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At least 1,297 records · Page 72Linked to original sources
PubMed2003

The systemic immune response is more prominent than the mucosal immune response in the pathogenesis of periodontal disease.

BACKGROUND/AIM: The diseased periodontium appears to express features of a systemic and a mucosal immune response. Our aims were to determine differences in immunoglobulin expression between gingivitis and periodontitis lesions and to ascertain whether immune and inflammatory cells were recruited into the diseased periodontium by the mucosal addressin adhesion molecule (MAdCAM-1). METHODS: In situ hybridization and immunohistochemistry were used to detect the expression of chemokines, adhesion molecules and immunoglobulins in tissue sections of gingival and granulation tissues excised from periodontitis-affected sites and of healthy tissue and gingivitis-affected tissue excised during crown-lengthening procedures. RESULTS: Greater numbers of plasma cells were observed in periodontitis gingival/granulation tissue lesions compared with gingivitis lesions. While IgA1 were predominant in all lesions, IgA2 and J-chain expressing plasma cells were present in increased proportions in gingival tissues compared with granulation tissue. Intracellular adhesion molecule-1 (ICAM-1) was higher in periodontitis than in gingivitis and interleukin-8 mRNA was higher in lesions with a pronounced neutrophil infiltrate. Vascular cell adhesion molecule-1 (VCAM-1) localized to the deep connective tissue and indicated the presence of a systemic type of immune response in this region. Periodontal tissues (n=71 biopsies) did not appear to express MAdCAM-1, in positive control sections of small intestine where it was detected. CONCLUSION: Overall, the systemic-type immune response is predominant, and although the mucosal immune response is minor and limited to the superficial tissues it may have an important role in the host defense to periodontal pathogens.

Adult↗
PubMed1989

An investigation of the general immune status and specific immune responsiveness to retinal-(S)-antigen in patients with chronic posterior uveitis.

Immunological abnormalities in endogenous posterior uveitis are widely reported but difficult to verify. We have therefore studied several immunological parameters in 14 patients with chronic posterior uveitis and compared the results with 14 healthy controls. Both the general immune status and the specific immune responsiveness to retinal S-antigen have been investigated. Results for the patient group as a whole were not significantly different from the control group. However the patients with severe eye disease (n = 4) had a reduced proliferative response to streptokinase-streptodornase antigen and two further individuals showed a general deficiency in functional cell mediated immunity. Circulating T-helper cells were marginally but not significantly reduced in patients. Responsiveness to bovine retinal S-antigen varied to a similar degree in both the patient and control groups. These findings indicate that, although severe uveitis may be associated with functional defects in cellular immunity in certain cases, in general the measurement of immune responsiveness of peripheral blood lymphocytes is unlikely to aid in the diagnosis or management of chronic posterior uveitis.

Adolescent↗
PubMed2006

SNAREing immunity: the role of SNAREs in the immune system.

The trafficking of molecules and membranes within cells is a prerequisite for all aspects of cellular immune functions, including the delivery and recycling of cell-surface proteins, secretion of immune mediators, ingestion of pathogens and activation of lymphocytes. SNARE (soluble-N-ethylmaleimide-sensitive-factor accessory-protein receptor)-family members mediate membrane fusion during all steps of trafficking, and function in almost all aspects of innate and adaptive immune responses. Here, we provide an overview of the roles of SNAREs in immune cells, offering insight into one level at which precision and tight regulation are instilled on immune responses.

Animals↗
PubMed2000

Enhancing immunity by dietary consumption of a probiotic lactic acid bacterium (Bifidobacterium lactis HN019): optimization and definition of cellular immune responses.

