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[Effect of progressive muscle relaxation using biofeedback on perceived stress, stress response, immune response and climacteric symptoms of middle-aged women].

PURPOSE: This study was aimed to evaluate the effect of progressive muscle relaxation training using biofeedback on perceived stress, stress response, immune response and climacteric symptoms. METHOD: This was a crossover, pre-post test design. The study subjects are 36 middle-aged women who were selected at 2 public health centers. The independent variable was Biofeedback training for 4 weeks, twice a week and home training for 4 weeks. Dependent variables were perceived stress, stress response, immune response, and climacteric symptoms measured with Hildtch's scale (1996). RESULT: Progressive muscle relaxation training using biofeedback was not effective in reducing perceived stress, but it was shown to be effective in reducing physiological stress responses such as pulse rate and EMG. Though blood pressure and skin conductance were repeatedly down, and skin temperature slowly increased, there were no statistically significant differences. Progressive muscle relaxation training using biofeedback was not effective in reducing serum cortisol, enhancing immune responses, or decreasing climacteric symptoms. CONCLUSION: The findings point to a pressing need for further, well-controlled and designed research with consideration in selection of subjects and instruments, frequency of measurements, the sampling method, and intervention modalities.

Adult↗

Genetic and phenotypic correlations between feather pecking behavior, stress response, immune response, and egg quality traits in laying hens.

The objective of the current study was to estimate genetic and phenotypic correlations among feather pecking (FP) behavior and stress response, immune response, and egg quality parameters. These traits have been measured in an F2 cross, coming from a cross between a high and a low FP line of laying hens. Heritabilities (h2) of stress response (32 wk), primary immune response to keyhole limpet hemocyanin (KLH) (36 wk) and Mycobacterium butyricum (39 wk), and egg quality parameters (35, 44, and 50 wk of age) were calculated. The h2 was 0.05 +/- 0.05 (SE) for stress response, 0.15 +/- 0.07 for antibody response to KLH, and 0.08 +/- 0.06 for antibody response to M. butyricum. The h2 for egg quality traits were in the range of 0.12 to 0.30. Significant phenotypic correlations were found between gentle FP in adult hens and stress response, egg weight at 44 and 50 wk, and egg deformation at 50 wk. Significant additive genetic correlations were found between severe FP in adult hens and antibody response to KLH (0.79 +/- 0.35), and between ground pecking in adult hens and egg deformation at 50 wk (0.63 +/- 0.26), and between ground pecking and eggshell strength at 35, 44, and 50 wk of age (-0.86 +/- 0.29, -0.81 +/- 0.20, -0.76 +/- 0.24, respectively).

Aging↗

Cell participation in immune response by immune ribonucleic acid. I. The role of T lymphocytes in immune response by immune RNA against T-dependent antigens.

T- and B-cell participation in the immune response induced by immune ribonucleic acid (iRNA) preparations against T-dependent antigens was studied using athymic nude, neonatally thymectomized (NT) and cyclophosphamide-treated (CY) mice. The iRNA(T + B) preparations were made from the spleen of BALB/c mice immunized with these antigens. Injection of the iRNA into nude or NT mice caused an increase in the number of specific rosette-forming cells (RFC) and of memory cells capable of responding to secondary stimulus with a small dose of the corresponding antigen. Injection with T-dependent antigens or with iRNA(T + B) did not cause any immune response in CY mice, suggesting depletion of the B-cell function. The iRNA(T) and iRNA(B) were prepared, respectively, from the thymuses of BALB/c mice and from the spleens of nude mice which had been immunized with T-dependent antigens. Injection of nude mice with both iRNA(T) and iRNA(B) caused an increase in the number of specific RFC and the secondary antibody formation response after boosting with a small dose of the corresponding antigen. Injection of iRNA(T) preparation into nude mice could induce the anamnestic response after boosting. However, neither of the iRNA(T) or iRNA(B) preparation could induce in nude mice the proliferation of the number of specific RFC. These results indicate the presence of at least two kinds of iRNA preparations against T-dependent antigens and that the cooperation of iRNA(T) and iRNA(B) was required for the induction of immune response against T-dependent antigens.

Animals↗

Cell preparation in immune response by immune ribonucleic acid. II. Independence of T lymphocytes in immune response against T-independent antigens.

