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PubMed1995

Specific secretory immune responses in the female genital tract following intranasal immunization with a recombinant adenovirus expressing glycoprotein B of herpes simplex virus.

Previously, we demonstrated that intranasal (i.n.) but not intraperitoneal (i.p.) immunization with a recombinant adenovirus vector expressing glycoprotein B (gB) of herpes simplex virus type 1 (HSV-1) induced mucosal immune responses and conveyed long-term protection to mice against an i.n. challenge with heterologous HSV-2. We now show that i.n. immunization of female mice with this same vector, AdgB8, provides secretory and serum-derived humoral immune responses in the genital tract. Intranasal immunization induced anti-HSVgB IgA and IgG in vaginal washes of mice, whereas i.p. immunization only induced IgG, which appeared to be serum-derived. Interestingly, intravaginal (ivag) immunization with AdgB8 resulted in little or no anti-HSVgB IgA and only low levels of specific IgG in vaginal washes. All three routes of inoculation induced gB-specific serum IgG and IgA; however, i.n. immunized mice demonstrated the highest level of serum anti-HSVgB IgA. Additionally, ivag boosting with AdgB8 did not significantly alter the serum or vaginal wash antibody responses in i.n. or i.p. immunized mice. The IgG to IgA ratios of gB-specific and total antibody titres in the serum and vaginal washes of i.n. immunized mice indicated that the IgA in the vaginal washes was likely to be secretory. Furthermore, the titres of anti-HSVgB IgA relative to total IgA were higher in vaginal washes than sera, suggesting that the gB-specific vaginal wash IgA present in i.n. immunized mice was locally produced.

Adenoviridae↗

PubMed2005

TLR9 expression is related to immune activation but is impaired in individuals with chronic immune activation.

Millions of individuals in developing countries are infected with helminths and other chronic infectious diseases, such as HIV-1, which lead to persistent immune activation and unbalanced immune state. We have suggested that the capacity of chronically immune activated individuals to protect themselves, cope with infections, and mount protective immunity following vaccination, is highly impaired. Here we examined the expression of toll-like receptor 9 (TLR9), as an essential component in the recognition of immunostimulating bacterial CpG-DNA motifs, in different subsets of human peripheral blood mononuclear cells (PBMC) obtained from chronically immune activated and non-activated individuals. TLR9 expression was correlated to immune cell activation and was upregulated following phytohemagglutinin or anti-CD3 activation. PBMC obtained from chronically immune activated individuals had a different overall pattern of TLR9 expression, including reduced upregulation of this receptor following additional immune activation, and diminished responsiveness to CpG-DNA stimulation, in comparison to non-activated individuals. These differences may partly account for the reduced capacity of chronically immune activated individuals to mount effective immune responses and strengthen the notion that the host immune background should be considered in the design and trial of potential adjuvants and vaccines.

Adolescent↗

PubMed2004

Oral immune regulation: a novel method for modulation of anti-viral immunity.

Chronic viral infections, including hepatitis B and C and human immunodeficiency virus (HIV) infections, afflict a significant part of the world's population. In many of these diseases, chronicity has been linked to defective anti-viral immunity that damages host tissues without producing viral clearance. Currently available therapeutic measures for chronic viral infections are limited. Oral immune regulation, the manipulation of immune responses towards antigens by their oral administration, is a relatively simple and antigen-specific immune-modulatory tool. Recent evidence suggests that induction of oral immune-regulation towards viral antigens may entail a complex immune effect, characterized by simultaneous enhancement and suppression of different elements of the immune response in a manner that benefits the host. Such manipulation of the immune response towards viruses may achieve a combination of upregulated specific anti-viral immunity and inhibition of immune-mediated damage. Oral immune regulation may prove to be an important addition to the available therapeutic arsenal for chronic viral infections.

Administration, Oral↗

PubMed1996

Modulation of anti-idiotypic immune response by immunization with the autologous M-component protein in multiple myeloma patients.