OBJECTIVE: To define the cellular basis for immune enhancement by a probiotic lactic acid bacteria strain (Bifidobacterium lactis HN019); and to determine whether immune enhancement can be optimized by delivery in oligosaccharide-enriched low-fat milk. DESIGN: A double-blind, three-stage before-and-after intervention trial. SETTING: Taipei Medical College Hospital, Taipei, Taiwan. SUBJECTS: Fifty healthy Taiwanese citizens (age range 41-81; median 60) randomly allocated to two groups. INTERVENTIONS: In stage 1 (run-in control stage) all subjects consumed reconstituted low-fat milk (LFM) for 3 weeks; in stage 2 (probiotic intervention) subjects consumed B. lactis in LFM (group A) or B. lactis in lactose-hydrolysed LFM (group B) for 3 weeks; in stage 3 all subjects returned to non-supplemented LFM for a further 3 weeks (washout stage). The innate immune functions of two different leucocyte types (polymorphonuclear (PMN) cells and natural killer (NK) cells) were assessed at four time points via in vitro analyses on peripheral blood samples. RESULTS: While consumption of LFM alone had no significant effect on immune responses, stage 2 results indicated significantly enhanced PMN cell phagocytosis and NK cell tumour killing activity following consumption of milk containing B. lactis. These increases levelled off following cessation of B. lactis consumption, but remained above the pre-treatment values. Increases in PMN and NK cell activity were greatest among subjects who consumed B. lactis in lactose-hydrolysed LFM. CONCLUSIONS: Dietary consumption of the probiotic bacterium B. lactis HN019 enhanced immune function of two different types of leucocytes; the degree of enhancement was increased by consuming B. lactis in an oligosaccharide-rich substrate. SPONSORSHIP: Financial support was provided by the New Zealand Dairy Board.

Adult↗
PubMed2006

The endogenous immune response modulates the course of IgA-immune complex mediated nephropathy.

In animal models of IgA nephropathy, the inevitable endogenous immune response to passively administered antigens alone or in complex with specific IgA mask the exact role each might play in pathogenesis. To delineate the role the immune response might play, we have developed a passive model with exclusive IgA-immune complex-mediated nephropathy in B-cell-deficient (BCD) mice. Glomerular IgA immune deposits were induced by administration of purified IgA antiphosphorylcholine and the specific pneumococcal C-polysaccharide (PnC) antigen daily for 2 weeks into BCD and wild-type (WT) mice. In BCD mice IgA+PnC deposits induced severe glomerular injury and renal dysfunction. In contrast, WT mice developed intense glomerular IgG and IgM and C3 co-deposits of the IgA+PnC with significantly less renal injury. Cytofluorometric analysis revealed that PnC induced in BCD, but not in WT, a rapid and dramatic increase in number of activated CD3(+)/CD69(+) T-cell population. The nuclear factor-kappa B (NF-kappaB) transcription factor was activated early and progressively increased in response to glomerular IgA+PnC deposits. These results suggest that nephritogenic IgA+PnC immune deposits induce glomerular and renal dysfunction through activation of the NF-kappaB. This inflammatory pathway is modulated by the endogenous cellular and antibody response to the antigen affecting the course of IgA nephropathy progression.

Animals↗
PubMed2006

Early-life immune challenge: defining a critical window for effects on adult responses to immune challenge.

Many aspects of mammalian physiology are functionally immature at birth and continue to develop throughout at least the first few weeks of life. Animals are therefore vulnerable during this time to environmental influences such as stress and challenges to the immune system that may permanently affect adult function. The adult immune system is uniquely sensitive to immune challenges encountered during the neonatal period, but it is unknown where the critical window for this programming lies. We subjected male Sprague-Dawley rats at postnatal day (P)7, P14, P21, and P28 to either a saline or lipopolysaccharide (LPS) injection and examined them in adulthood for differences in responses to a further LPS injection. Adult febrile and cyclooxygenase-2 responses to LPS were attenuated in rats given LPS at P14 and P21, but not in those treated at P7 or P28, while P7-LPS rats displayed lower adult body weights than those treated at other times. P28-LPS rats also tended to display enhanced anxiety in the elevated plus maze. In further experiments, we examined maternal-pup interactions, looking at the mothers' preference in two pup-retrieval tasks, and found no differences in maternal attention to LPS-treated pups. We therefore demonstrate a 'critical window' for the effects of a neonatal immune challenge on adult febrile responses to inflammation and suggest that there are other critical time points during development for the programming of adult physiology. We also show that the neonatal LPS effects on the adult immune system are not likely due to overt differences in maternal attention.

Aging↗
PubMed2004

DNA immunization encoding the secreted nonstructural protein 3 (NS3) of hepatitis C virus and enhancing the Th1 type immune response.