The immune response of congenitally athymic (nude) mice induced by immune ribonucleic acid (iRNA) to lipopolysaccharides of Escherichia coli 0-55 (LPS) was studied. The thymus-independent nature of the immune response of mice to LPS was confirmed and nude mice responded to LPS in a manner similar to normal mice. An iRNA preparation extracted from the spleen of nude mice immunized with LPS could induce the proliferation of rosette-forming cells (RFC) in nude mice. iRNA preparations were insensitive to treatment with deoxyribonuclease and pronase, but were inactivated by ribonuclease treatment. The active fraction of the iRNA preparation had sedimentation values in a sucrose density gradient between 7 and 16 S and comprised only a small fraction of the total RNA present in the spleen cells, thereby indicating that the active moiety was one or more species of RNA. The anamnestic response was induced by treatment with iRNA made from the spleen of nude mice immunized with LPS. An increase in the number of rosette-forming cells (RFC), plaque forming cells (PFC) and formation of humoral antibody to LPS was seen after injection with a small amount of LPS 4 weeks after iRNA treatment.

Animals↗

Local and distant recurrences in rectal cancer patients are predicted by the nonspecific immune response; specific immune response has only a systemic effect--a histopathological and immunohistochemical study.

BACKGROUND: Invasion and metastasis is a complex process governed by the interaction of genetically altered tumor cells and the immunological and inflammatory host response. Specific T-cells directed against tumor cells and the nonspecific inflammatory reaction due to tissue damage, cooperate against invasive tumor cells in order to prevent recurrences. Data concerning involvement of individual cell types are readily available but little is known about the coordinate interactions between both forms of immune response. PATIENTS AND METHODS: The presence of inflammatory infiltrate and eosinophils was determined in 1530 patients with rectal adenocarcinoma from a multicenter trial. We selected 160 patients to analyze this inflammatory infiltrate in more detail using immunohistochemistry. The association with the development of local and distant relapses was determined using univariate and multivariate log rank testing. RESULTS: Patients with an extensive inflammatory infiltrate around the tumor had lower recurrence rates (3.4% versus 6.9%, p = 0.03), showing the importance of host response against tumor cells. In particular, peritumoral mast cells prevent local and distant recurrence (44% versus 15%, p = 0.007 and 86% versus 21%, p < 0.0001, respectively), with improved survival as a consequence. The presence of intratumoral T-cells had independent prognostic value for the occurrence of distant metastases (32% versus 76%, p < 0.0001). CONCLUSIONS: We showed that next to properties of tumor cells, the amount and type of inflammation is also relevant in the control of rectal cancer. Knowledge of the factors involved may lead to new approaches in the management of rectal cancer.

Adenocarcinoma↗

Transforming growth factor-beta 1 derived from biliary epithelial cells may attenuate alloantigen-specific immune responses.

Immune response to liver allografts may be different from that to other organ transplants since immunological manipulation easily attenuates immune-response to liver allografts. Numerous studies on the alloantigen-specific immune response have been carried out, however, the precise mechanisms involved in this attenuation are not clear yet. Here we suggest the attenuation of alloantigen-specific immune response by TGF-beta 1 derived from biliary epithelial cells. The transforming growth factor-beta 1 (TGF-beta 1) expression in rat liver was examined immunohistologically. Rat biliary epithelial cells (BEC) were purified from the perfused liver and added to allogeneic mixed lymphocyte reaction (allo-MLR) to assess their attenuating potential on allo-MLR and alloantigen-specific cytotoxic T lymphocyte (allo-CTL) induction. Immunohistological investigation revealed the expression of TGF-beta 1 in biliary epithelial cells. Both purified biliary epithelial cells and TGF-beta 1 attenuated allo-MLR and allo-CTL induction in a dose-dependent manner, and anti-TGF-beta 1 antibody partially relieved this attenuation. This study reveals that biliary epithelial cells, the major target cells of allo-antigen specific immune response, contain TGF-beta 1 and that they have a capacity to attenuate allo-MLR and allo-CTL induction.

Animals↗

Inflammatory cytokines in the brain: does the CNS shape immune responses?

Immune responses in the central nervous system (CNS) have traditionally been regarded as representing the intrusion of an unruly, ill-behaved mob of leukocytes into the well-ordered and organized domain of thought and reason. However, results accumulated over the past few years suggest that, far from being an immunologically privileged organ, T lymphocytes may be regular and frequent visitors to the CNS, for purposes of immune surveillance. Here, Trevor Owens and colleagues propose that the brain itself can regulate or shape immune responses therein. Furthermore, given that the immune cells may be subverted to autoimmunity, they suggest that the study of inflammatory autoimmune disease in the brain may shed light on the ability of the local environment to regulate immune responses.

Animals↗

Alcohol-mediated polarization of type 1 and type 2 immune responses.