Multiple myeloma is characterized by a proliferation of clonal B lymphocytes and plasma cells. The idiotypic structure of clonal immunoglobulin (Ig) expressed on the tumour B-cell surface can be regarded as a tumour-specific antigen and, as such, a potential target for anti-idiotypic T and B-cells in an immune regulation of the tumour-cell clone. Active immunization using the autologous mono-clonal Ig as a 'vaccine' was shown to induce tumour-specific immunity in murine B-cell tumours and in human B-cell lymphoma. With the aim to induce or amplify an anti-idiotypic response in multiple myeloma, five stage I-III patients were repeatedly immunized with the autologous monoclonal IgG. Induction of idiotype-specific cellular immunity was analysed in vitro by an enzyme-linked immunospot assay (interferon-gamma and interleukin-4 secreting cells). B cells secreting anti-idiotypic IgM antibodies were also analysed. An anti-idiotypic T-cell response was amplified 1.9-5-fold in three of the five patients during immunization. The number of B cells secreting anti-idiotypic antibodies also increased in these three patients. In two of the patients induction of idiotype-specific immunity was associated with a gradual decrease of blood CD19+ B cells. The induced T-cell response was eliminated during repeated immunization. Further studies are warranted to optimize the immunization schedule in order to achieve a long-lasting T-cell immunity against idiotypic determinants on the tumour clone. A role for immunity in controlling the tumour clone remains to be established.

Adult↗

PubMed2006

Immune gene networks of mycobacterial vaccine-elicited cellular responses and immunity.

Gene networks of protective lymphocytes after immune activation with live attenuated vaccines remain poorly characterized. Because Mycobacterium bovis bacille Calmette-Guérin (BCG) vaccine can confer protection against fatal forms of tuberculosis in humans and monkeys, we made use of macaque models to optimally study immune gene networks after BCG vaccination/infection. We first established and validated a large-scale real-time quantitation system and then used it to measure expression levels of 138 immune genes after BCG vaccination/infection of rhesus macaques. Systemic BCG vaccination induced up to 600-fold increases in expression of 78 immune genes among the 138 genes tested at the time when BCG-elicited T cell responses and immunity were apparent. These up-regulated transcripts constituted multiple gene networks that were linked to various aspects of immune function. Surprisingly, the up-regulation of most of these immune genes in the gene networks occurred at 1 week and was sustained at > or = 6 weeks after BCG vaccination/infection. Although early activation of immune gene networks was an immune correlate of anti-BCG immunity, prolonged up-regulation of these networks coincided with the development of vaccine-elicited T cell responses after BCG vaccination/infection. These findings provide molecular evidence suggesting that the BCG-induced gene networks may represent global transcriptomes and proteomes underlying the development of T cell responses and, ultimately, immunity to mycobacteria.

Animals↗

PubMed2002

Endogenous interleukin-4 downregulates the type 1 CD4 T cell-mediated immune response induced by intramuscular DNA immunization.

Intramuscular (i.m.) administration of eukaryotic plasmid vectors containing foreign genes is a general immunization strategy capable of inducing protective type 1 immune responses against viral, bacterial, fungal, and parasitic infections. We have described that immunization with a plasmid containing a gene encoding a parasite antigen elicits specific type 1 protective immune responses against experimental infection with the human protozoan parasite Trypanosoma cruzi. However, we had evidence suggesting that DNA immunization concomitantly activated specific type 2 immune responses. To determine precisely the influence of the type 2 cytokine interleukin-4 (IL-4) during DNA immunization, we compared the immune responses of genetically modified IL-4-deficient or wild-type (wt) BALB/c mice. IL-4-deficient mice had a significantly lower ratio of specific serum IgG1/IgG2a, and on in vitro restimulation with antigen, their spleen cells secreted significantly higher amounts of interferon-gamma (IFN-gamma). In contrast, absence of IL-4 did not affect total serum antibody response, T cell proliferative responses, or activation of IFN-gamma-producing CD8(+) T cells. Our results suggested that in contrast to conventional adjuvants, such as alum and complete Freund's adjuvant, specific IgG1 in DNA-immunized BALB/c mice was highly dependent on IL-4. To our knowledge, our study provides the first evidence that endogenous IL-4 selectively downregulates the type 1 CD4(+) T cell-mediated immune response induced by i.m. genetic immunization, a fact that may have implications for the design of certain DNA vaccines.

Animals↗

PubMed1997

Nutrition and immunity in the elderly: modification of immune responses with nutritional treatments.