To induce a sustained and specific cellular immune response to hepatitis C virus (HCV), DNA immunization of mice was performed using plasmids containing the HCV nonstructural gene 3 (HCV/NS3). Plasmids were constructed such that the NS3 gene was expressed in a secreted form, a nonsecreted form or as a membrane-bound antigen. The plasmid encoding the secreted antigen induced the strongest humoral and cellular immunity and favoured the T-helper type 1 (Th1) pathway as shown by cytokine profiles and switching of antibody subclasses. Our study indicates that DNA immunization with a secreted form of HCV/NS3 is an effective means of inducing primary Th1 immune responses in the murine model.

Animals↗
PubMed1999

Humoral immune responses in periodontal disease may have mucosal and systemic immune features.

The humoral immune response, especially IgG and IgA, is considered to be protective in the pathogenesis of periodontal disease, but the precise mechanisms are still unknown. Immunoglobulins arriving at the periodontal lesion are from both systemic and local tissue sources. In order to understand better the local immunoglobulin production, we examined biopsy tissue from periodontitis lesions for the expression of IgM, IgG, IgA, IgE and in addition the IgG and IgA subclasses and J-chain by in situ hybridization. Tissues examined were superficial inflamed gingiva and the deeper granulation tissue from periodontal sites. These data confirm that IgM, and IgG and IgA subclass proteins and J-chain can be locally produced in the periodontitis tissues. IgG1 mRNA-expressing cells were predominant in the granulation tissues and in the gingiva, constituting approx. 65% of the total IgG-expressing plasma cells. There was a significantly increased proportion of IgA-expressing plasma cells in the gingiva compared with the granulation tissue (P < 0.01). Most of the IgA-expressing plasma cells were IgA1, but a greater proportion expressed IgA2 mRNA and J-chain mRNA in the gingival tissues (30.5% and 7.5%, respectively) than in the periodontal granulation tissues (19% and 0-4%, respectively). The J-chain or dimeric IgA2-expressing plasma cells were located adjacent to the epithelial cells, suggesting that this tissue demonstrates features consistent with a mucosal immune response. Furthermore, we were able to detect the secretory component in gingival and junctional epithelial cells, demonstrating that the periodontal epithelium shares features with mucosal epithelium. In contrast, deeper tissues had more plasma cells that expressed IgM, and less expressing IgA, a response which appears more akin to the systemic immune response. In conclusion, this study suggests that immune mechanisms involved in the pathogenesis of periodontitis may involve features of both the mucosal and systemic immune systems, dependent on tissue location.

Adult↗
PubMed2003

In vivo immunization following virus suppression: a novel approach for inducing immune control in chronic hepatitis B.

summary. Antiviral treatment of patients with active chronic hepatitis B may lead to significant reduction in morbidity and mortality. However, after stopping nucleoside therapy, relapse rates are high in those without acquired specific immunity. We have treated two chronic hepatitis B patients with in vivo immunization. In vivo immunization aims to optimize conditions for an effective immune response: following rapid and profound virus suppression by interferon-lamivudine combination therapy, lamivudine is withdrawn intermittently for 4 weeks during continued interferon therapy. In both patients with profound virus suppression a rapid rebound in viral replication was observed after lamivudine withdrawal; despite continued interferon. These periods of renewed viral replication were followed by rises in hepatitis activity. After re-introduction of lamivudine HBV DNA became undetectable by PCR followed by normalization of serum ALT. These observations are a stimulus to further explore the concept of in vivo immunization as a novel therapeutic approach for chronic hepatitis B.

Adult↗
PubMed1997

Immunization with alum-collagen II complex suppresses the development of collagen-induced arthritis in rats by deviating the immune response.

Collagen-induced arthritis (CIA) is an experimental rat model sharing a number of features with human rheumatoid arthritis (RA). The model is associated with a proinflammatory (TH1) type of immune response and treatments with cytokines associated with TH2 immune responses are beneficial. Since agents with TH1-inducing properties, such as Freund's incomplete adjuvant (FIA), are necessary for disease induction, it is of interest to investigate whether an adjuvant with TH2-inducing properties affects CIA in a different way than does FIA. The authors studied arthritis development in DA rats after immunization with the TH2 stimulatory adjuvant alum adsorbed to rat collagen type II (CII) or collagen II fragments. Such treatments suppressed disease development both prophylactically and therapeutically. This beneficial effect of alum-CII immunization was associated with an increase in the IgG1 anti-CII antibody response as compared to untreated rats or rats pretreated with alum alone. Treatment with alum without the addition of collagen did not have any clinical effect. In addition, alum-CII treated rats had a significantly higher expression of IL-4 mRNA than untreated rats in the lymph nodes, 7 days after CIA induction. The authors suggest that alum-CII induces a TH2 immune response against rat CII which counteracts the development of CIA.

