responses and therapeutic immunity.

Dendritic cell (DC) therapies are currently being evaluated for the treatment of cancer. The majority of ongoing clinical trials use DCs loaded with defined antigenic peptides or proteins, or tumor-derived products, such as lysates or apoptotic cells, as sources of Ag. Although several theoretical considerations suggest that DCs expressing transgenic protein Ags may be more effective immunogens than protein-loaded cells, methods for efficiently transfecting DCs are only now being developed. In this study we directly compare the immunogenicity of peptide/protein-pulsed DCs with lentiviral vector-transduced DCs, and their comparative efficacy in tumor immunotherapy. Maturing, bone marrow-derived DCs can be efficiently transduced with lentiviral vectors, and transduction does not affect DC maturation, plasticity, or Ag presentation function. Transduced DCs efficiently process and present both MHC class I- and II-restricted epitopes from the expressed transgenic Ag OVA. Compared with peptide- or protein-pulsed DCs, lentiviral vector-transduced DCs elicit stronger and longer-lasting T cell responses in vivo, as measured by both in vivo killing assays and intracellular production of IFN-gamma by Ag-specific T cells. In the B16-OVA tumor therapy model, the growth of established tumors was significantly inhibited by a single immunization using lentiviral vector-transduced DCs, resulting in significantly longer survival of immunized animals. These results suggest that compared with Ag-pulsed DCs, vaccination with lentiviral vector-transduced DCs may achieve more potent antitumor immunity. These data support the further development of lentiviral vectors to transduce DCs with genes encoding Ags or immunomodulatory adjuvants to generate and control systemic immune responses.

Animals↗
PubMed2006

Humoral immune response to flagellin requires T cells and activation of innate immunity.

Bacterial flagellin, the primary structural component of flagella, is a dominant target of humoral immunity upon infection by enteric pathogens and in Crohn's disease. To better understand how such responses may be regulated, we sought to define, in mice, basic mechanisms that regulate generation of flagellin-specific Igs. We observed that, in response to i.p. injection with flagellin, generation of flagellin-specific Ig required activation of innate immunity in that these responses were ablated in MyD88-deficient mice and that flagellin from Helicobacter pylori, which is known not to activate TLR5, also did not elicit Abs. Mice lacking alphabeta T cells (TCRbeta(null)) were completely deficient in their ability to make flagellin Abs in various contexts indicating that, in contrast to common belief, generation of flagellin-specific Ig is absolutely T cell dependent. In contrast to Ab responses to whole flagella (H serotyping), responses to flagellin monomers displayed only moderate serospecificity. Whereas neither oral nor rectal administration of flagellin elicited a strong serum Ab response, induction of colitis with dextran sodium sulfate resulted in a MyD88-dependent serum Ab response to endogenous flagellin, suggesting that, in an inflammatory milieu, TLR signaling promotes acquisition of Abs to intestinal flagellin. Thus, acquisition of a humoral immune response to flagellin requires activation of innate immunity, is T cell dependent, and can originate from flagellin in the intestinal tract in inflammatory conditions in the intestine.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Prevention of hepatitis A through active or passive immunization: Recommendations of the Advisory Committee on Immunization Practices (ACIP).

Routine vaccination of children is the most effective way to reduce hepatitis A incidence nationwide over time. Since licensure of hepatitis A vaccine in 1995, this strategy has been implemented incrementally, starting with the recommendation of the Advisory Committee on Immunization Practices (ACIP) in 1996 to vaccinate children living in communities with the highest rates of infection and disease. These updated recommendations represent the next phase of this hepatitis A immunization strategy. Vaccination of children living in states and communities with consistently elevated rates of hepatitis A will provide protection from disease and is expected to reduce the overall incidence of hepatitis A. This report updates the ACIP's 1996 recommendations on the prevention of hepatitis A through immunization (MMWR 1996;45:[No. RR-151) and includes a) new data about the epidemiology of hepatitis A; b) recent findings about the effectiveness of community-based hepatitis A vaccination programs; and c) recommendations for the routine vaccination of children in states, counties, and communities with rates that are twice the 1987-1997 national average or greater (i.e., > or = 20 cases per 100,000 population) and consideration of routine vaccination of children in states, counties, and communities with rates exceeding the 1987-1997 national average (i.e., > or = 10 but <20 cases per 100,000 population). Unchanged in this report are previous recommendations regarding the vaccination of persons in groups at increased risk for hepatitis A or its adverse consequences and recommendations regarding the use of immune globulin for protection against hepatitis A.