Nutrition has a strong influence on the immune system of the elderly. Aging induces dysregulation of the immune system, mainly as a result of changes in cell-mediated immunity. Aging is associated with changes to the equilibrium of peripheral T and B lymphocyte subsets, such as decreases in the ratios of mature to immature, naive to memory, T helper 1 subset (TH1) to TH2, and CD5- to CD5+ cells. As a consequence, cell-mediated immune responses are weaker and neither cell-mediated nor humoral responses are as well adapted to the antigen stimulus. Undernutrition, common in aged populations, also induces lower immune responses, particularly in cell-mediated immunity. Protein-energy malnutrition is associated with decreased lymphocyte proliferation, reduced cytokine release, and lower antibody response to vaccines. Micronutrient deficits, namely of zinc, selenium, and vitamin B-6, all of which are prevalent in aged populations, have the same influence on immune responses. Because aging and malnutrition exert cumulative influences on immune responses, many elderly people have poor cell-mediated immune responses and are therefore at a high risk of infection. Nutritional therapy may improve immune responses of elderly patients with protein-energy malnutrition. Supplementation with high pharmacologic doses of a single nutrient (zinc or vitamin E) may be useful for improving immune responses of self-sufficient elderly people living at home. Therefore, nutritional deficiency must be treated in the elderly to reduce infectious risk and possibly slow the aging process.

Aged↗

PubMed2001

Intravenous Rh immune globulin for treating immune thrombocytopenic purpura.

Intravenous Rh [corrected] immune globulin was licensed by the U. S. Food and Drug administration in 1995 for the treatment of acute and chronic immune thrombocytopenic purpura in children and chronic immune thrombocytopenic purpura in adults. In 1996, the American Society of Hematology published a practice guideline for immune thrombocytopenic purpura, but treatment recommendations of necessity were formulated using only results of early clinical trials with intravenous Rh immune globulin. To date, there are no published results of large-scale clinical trials comparing conventional doses of intravenous immune globulin with the most promising dose range for intravenous Rh immune globulin (50-75 microg/kg). However, clinical experience is accumulating to indicate that intravenous Rh immune globulin is as effective, probably safer, and easier to administer than intravenous immune globulin. Acute intravascular hemolysis after infusions of intravenous Rh immune globulin for immune thrombocytopenic purpura has been reported with an estimated incidence of 1 in 1,115 patients. The risk factors for this adverse event have not been defined.

Adult↗

PubMed1995

Differential induction of carrier antigen-specific immunity by Salmonella typhimurium live-vaccine strains after single mucosal or intravenous immunization of BALB/c mice.

In this study, we constructed strain KR21 (chi 4550 delta cya delta crp delta asd/pYA292asd(+)-toxC+) and compared it with BRD847 (aroA aroD/pnirB-toxC) for the ability to induce humoral and cellular immunity after a single oral or intravenous immunization in 3- to 4-week-old BALB/c mice. ToxC-specific serum immunoglobulin G (IgG) was detectable in animals orally immunized with either BRD847 or KR21. However, after intravenous immunization, IgG was detected only in BRD847-immunized animals. Measurement of immunoglobin types IgG1 and IgG2a suggests that a Th1 cellular response is prominent after immunizations with either system. ToxC-specific IgA was detected in fecal and vaginal samples of animals immunized orally and intravenously with BRD847, while those immunized with KR21 failed to show fecal or vaginal IgA responses. Delayed-type hypersensitivity was used as a measure of induction of T-cell responses in vivo. Mice immunized either orally or intravenously with BRD847 showed significant ear swelling responses after ToxC injections, while KR21-immunized animals failed to show a cellular response. These data indicate that the aroA aroD/pnirB system holds greater potential for inducing global immunity after a single dose when directly compared with the balanced lethal system (delta cya delta crp delta asd/pYA292asd+).

Administration, Oral↗

PubMed2002

Immunization with the Chlamydia trachomatis mouse pneumonitis major outer membrane protein by use of CpG oligodeoxynucleotides as an adjuvant induces a protective immune response against an intranasal chlamydial challenge.

Recently, we have shown that a vaccine consisting of a purified preparation of the Chlamydia trachomatis mouse pneumonitis (MoPn) major outer membrane protein (MOMP) and Freund's adjuvant can protect mice against a genital challenge. Here, we wanted to determine if CpG motifs could be used as an immune modulator to the MOMP to induce protection in mice against an intranasal (i.n.) challenge. One-week-old BALB/c mice were immunized intramuscularly and subcutaneously either once or three times at 2-week intervals with MOMP and CpG suspended in aluminum hydroxide (alum). Negative controls received ovalbumin, CpG, and alum. Positive controls were immunized i.n. with C. trachomatis MoPn elementary bodies (EB). Six weeks after the last immunization, mice were challenged i.n. with 10(4) inclusion-forming units (IFU) of the C. trachomatis MoPn serovar. Mice that received MOMP, CpG, and alum had a strong immune response, as shown by a high titer of serum antibodies to Chlamydia and significant lymphoproliferation of T-cells following stimulation with C. trachomatis EB. After the i.n. challenge mice immunized with MOMP, CpG, and alum showed significantly less body weight loss than the corresponding control mice immunized with ovalbumin, CpG, and alum. Ten days after the challenge the animals were euthanized, their lungs were weighed, and the numbers of IFU in the lungs were determined. The average weight of the lungs of the mice immunized with MOMP, CpG, and alum was significantly less than average weight of the lungs of the mice immunized with ovalbumin, CpG, and alum. Also, the average number of IFU recovered per mouse immunized with MOMP, CpG, and alum was significantly less than the average number of IFU per mouse detected in the mice inoculated with ovalbumin, CpG, and alum. In conclusion, our data show that CpG sequences can be used as an effective adjuvant with the C. trachomatis MoPn MOMP to elicit a protective immune response in mice against a chlamydial respiratory challenge.