Alum Compounds↗
PubMed2000

Interleukin-10 produced by the innate immune system masks in vitro evidence of acquired T-cell immunity to E. coli.

Bacteria trigger stimulation of antigen-specific, as well as innate, immune responses. Cytokines and other products of cells belonging to the innate immune system may interfere with the detection of acquired immunity to whole bacteria in vitro. Proliferation and cytokine production by human blood mononuclear cells in response to a whole UV-killed Escherichia coli was compared with the response to commonly used antigen preparations: purified protein derivative (PPD), Candida albicans and influenza proteins. E. coli induced a weaker proliferative response with later onset than did the other antigens, and production of interferon (IFN)-gamma comparable with that in response to C. albicans and influenza vaccine, but lower than that induced by PPD. Both proliferation and IFN-gamma production were abolished by removal of CD4 cells or blocking of HLA-D, but not CD1 antigen-presenting molecules. Purified lipopolysaccharide (LPS) induced neither proliferation nor IFN-gamma production. None of the antigen preparations stimulated interleukin (IL)-4 production but, in contrast to the other antigens, whole E. coli, as well as purified O6 LPS, induced large quantities of IL-10. IL-10 production was independent of CD4 cells or HLA-D molecules. Blocking of IL-10 by neutralizing antibodies increased both E. coli-induced proliferation and IFN-gamma production markedly. Conversely, the addition of whole E. coli or LPS to cultures stimulated with other antigens (C. albicans or Staphylococcus aureus) down-regulated proliferative and IFN-gamma responses, an effect which was at least partly IL-10 dependent. The results indicate a substantial T-cell memory to commensal E. coli, but suggest that the evidence of such memory, e.g. proliferation and IFN-gamma production, is effectively prevented by IL-10 and perhaps other factors produced by monocytes in response to bacteria. Thus, the innate immune responses must be taken into account when acquired immune responses to microbes are measured.

Antigens, CD1↗
PubMedDate not supplied

Effect of copper on growth and serum constituents of immunized and non-immunized rabbits infected with Trypanosoma brucei.

Seventy-two five-week-old New Zealand White rabbits were divided into three groups and fed a basal diet containing 0, 125 or 250 ppm supplemental Cu for 4 weeks before each Cu-group was further subdivided into three lots of 8 rabbits each. One subgroup was immunized with Trypanosoma brucei before being infected with the same parasite, another subgroup was infected without immunization while the third subgroup was neither immunized nor infected. Parasitemia slightly depressed growth and efficiency of feed utilization while supplemental Cu at 125 and 250 ppm improved both parameters in rabbits. Immunization conferred slight protection on body weight losses by the infected rabbits while supplemental Cu at 250 ppm alone or in combination with immunization completely obliterated the effects of infection on growth performance. Infection depressed haematocrit, haemoglobin, and serum glucose, while the alkaline phosphatase activity was increased. Supplemental Cu significantly increased both haemoglobin and serum glucose levels. Supplemental Cu reversed the effects of parasite infection on blood constituents. The study indicates that Cu may not only promote growth but will also suppress the effects of parasitemia on performance and serum profile of rabbits infected with trypanosomes.

Alkaline Phosphatase↗
PubMed2000

DNA-Based immunization produces Th1 immune responses to hepatitis delta virus in a mouse model.