Adult↗
PubMed2000

Leptin and the immune system: how nutritional status influences the immune response.

Several observations suggest the presence of an interaction between immune and the endocrine systems. Leptin is an adipocyte-derived hormone, that belongs structurally to the long-chain helical cytokine family such as interleukin-2 (IL-2), interleukin-12 (IL-12), growth hormone (GH), and signals by a class I cytokine receptor (Ob-R). This cytokine represents an important link between fat mass on the one side and the regulation of energy balance and reproductive function on the other. Indeed, obese leptin-deficient ob/ob mice display low body temperature, hyperphagia, infertility and evidence of immune defects with lymphoid organ atrophy, mainly affecting thymic size and cellularity. Acute starvation, associated with decreased leptin levels, causes thymic atrophy and reduces the delayed type hypersensitivity (DTH) reaction to antigens in normal mice, resembling that observed in ob/ob mice. Leptin replacement reverses the immunosuppressive effects of acute starvation in mice. Leptin differentially affects the in vitro proliferation and cytokine production by naive and memory T cells, increasing IL-2 secretion and proliferation of naive T cells, while inducing IFN-g production in memory T cells with little effect on their proliferation. Presence of leptin seems to be necessary for the induction and maintenance of the pro-inflammatory Th1 immune response. These findings support the hypothesis that leptin plays a key role in linking nutritional state to the T cell function. According to this view, leptin might represent an important target for immune intervention in a variety of pathophysiological conditions.

Animals↗
PubMed1999

[Physiology and physiopathology of the immune system: initiation and termination of immune responses].

The immune system is regulated in a complex fashion that allows flexibility in the response to pathogens and enables close control at multiple points, to prevent an undesired response. Indeed, for effective action, it is not only essential that the immune system possesses good effectors, but that the performance of the effectors be properly monitored back to avoid autoimmune reactions or excessive inflammatory response that might imperil the fitness of the organism. Herein, we show the importance of the dendritic cell population in the initiation of an effective immune response and we describe an experimental approach to optimize the dendritic cell-based immunotherapy in cancer murine models. We also characterize a T cell activation-limiting mechanism that is likely to play a physiological role in the down-regulation of the immune responses.

Animals↗
PubMed1998

[Persistence of HB vaccine immune protection and response to hepatitis B booster immunization].

OBJECTIVE: To determine the persistence of immune protection of China-made, plasma-derived HBV vaccine in infants and the time table of booster immunization. METHODS: Serological effect of 7-year follow-up study and antibody response of an experimental study on booster were detected using radioimmunoassay. RESULTS: The protective anti-HBs positive rates of 1,018 children, who were vaccinated according to the regimen of three doses of 10 micrograms HBV vaccine, declined from 75.0% during the first two years to 48.2% at 7 years after the first dosages, however, the positive rates for HBsAg and anti-HBc always fluctuated at low frequency. 144 children aged 6 or 7 years old, who received the HBV vaccine in their infancy and were negative for both HBsAg and anti-HBc before booster, were selected from 1,018 children of the follow-up study and boosted with 1 microgram (intradermally) or 2 micrograms (hypodemically) HBV vaccine. Their anti-HBs GMT and anti-HBs positive rate were 190.6 mIU/ml and 89.6% at one month after booster, significantly higher than 14.7 mIU/ml and 54.9% before booster (P < 0.01), and declined back to 25.3 mIU/ml and 75.5% at 12th month; among 65 children with the anti-HBs negative before booster, 40 of them had the level of anti-HBs > or = 100 mIU/ml one month after booster, suggesting the retention of immunological memory in most of them. CONCLUSIONS: No need for revaccination against hepatitis B at 7th year after the initial immunization due to better persistence of immune protection of the vaccine.

Child↗
PubMed2002

Immune restoration disease in HIV patients: aberrant immune responses after antiretroviral therapy.