Immune responses of alcoholics are often compromised, placing them at increased risk for frequent and severe infections. We demonstrate, using a murine model that parallels human alcoholism, that ethanol consumption polarizes adaptive immune responses by CD4+ T helper lymphocytes (Th). Alcohol impairs Th1-regulated cell-mediated, although Th2-regulated humoral responses are largely unimpaired and may be enhanced. Ethanol's effect is most pronounced during the early or cognitive phase of the immune response, when antigen-presenting cells (APC) interact with T cells. We find that alcohol does not act directly upon T cells, but upon APC. Consequences of this interaction of alcohol with APC in vivo are diminished Th1-mediated delayed hypersensitivity (DTH) reactions, while at the same time increased Th2-regulated serum IgE levels are seen. Further ethanol consumption leads to decrease affinity of the IgG2a and IgG2b Th1-regulated antibody isotypes.

Animals↗

Experimental porcine eperythrozoonosis: T-lymphocyte suppression and misdirected immune responses.

Immune responses and hematologic alterations were investigated in splenectomized pigs after IM inoculation with Eperythrozoon suis. Early hematologic alterations were massive parasitism of RBC, severe hypoglycemia, moderate bilirubinemia, and mild anemia; later findings included severe anemia, minimal parasitism of RBC, spontaneous agglutination of RBC at 25 C and 4 C which was reversible at 37 C, transient thrombocytopenia, and mild bilirubinemia. The humoral immune responses consisting of a transitory hyperglobulinemia and increase of indirect hemagglutination (IHA) titers against E suis were attributed to immunoglobulin M cold agglutinins. Cell-mediated immune responses, measured by phytohemagglutinin- and pokeweed mitogen-induced lymphocyte blastogenesis, were reduced after massive parasitemia. Blastogenesis induced by Escherichia coli lipopolysaccharide mitogen was increased before the hyperglobulinemia and an increase in IHA titer. There was an increase in the uptake of [3H]thymidine by lymphocytes cultured without mitogens after the decline in total globulin concentration and IHA titer.

Anaplasmataceae Infections↗

A distinct role for interleukin-13 in Th2-cell-mediated immune responses.

Immune responses elicited by allergic reactions and parasitic worm infections are characterised by the induction of T helper 2 (Th2) cells. These cells secrete cytokines such as interleukin-4 (IL-4), IL-5 and IL-13, which induce the production of immunoglobulin E (IgE) and eosinophils [1,2]. Previous studies using gastrointestinal nematodes to elucidate the role of Th2-cell-mediated immune responses have demonstrated a causal relationship between T cells and worm expulsion (reviewed in [3]). Although it has been proposed that IL-4 played a central role in these responses, recent studies demonstrated that IL-4-/- mice expel the parasitic gastrointestinal nematode Nippostrongylus brasiliensis normally [4], suggesting that another T-cell mediator is required for efficient worm clearance. Using IL-13-/- mice, we have demonstrated that, unlike wild-type and IL-4-/- mice, the IL-13-/- animals failed to clear N. brasiliensis infections efficiently, despite developing a robust Th2-like cytokine response to infection. Furthermore, treatment of the IL-13-/- mice with exogenous IL-13 resulted in a reduction in the numbers of worms recovered. The IL-13-/- animals also failed to generate the goblet cell hyperplasia that normally occurs coincident with worm expulsion. This observation may link IL-13 with the production of intestinal mucus which is believed to facilitate worm expulsion. These data support a unique role for IL-13 in Th2-cell-mediated immune responses and demonstrate that IL-13 and IL-4 are not redundant.

Animals↗

The effectiveness and limitations of immune memory: understanding protective immune responses.

Immune memory is the foundation of the practise of vaccination. Research on the molecular and cellular events leading to generation and development of memory T and B lymphocytes explain why there are heightened secondary immune responses after an initial encounter with antigen. In this review, we discuss how clonal expansion, targeted tissue localisation, more efficient antigen recognition and more proficient effector functions contribute to the improved effectiveness of memory cells. Despite the enhanced efficacy of memory cells and the recall immune response, there are numerous experimental and empirical examples in which protection provided by vaccines are short-lived, particularly against pathogens that replicate and cause pathology at their site of entry. In the absence of active immune effector activities, the ability of memory cells to respond quickly enough to control this type of infection is limited. The protective efficacy of bovine herpes virus-1 vaccines in experimental and field challenge conditions are used to illustrate the concept that full protection from disease conferred by vaccination requires the presence of active immune effector mechanisms. Thus, regardless of the many successful technological advances in vaccine design and better understanding of mechanisms underlining induction of memory responses by vaccination, we should recognise that vaccine immunoprophylaxis has limitations. Expectations for vaccines should be realistic and linked to the understanding of host immune responses and knowledge regarding the pathogen and disease pathogenesis.