Hepatitis delta virus (HDV) superinfection is one of the major causes of fulminant hepatitis in endemic areas of hepatitis B virus (HBV) infection. Currently, there is no effective treatment or vaccine against HDV superinfection. DNA-based immunization is a promising antiviral strategy to prevent or treat persistent viral infections. In this study, we investigated the immunological effects of DNA vaccines against HDV in BALB/c mice. Plasmid (pD) encoding large hepatitis D antigen (L-HDAg), or plasmid (pS/pD) coexpressing hepatitis B surface antigen (HBsAg) and L-HDAg, were injected into mice intramuscularly. The seroconversion rate, anti-HBs levels, anti-HDV titers, T-cell proliferation responses, and T-helper (Th)-release cytokine profiles were analyzed. Mice immunized with plasmids, pS/pD or pD, produced low, but significant, titers of anti-HDV antibodies. In contrast, pS/pD induced much stronger anti-HBs titers in the immunized animals. Interestingly, splenic lymphocytes derived from pS/pD-inoculated mice demonstrated significant proliferation responses to recombinant HBsAg and HDAg, and resulted in a Th1-like immune response as suggested by the production of interferon gamma (INF-gamma) and interleukin-2 (IL-2), but not IL-4. The splenic lymphocyte derived from the pD-inoculated mice showed a similar Th1 response to the stimulation of HDAg, but not to HBsAg. In conclusion, our results suggest that DNA vaccines against HDV can induce significant cellular immune responses with a Th1 preference. HBV and HDV coimmunization can be performed by DNA vaccines. These results are promising for the future development of prophylactic and therapeutic HDV vaccines.

Animals↗
PubMed2001

Immediate and longterm effects of immune stimulation: hypothesis linking the immune response to subsequent physical and psychological wellbeing.

We hypothesize that antigenic stimuli in susceptible persons during key developmental life stages alters neuroendocrine-immune organization and leads to the development of aberrant immune and neuroendocrine responses to subsequent environmental stressors, with longterm physical and psychological consequences. The release of interleukin-1beta (IL-1beta) and other proinflammatory cytokines associated with the immune response during times when individuals are most vulnerable to the effects of environmental influences activates the hypothalamic-pituitary-adrenal (HPA) axis and leads to maladaptive responses to subsequent stressors. The primed HPA axis is reactivated by proinflammatory cytokines, resulting in the secretion of corticotropin-releasing hormone (CRH) and cortisol, followed by physical and psychological effects that feedback on the HPA axis to produce an array of outcomes affecting general wellbeing. Through the release of histamine and other mediators and their effects on the mast cell-leukocyte cytokine cascade, immune stimuli in susceptible persons increase allergic inflammation and magnify stressors' effects through the release of HPA-axis-activating cytokines, such as IL-1beta, that drive the axis and reinforce the physiological and behavioral effects. Thus, specific proinflammatory cytokines and allergic reactions initiate, promote, and maintain immune-stimulus-associated HPA axis activity, and with CRH and cortisol, participate in a positive feedback loop, resulting in aberrant, maladaptive responses to physical or psychological stressors, with outcomes such as depression, hyperalgesia, and pain-related behavior.

Adrenal Glands↗
PubMed1997

Immune aspects of endometriosis: relevance of the uterine mucosal immune system.

Endometriosis is classically defined as the growth of endometrial cells at sites outside the uterus. It is a common disease characterized by infertility, chronic pain and adhesion formation. Immune dysregulation, evidenced by decreased clearance of endometrial cells and aberrant production of cytokines by peritoneal fluid leukocytes, has been proposed as a mechanism which allows implantation and growth of ectopic endometrium. Cytokines are primary components of intercellular signaling between uterine epithelial and stromal cells, leukocytes, and the developing conceptus. Because their production is regulated by sex hormones, cytokines are well-placed to play a key role in the extensive tissue remodeling required to accommodate menstruation, implantation and pregnancy. Understanding this specialized hormonally-responsive mucosal immune system within the uterus will be critical to understanding the potential importance of the immune system in the pathogenesis of endometriosis. In this review, highlights of studies describing leukocyte populations, cytokines and cytokine receptors in uterine and ectopic endometrium and their proposed role in the regulation of immune processes and endometrial growth are presented, followed by a review of current data on immune aspects of endometriosis. Studies directed at investigating the hormonal regulation of cytokine secretion by uterine and peritoneal cell populations, and the effect of cytokines on endometrial proliferation, should provide a more complete understanding of their potential role in normal uterine growth and in the pathogenesis of endometriosis.

Ascitic Fluid↗
PubMed1993

Prophylactic administration of respiratory syncytial virus immune globulin to high-risk infants and young children. The Respiratory Syncytial Virus Immune Globulin Study Group.