Adjuvants, Immunologic↗

PubMed2004

Immunoglobulin E and eosinophil-dependent protective immunity to larval Onchocerca volvulus in mice immunized with irradiated larvae.

Mice immunized with irradiated Onchocerca volvulus third-stage larvae developed protective immunity. Eosinophil levels were elevated in the parasite microenvironment at the time of larval killing, and measurements of total serum antibody levels revealed an increase in the immunoglobulin E (IgE) level in immunized mice. The goal of the present study was to identify the role of granulocytes and antibodies in the protective immune response to the larval stages of O. volvulus in mice immunized with irradiated larvae. Immunity did not develop in mice if granulocytes, including both neutrophils and eosinophils, were eliminated, nor did it develop if only eosinophils were eliminated. Moreover, larvae were killed in naïve interleukin-5 transgenic mice, and the killing coincided with an increase in the number of eosinophils and the eosinophil peroxidase (EPO) level in the animals. To determine if EPO was required for protective immunity, mice that were genetically deficient in EPO were immunized, and there were no differences in the rates of parasite recovery in EPO-deficient mice and wild-type mice. Two mouse strains were used to study B-cell function; micro MT mice lacked all mature B cells, and Xid mice had deficiencies in the B-1 cell population. Immunity did not develop in the micro MT mice but did develop in the Xid mice. Finally, protective immunity was abolished in mice treated to eliminate IgE from the blood. We therefore concluded that IgE and eosinophils are required for adaptive protective immunity to larval O. volvulus in mice.

Animals↗

PubMed2001

Induction of type 1 immune pathology in the brain following immunization without central nervous system autoantigen in transgenic mice with astrocyte-targeted expression of IL-12.

IL-12, a cytokine produced by microglia, may regulate cellular immunity at a localized level in the CNS. To investigate this further, we examined the consequences of peripheral immune stimulation without specific autoantigen in wild-type or transgenic (termed GF-IL12) mice with astrocyte production of the bioactive IL-12 p75 heterodimer. Active immunization with CFA and pertussis toxin, a procedure known to stimulate a robust type 1-biased immune response, produced CNS immune pathology from which GF-IL12 but not wild-type mice developed signs of clinical disease consisting of loss of activity, piloerection, mild tremor, and motor change. All immunized mice had some degree of mononuclear cell infiltration into the brain; however, the severity of this was markedly increased in GF-IL12 mice where leukocytes accumulated in perivascular and parenchymal locations. Accumulating cells consisted of CD4(+) and CD8(+) T cells and macrophage/microglia. Moreover, expression of cytokines (IFN-gamma and TNF), chemokines (IFN-inducible protein-10 and RANTES), the immune accessory molecules, MHC class II, B7.2, ICAM-1 and VCAM-1, and NO synthase-2 was induced in the CNS of the GF-IL12 mice. Therefore, peripheral immunization of GF-IL12 but not wild-type mice can provoke active type 1 immunity in the brain-a process that does not require CNS-specific immunizing autoantigen. These findings indicate that the cytokine milieu of a tissue can dramatically influence the development of intrinsic immune responses and associated pathology.

Animals↗

PubMed1975

Duration of circulating and secretory antibody and cell-mediated immunity following immunization.