Animals↗

Correlation between in vivo humoral and in vitro cellular immune responses following immunization with hepatitis B surface antigen (HBsAg) vaccines.

To study the regulation of the human immune response to hepatitis B surface antigen (HBsAg) we have carefully monitored the in vivo humoral and in vitro cellular immune responses to HBsAg in 50 subjects receiving four doses of hepatitis B vaccine according to a 0, 1, 2, 12 month vaccination scheme. Twenty-three subjects were given a plasma-derived vaccine (Hevac B) and 27 received a recombinant HBsAg vaccine (yeast-derived; Engerix-B). The humoral and cellular immune responses were measured before vaccination (day 0); 6 days after the second dose (day 36); 6 days (day 66), 2 months (day 120) and 10 months (day 365) after the third dose and 1 month after the fourth dose (day 395). Based on the kinetics of the humoral immune responses, the vaccinees could be classified into fast, intermediate and slow/non-responders. Based on the magnitude of the immune response (anti-HBs titre) on day 395, the vaccinees could be divided into high (> or = 2000 U l-1) and low (< or = 2000 U l-1) responders. A close correlation between the kinetics and the magnitude of the humoral immune response was observed. The in vivo anti-HBs response was measured using commercially available immunoradiometric assays. The in vitro cellular immune response was measured using an HBsAg-specific lymphoproliferation assay. Because of interassay variability the results were considered as dichotomous variables (proliferation versus non-proliferation) for further data analysis. A statistically significant correlation was observed between the kinetics and magnitude of the humoral immune response on the one hand and the in vitro anti-HBs response on the other hand.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

LPS regulation of the immune response: suppression of immune responses to orally administered T-independent antigen.

The regulation of immune responses to gastrically administered TI antigens has been investigated, and the characterization of a regulatory cell population has been performed. Intragastric administration of TNP-haptenated homologous erythrocytes (TNP-MRBC) induced splenic IgM anti-TNP PFC responses in LPS nonresponsive C3H/HeJ mice that were higher than those in LPS-responsive C3H/HeN mice and similar to those noted in athymic (nu/nu) C3H/HeN animals. The simultaneous intragastric administration of LPS with TNP-MRBC augmented immune responses in a manner similar to that previously reported for parenterally administered LPS and antigen. Further, LPS-induced augmentation of TNP-MRBC responses was greater in athymic mice. These findings were substantiated using in vitro spleen cultures. Intragastric challenge with a 2nd TI antigen, TNP-LPS, induced approximately 8-fold higher splenic anti-TNP PFC responses in athymic C3H/HeN mice compared with those in euthymic littermates. By admixture of B and T cell populations, it was demonstrated that the host responsiveness to TNP-LPS was negatively regulated by suppressor cells. Suppressive activity resided in a Thy 1.2-bearing, irradiation-resistant, nylon wool-nonadherent cell population. These cells could be demonstrated in spleen and Peyer's patches from young or old LPS-responsive C3H/HeN mice, but not in tissues from LPS nonresponsive C3H/HeJ mice. The specificity of the regulator cells was not limited to TNP-LPS responses, since immune responsiveness to another TI antigen, TNP-dextran, was also under the control of this cell population. These studies confirm the TI nature of TNP-MRBC and indicate that immune responses to gastrically administered antigens such as TNP-LPS, TNP-dextran, and possibly TNP-MRBC are negatively regulated by a suppressor T cell population. A role for endogenous LPS in the generation of regulator cells and the effect of these cells on host responses to gut-derived antigens is discussed.

Administration, Oral↗

Synthetic oligodeoxynucleotide containing CpG motif induces an anti-polysaccharide type 1-like immune response after immunization of mice with Haemophilus influenzae type b conjugate vaccine.

Synthetic oligodeoxynucleotides containing CpG motifs [immunostimulatory sequences (ISS)] have been described as potent adjuvants of type 1 immune responses when co-administered with protein or peptide vaccines. To investigate their role in the immune response to polysaccharides (CHO), different preparations of anti-Haemophilus influenzae type b (Hib) conjugate vaccine were administered to mice. The unconjugated CHO did not induce the synthesis of specific antibodies even in the presence of ISS. On the other hand, anti-CHO-specific antibodies significantly increased in the presence of ISS, when tetanus (TT) or diphtheria [cross-reacting material (CRM)] toxoid-conjugated CHO were used to immunize mice. The adjuvant effect was also observed for the immune response against the carrier protein (TT and CRM). ISS insured an early and long-lasting specific IgG production. The effects of ISS on the anti-CHO immune response could be attributed to the amplification of the T help provided by the carrier. The analysis of anti-CHO IgG subclasses showed a significant increase of IgG2a and IgG3 in the presence of ISS. ISS caused a rapid release of IL-12 and IFN-gamma in sera from treated mice. This data provide a first evidence for the ability of ISS to induce an anti-CHO type 1-like immune response and demonstrate that ISS have the potential to increase host antibody response against both the CHO and the protein component of a conjugated vaccine.