BACKGROUND: Infants with cardiac disease or prematurity are at risk for severe illness caused by respiratory syncytial virus. Immune globulin with a high titer of antibodies against respiratory syncytial virus may offer infants and young children at risk protection from this serious, common respiratory illness. METHODS: We studied 249 infants and young children (mean age, eight months) who had bronchopulmonary dysplasia due to prematurity (n = 102), congenital heart disease (n = 87), or prematurity alone (n = 60). Respiratory syncytial virus immune globulin was given monthly to some of these children in either a high dose (750 mg per kilogram of body weight; n = 81) or low dose (150 mg per kilogram; n = 79); 89 controls received no immune globulin. Group assignments were random. Assessments of respiratory illness and management were conducted without knowledge of the children's group assignments. RESULTS: There were 64 episodes of respiratory syncytial virus infection: 19 in the high-dose group, 16 in the low-dose group, and 29 in the control group. In the high-dose group there were fewer lower respiratory tract infections (7, vs. 20 in the control group; P = 0.01), fewer hospitalizations (6, vs. 18 in the control group; P = 0.02), fewer hospital days (43, vs. 128 in the control group; P = 0.02), fewer days in the intensive care unit (P = 0.05), and less use of ribavirin (P = 0.05). In the low-dose group there was a significant reduction only in the number of days in the intensive care unit (P = 0.03). Adverse events during the 580 infusions were generally mild and included fluid overload (in five children), oxygen desaturation (eight), and fever (six). Six children died: three in the high-dose group, three in the low-dose group, and none in the control group (P = 0.15), but no death was attributed to the use of immune globulin or to illness caused by respiratory syncytial virus. CONCLUSIONS: Administration of high doses of respiratory syncytial virus immune globulin is a safe and effective means of preventing lower respiratory tract infection in infants and young children at high risk for this disease.

Antibodies, Viral↗
PubMed1987

Theoretical implications of cellular immune reactions against helper lymphocytes infected by an immune system retrovirus.

The breakdown of the immune system induced by the human immunodeficiency virus might be due to the active immune destruction of human immunodeficiency virus-infected helper T lymphocytes expressing viral antigens. By numerical simulation, we have studied possible consequences that a hypothetical immunodeficiency virus (IDV) may have on the cellular immune response by using a mathematical model. In this model, IDV infects CD4+ (helper) T cells and is actively synthesized by the immunologically activated helper T cells. Infected helper T cells synthesizing IDV express antigenic determinants specific for IDV and trigger a cellular immune response against themselves that is mediated by cytotoxic T cells and cytotoxic macrophages. The dynamic evolution of the model in the case of mixed-type infections with IDV and with another pathogen that evokes a cell-mediated immune response shows strong interactions between both simultaneous infections. The model might be of value to elucidate the dynamics leading to opportunistic infections. Furthermore, a pivotal role for immunological stimulation in the progressive exacerbation of the disease can be demonstrated.

Antigens, Viral↗
PubMed2001

The mucosal immune system: from specialized immune defense to inflammation and allergy.

The mucosal immune system is a first line of defense against foreign antigens, including microbial and dietary antigens. Under normal circumstances, the mucosal immune system employs tightly regulated dynamic mucosal intra- and internets consisting of inductive and effector sites for the induction of an appropriate immunological homeostasis between the host and mucosal environments. The common mucosal immune system (CMIS), which interconnects between inductive (e.g. Peyer patch) and effector (e.g. intestinal lamina propria) tissues for the induction of the IgA response, is well characterized. Recent results provide strong evidence for the presence of a CMIS-independent IgA induction pathway. Two distinct subsets of mucosal IgA-committed B cells termed B-1 and B-2, are associated with CMIS-independence and CMIS-dependent cascades respectively. In some cases, the breakdown of this tightly regulated mucosal immune system leads to pathological responses to different gut environmental antigens. As a result, disorders such as inflammatory bowel disease (e.g. IBD) and allergic gastroenteropathy can be evoked in the gastrointestinal tissues. Recently, many studies have described possible molecular and cellular mechanisms for this dysfunction in the gastrointestinal tissues by using murine models with specific gene manipulation. In this review we summarize recent findings from our group concerning the CMIS-dependent and CMIS-independent IgA induction pathways and gastrointestinal diseases (IBD and intestinal allergic diseases). These observations may provide useful information for the development of new mucosal immune therapy.

Animals↗