An important consideration in evaluating vaccines is the duration of immunity. The only really important measure of this immunity is the protection against infections and/or illness at various time intervals, following natural or artificial challenge. There are few data of this sort, more commonly immunity is estimated by measuring serum antibody, in many instances an erroneous measure. Serum antibody levels to respiratory viruses fall only slightly 6 months following infection or immunization. It is difficult to assess the duration of antibody for much longer than this, because of problems with intercurrent infection. With respiratory bacterial infections, e.g. pneumococcal pneumonia, parenterally-induced immunity probably lasts for only several months. Secretory antibody induced by inactivated viral vaccines, seems to persist for about a year, after having reached a peak level at about 4-6 weeks following immunization. Work with the live attenuated polio virus vaccine indicates longer lasting immunity, with detectable antibody persisting for up to 34 months. Restimulation with the inactivated polio virus vaccine produced no evidence of a secondary response (memory). Following booster immunization with influenza very little evidence of memory is seen. Cell-mediated immunity (CMI): in guinea pigs BCG sensitization can be demonstrated for at least 2-9 months. In humans, intracutaneous BCG immunization leads to positive tuberculin reaction in 6-10 weeks, and skin sensitivity lasts an average of about 4 years. There is contradicting data as to the duration of protection against infection following BCG immunization. Local and systemic CMI have been shown to exist independently of each other in experimental animals and man.

Animals↗

PubMed1989

Induction of tumor-specific in vivo protective immunity by immunization with tumor antigen-pulsed antigen-presenting cells.

The present study investigates the role of APC in inducing tumor-specific in vivo protective immunity. Thy-1+ cell-depleted, Mac-1+ cell-enriched fraction of normal BALB/c spleen cells were used as a source of APC. These APC were cultured in vitro with the membrane fraction isolated from CSA1M fibrosarcoma derived from BALB/c strain. The administration of such APC into naive BALB/c mice generated the capacity of these animals to reject the subsequently challenged viable CSA1M tumor cells. Although the induction of anti-CSA1M in vivo protective immunity required three consecutive immunizations with more than 10(5) APC which had been pulsed in vitro with 200 to 300 micrograms protein of CSA1M membrane fraction, the immunity was induced irrespective of whether APC were administered via s.c., i.v., or i.p. route. This immunity was tumor-specific, inasmuch as the inoculation of CSA1M or Meth A fibrosarcoma membrane component-pulsed APC resulted in the selective immunity against the challenge with homologous types of tumor cells. The CSA1M-specific in vivo protective immunity was also induced by injecting APC pulsed with solubilized CSA1M membrane components. Moreover, it was demonstrated that the efficiency for inducing anti-CSA1M immunity was much higher in the utilization of tumor Ag-pulsed APC than in the immunization with tumor Ag emulsified in CFA. These results indicate the critical role of APC in generating tumor rejection immunity in vivo and this model presents a novel approach to induce tumor-specific immunity without using tumor cells themselves.

Animals↗

PubMed1985

Cross-reactive cellular and humoral immunity to carcinogen-induced chicken fibrosarcomas. I. Protective cross-immunity between transplantable tumor lines.

Dimethylbenz[a]anthracene (DMBA)-induced transplantable fibrosarcomas in B2 homozygous chickens (SC line) grow progressively in normal chickens, but are rejected by chickens immunized previously with irradiated tumor cells and Corynebacterium parvum. Tumor-immune chickens resist challenge by the immunizing tumor lines as well as by some, but not all, fibrosarcoma lines. The pattern of cross-reactivity between four DMBA-induced transplantable tumor lines was examined in detail. Ability to reject a tumor challenge correlated very well (p less than 0.001) with the presence of delayed-type hypersensitivity (DTH) to that tumor. Immunization with one of two of the DMBA-induced lines tested also caused rejection of transplantable tumors developed from methylcholanthrene-induced and benzo(a)pyrene-induced primary fibrosarcomas. Although immunization with tumor caused DTH to chicken embryo fibroblasts (CEF), immunization with CEF failed to cause protective immunity or DTH to tumors. Presence of protective immunity, where tested, also correlated with the ability of spleen cells from immune donors to inhibit tumor growth in Winn tests. Humoral immunity exhibited even greater cross-reactivity than did cellular immunity. Distinct patterns of cross-reactivity were nevertheless observed with respect to the serum antibodies as detected in ELISA. Two of these patterns were also observed in several sera from primary tumor-bearing chickens, both including reactivity with CEF. Such reactivity was absent from normal chicken sera.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1997

[Is the immune system our sixth sense? Relation between the immune and neuroendocrine systems].