Adjuvants, Immunologic↗

Cell-mediated and humoral immune responses in immunized and/or Dermatobia hominis infested rabbits.

The cell-mediated and humoral immune response of rabbits to antigens from larvae of Dermatobia hominis were analyzed by leucocyte migration inhibition factor assay (MIF), immunodiffusion (ID) and passive hemagglutination (PH) test in rabbits immunized with D. hominis extract, in rabbits immunized and infested with the parasite and rabbits infested with D. hominis. Twenty rabbits were divided into five groups: Group 1, rabbits immunized with a crude antigen extract, evaluated for 40 weeks at 4 week intervals; Group 2, rabbits immunized and infested with newly hatched larvae at 14 weeks post immunization (PI) and evaluated as Group 1; Group 3, rabbits immunized, evaluated for 28 weeks at 2 week intervals; Group 4, rabbits immunized and infested at 4 weeks PI and evaluated as Group 3; Group 5, rabbits infested and evaluated for 24 weeks at 2 week intervals. Different patterns of reactivity were observed in the infested and immunized animals: immunized rabbits developed antibodies and cellular immune responses earlier and at higher levels during immunization than the infested rabbits; the infestation at 14 weeks PI, when the cell-mediated and humoral immune response began to decrease, or at 4 weeks PI when these parameters were at higher levels, elicited an anamnestic response. After the spontaneous elimination of larvae by the host, from the 4th week PI onwards, high titers of antibodies and migration inhibition indices were maintained for a long period. These results suggest that the onset of cellular and humoral immune responses after immunization may be important as a biological control of myiasis and contribute to better understanding of the immune defense mechanism of the host against D. hominis.

Animals↗

A simple method to test the ability of individual viral proteins to induce immune responses.

Immune responses to a mouse fibroblast line, transfected with a plasmid that causes expression of the rabies virus glycoprotein under the control of a simian virus 40 early promoter, were studied. Transfected cells were shown to be recognized in vitro by a panel of monoclonal antibodies directed to conformational epitopes of the different antigenic sites of the glycoprotein. They stimulated rabies virus glycoprotein-specific T helper cells in the presence of antigen-presenting cells and were, furthermore, recognized by rabies virus-induced cytolytic T cells. In vivo, immunization of H-2-compatible mice with the transfected cell line led to a rabies virus glycoprotein-specific antibody response, and to protection against a subsequent challenge with live virus. We propose this procedure, i.e. use of cell lines transfected with plasmids expressing a viral protein under a mammalian promoter, as a simple and inexpensive method to screen individual viral proteins for their ability to elicit immune responses, including T helper cells, cytolytic T cells, antibodies, and protection against viral challenge.

Animals↗

Sex differences in immune responses and immune reactivity to stress in adolescents.

The immune system is the body's major defense mechanism against disease. However, psychosocial factors, such as stress, can modulate various immune responses. Although they have been examined in adult humans and other animals, sex differences in immune responses and immune reactivity to stress have rarely been examined in adolescents, particularly comparing healthy and asthmatic adolescents. In 151 healthy and asthmatic high school adolescents (91 females and 60 males), natural killer cell (NK) cytotoxicity, polymorphonuclear leukocyte (PMN) superoxide release, lymphocyte proliferative responses, and CD subsets were measured twice: once during mid-semester and again during final examinations. There was little difference in these measures between healthy and asthmatic adolescents. Similarly, only sex difference was noted in NK cytotoxicity at a 25:1 effector-to-target cell ratio, with males showing significantly higher responses than females. For PMN superoxide release, females significantly increased their responses during final examinations, whereas males demonstrated no changes. For lymphocyte proliferative responses, both females and males increased their responses during final examinations, but the magnitude of increase was much greater in males. Furthermore, racial comparisons indicated that African American adolescents (n = 16), as compared with Caucasian adolescents (n = 128), had significantly higher responses in PMN superoxide release to N-Formyl-Met-Leu-Phe (FMLP) activation during mid-semester and lymphocyte proliferative responses at both time points. Nevertheless, the overall findings indicate limited differences in immune responses and immune reactivity to stress in adolescents between males and females, healthy and asthmatic adolescents, and Caucasians and African Americans. However, further investigations with larger samples are warranted.

Adolescent↗