Suppression of HIV replication by antiretroviral therapy has various effects on the immune system of HIV-infected patients. Whereas protective pathogen-specific immune responses are restored in some patients, others have persistent immunodeficiency or produce immunopathological responses against opportunistic pathogens that cause immune restoration disease (IRD). Significant morbidity and even mortality may result from IRDs associated with infections by mycobacteria, herpesviruses, hepatitis viruses or the JC virus. Preliminary evidence from our studies suggests that immune responses in patients with IRD may be dysregulated and affected by immunogenetic factors. Thus, herpesvirus IRDs were associated with increased plasma levels of bioavailable interleukin-6 and soluble CD30, while mycobacterial and herpesvirus IRDs were associated with a major histocompatibility complex gene haplotype and/or alleles of particular cytokine genes. A greater understanding of pathogenic mechanisms and the immunogenetics of IRDs may lead to improved preventive and management strategies.

AIDS-Related Opportunistic Infections↗
PubMed2000

[The protective immunity in mice immunized with FhGST or AsGST against Schistosoma japonicum cercariae].

OBJECTIVE: To study the protective immunity against Schistosoma japonicum (Sj) cercariae challenge in mice immunized with FhGST or AsGST. METHODS: There groups of Kunming mice were immunized three times with rSjGST, FhGST and AsGST, respectively. Then 30 cercariae of Schistosoma japonicum were given per mouse by abdominal skin inoculation. Six weeks later, all mice were killed to collect adult worms, liver, spleen and large intestine for worm count and egg count. RESULTS: The worm burden was reduced by 27.8%-36.4% in the three immune groups compared with the two control groups (P < 0.05). rSj26GST, FhGST and AsGST significantly decreased the number of eggs deposited in the tissues. CONCLUSION: FhGST and AsGST could induce protection against S. japonicum cercariae infection.

Animals↗
PubMed2003

Primary immune deficiencies unravel the molecular basis of immune response.

Primary immune deficiencies (PID) represent inborn errors of immunity. Over the years, detailed analysis of the clinical and laboratory features associated with these unique and rare disorders have shed light on the complex array of signals and processes that govern development and activation of the immune system. While the first examples of PID pertained to severe defects in lymphoid development, more recently a variety of gene defects have been identified in humans that do not compromize the ability to generate lymphocytes, but rather result in profound immune dysregulation. In many cases, identification of the molecular and cellular bases of PID has preceeded development of animal models by gene targeting. Finally, since the very first cases reported in humans, PID have also represented a unique tool to investigate the efficacy of novel therapeutic approaches (from molecular therapy to hematopoietic stem cell transplantation to somatic cells gene therapy), that have been applied or may apply to a variety of more common human diseases.

Cytokines↗
PubMedDate not supplied

Prolactin triggers pro-inflammatory immune responses in peripheral immune cells.

The peptide hormone prolactin (PRL) is produced by specialized cells in the anterior pituitary gland and in a number of sites outside the pituitary. Its biological actions consist of various roles in reproduction, lactation, and of a number of homeostatic biological activities that also include immune functions. Elevated serum PRL concentrations often correlate with abnormalities in immune responses. To determine the influence of PRL on human immune cells, human whole blood cultures were stimulated with lipopolysaccharide (LPS), supplemented with various concentrations of human recombinant PRL. We found that PRL, at concentrations achievable during pregnancy, anesthesia and medication, significantly amplified interleukin (IL)-12 and tumor necrosis factor-alpha (TNF-alpha) synthesis in LPS-stimulated cultures, in a dose-dependent manner. Conversely, synthesis of the anti-inflammatory cytokine IL-10 only increased significantly at very high concentrations of supplemented PRL. PRL alone was not able to induce any measurable secretion of TNF-alpha, IL-10, or IL-12 in non-stimulated, whole blood cultures. However, we demonstrated that PRL, by itself or in combination with LPS, causes an increase in the binding activity of the transcription factors nuclear factor-kappaB (NFkappaB) and interferon regulatory factor-1 (IRF-1), which are known to promote TNF-alpha and IL-12 secretion. These data suggest that PRL promotes pro-inflammatory immune responses via NFkappaB and IRF-1, which may affect pathophysiological processes in physiological hyperprolactinemic states.

Blood Cells↗