There is an overwhelming evidence that cytokines, peptide hormones and neurotransmitters, as well as their receptors, are present in the brain, endocrine and immune systems. The structure and pattern of synthesis of these peptides by leukocytes appear similar to those synthesized in the neuroendocrine system, although some differences exist. Once secreted, these peptide hormones may function as endogenous regulators inside of the each system and also in bidirectional communication between the immune and neuroendocrine systems. Such communication suggest an immunoregulatory role for the brain and a sensory function for the immune system which may sense stimuli that are not recognized by the central and peripheral nervous systems (noncognitive stimuli). The plasma hormone concentrations contributed by lymphocytes usually do not reach the levels required when the pituitary gland is the source, but because immune cells are mobile, they have the potential to deposit the hormone locally at the target site. Several immunoregulatory cytokines, including IL-1, IL-2, IL-6, IFN-gama and TNF are produced not only in the immune system but in the neuroendocrine system as well. They have profound effects on neuroendocrine functions especially on hypothalamic pituitary axes. Neuroendocrine influences that modulate the immune function mainly include mental and physical stress. It can reduce the resistance of organism to infectious diseases and malignancies by compromising the immune system directly or indirectly. The brain is not an immunologically privileged site and therefore may become the target of immunologic attacks resulting in neuroimmunological diseases with an autoimmune component. The impact of psychological and psychosocial factors on the immune system is studied by psychoneuroimmunology whereas neuroendocrine immunology is generally interested in the interactions between the immune and neuroendocrine systems under physiological and pathological conditions. The recognition of the identity of ligands and receptors in the immune, nervous, and endocrine systems suggest a radically altered view of the immune systems impact on other tissues and organ systems, and vice versa. This will undoubtedly change our understanding of physiology, and consequently should profoundly impact the practice of medicine. (Tab. 5, Fig. 4, Ref. 85.)

Animals↗

PubMed1979

Dissociation of anti-tumor immune responses in rats immunized with solubilized tumor-associated antigens from a methylcholanthrene-induced fibrosarcoma.

Soluble tumor antigens were prepared from chemically-induced rat fibrosarcoma KMT-17 cells by various methods [Na-deoxycholate (DOC), 3 M-KCI extraction, and crude membrane preparations by mechanical disruption]. Soluble tumor antigens prepared by DOC extraction (DOC-STA) could be detected by a radioisotopic footpad assay (FPA) and they showed the strongest antigenic activity in KMT-17 immune rats. Anti-tumor immune responses in rats previously immunized with DOC-STA were measured by FPA, Winn assay, and transplantation resistance. Significant responses detected by the FPA and Winn assay were demonstrated in rats immunized with DOC-STA. However, rats previously immunized with DOC-STA showed a significant enhancement of tumor growth when challenged with KMT-17 cells. This enhancement was specific for the tumor line used. Normal rats which received adoptive transfer of thymus and spleen cells from rats immunized with DOC-STA produced specific enhancement of tumor growth as compared with non-treated rats. Administration of cyclophosphamide before immunization with DOC-STA abrogated the enhanced tumor growth in the host. These results suggest that immunization with soluble tumor antigens specifically enhanced tumor grwoth by the induction of immunosuppressor cells. Dissociation between the anti-tumor immunity detected by the FPA and Winn assay and the enhanced tumor growth detected by transplantation resistance in rats immunized with DOC-STA is discussed.

Animals↗

PubMed2003

Stress applied during primary immunization affects the secondary humoral immune response in the rat: involvement of opioid peptides.

The effect of unpredictable, inescapable and uncontrollable electric tail shocks (ES) on the humoral immune response to bovine serum albumin (BSA) was investigated in the rat. Contributions of the procedures that accompany shock delivery, such as witnessing the ES procedure (stress witnessing, SW) and exposure to the apparatus for shock delivery (apparatus control, AC) to the changes in specific immunity induced by ES were also tested. All procedures were applied during primary and/or secondary immunization. It was demonstrated that exposure to ES during primary immunization with BSA significantly suppressed specific anti-BSA antibody production after secondary and tertiary immunization with the same antigen. Exposure to the SW procedure during primary immunization with BSA enhanced the specific antibody level after secondary immunization, while exposure to the apparatus alone did not influence the development of either the primary or secondary humoral immune response to BSA. Both ES-induced suppression and SW-induced potentiation of the humoral immune response were partially inhibited by prior treatment with the opioid receptor antagonist naloxone. Additionally, treatments with the opioid peptides methionine- and leucine-enkephalin decreased anti-BSA antibody level, mimicking to some extent the effects of ES. It is suggested that ES and endogenous opioid peptides had long-term effects on humoral immunity through mechanisms involving immunologic memory.

Animals↗