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PubMed2006

Protective effect of melatonin against propoxur-induced oxidative stress and suppression of humoral immune response in rats.

Effect of melatonin in attenuation of propoxur induced oxidative stress and suppression of humoral immune response was studied in rats. Oral administration of propoxur (10 mg/kg) increased lipid peroxidation in serum after 28 days treatment. Superoxide dismutase, catalase and glutathione were also altered following propoxur exposure. In addition propoxur exposure markedly suppressed humoral immune response as assessed by antibody titre and plaque forming cell assay. Simultaneous treatment with melatonin (5 mg/kg, ip) markedly attenuated the effect of propoxur on (a) lipid peroxidation, (b) oxidative stress parameters and (c) immunotoxicity. Results have been discussed in the light of possible immunopotentiating and antioxidant effects of melatonin to understand the influence of oxidative stress on propoxur induced immunomodulation.

Animals↗
PubMed2001

[Detection of humoral immune response to inner ear proteins in patients with sensorineural hearing loss].

BACKGROUND: The precise mechanism of inner ear disease is still unknown. An autoimmune reaction could be one of several possible pathogenic factors involved in progressive sensorineural hearing loss. Heat shock protein 70 is suggested to play an important role in the development of autoimmune diseases. The aim of this study is the investigation of humoral immune reactivity to inner ear components in patients with sensorineural hearing loss. METHODS: The presence of antibodies to inner ear components was determined by immuno-blotting extracted bovine or human inner ear proteins. Study groups consisted of patients with idiopathic progressive sensorineural hearing loss (group A), patients with Menière's disease (group B), patients with sudden hearing loss (group C), patients with otosclerosis (group D), patients with Cogan's disease (group E), and individuals without hearing problems (group F). RESULTS: 40% of the patients with progressive sensorineural hearing loss showed reactivity against a 68-kDa protein extracted from bovine inner ear. In contrast to this, only 5% of healthy individuals and 10% with Menière's disease showed reactivity against the 68-kDa protein from bovine inner ear or against bovine heat shock protein 70. Some of the patients who showed reactivity against bovine inner ear proteins were tested with human inner ear and human heat shock protein 70; all of these showed reactivity. Approximately 6% of the patients with sudden hearing loss (group C), otosclerosis (group D), and Cogan's disease (group E) showed reactivity to inner ear proteins. A non-specific humoral immune reaction against inner ear proteins with molecular weights of 30, 40, 50, 60, and 220 kDa was observed in all patients. DISCUSSION: These results indicate a humoral immune reactivity against heat shock protein 70, which might be responsible for the pathogenesis of progressive sensorineural hearing loss.

Adult↗
PubMed2001

[Proinflammatory cytokines in humoral immune response].

Proinflammatory cytokines secreted by cells involved in inflammatory process play a key role in the regulation of immune responses, both cellular and humoral immune response. Through their influence on T-helper lymphocytes and antigen presenting cells including lymphocytes B, they induce secretion of secondary cytokines and, in cooperation with them, promote activation and proliferation of lymphocytes B and production of variety of classes of immunoglobulins. Cytokines interact with their specific receptors which usually occur both in membrane bound and soluble form. The purpose of this article was to evaluate the relationships between primary cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) and other cytokines, lymphocytes T-helper and lymphocytes B in the light of current opinions regarding this matter.

Antibody Formation↗
PubMed1990

Monoclonal anti-idiotypic antibodies induce humoral immune responses specific for simian virus 40 large tumor antigen in mice.

Mouse monoclonal anti-Id antibodies were generated against a mouse mAb (Ab-1) preparation specific for SV40 large tumor Ag (T-Ag). Four monoclonal anti-Id preparations each inhibited the binding of the monoclonal anti-SV40 T-Ag Ab-1 preparation to SV40 T-Ag. These anti-Id preparations appeared to recognize similar idiotopes on the monoclonal anti-SV40 T-Ag Ab-1 based on competitive cross-inhibition studies. One of these anti-Id preparations, designated 57B, was examined further for its in vivo modulatory capacity in mice. This anti-Id induced an Ab-3 response in BALB/c mice that recognized SV40 T-Ag (Ag+) and expressed an Id that was shared by the monoclonal anti-SV40 T-Ag Ab-1 preparation (Id+). The Id expressed on the Ab-3 differed from the Id induced in BALB/c mice immunized with the nominal SV40 T-Ag. Furthermore, characterization of the humoral immune response induced by anti-Id immunization indicated that the Ab-3 also recognized different epitopes on SV40 T-Ag when compared to the anti-SV40 T-Ag Ab-1 preparation used to generate the anti-Id. These studies indicate that monoclonal anti-Id can be used to induce humoral immune responses to a viral encoded tumor-associated Ag in vivo with 1) and Id specificity that differs from that expressed on antibodies produced by immunization with the nominal Ag and 2) an epitope specificity distinct from the Ab-1 preparation used for the production of the anti-Id.

Animals↗
PubMed2002

Humoral immune response and protection from viral infection in mice vaccinated with inactivated MHV-68: effects of type I interferon.

Infection of mice by murine gammaherpesvirus 68 (MHV-68) represents a suitable animal model in which to investigate the immune response against gammaherpesviruses and to test the efficacy of vaccination strategies. In this study, we evaluated the efficacy of heat-inactivated MHV-68 as a vaccine as well as the adjuvant activity of type I interferon (IFN-I) administered together with the vaccine. Mice vaccinated with inactivated MHV-68 and subsequently infected with the virus exhibited a significant augmentation of the virus-specific humoral immune response and a considerable inhibition of MHV-68 acute replication in the lungs compared with unvaccinated control mice. The coadministration of IFN-I with inactivated MHV-68 significantly enhanced the humoral immune response elicited by the vaccine by stimulating the production of virus-specific IgG2 antibodies but did not significantly enhance protection from viral challenge. We conclude that IFN-I, recently shown to exhibit a powerful adjuvant activity to a poorly immunogenic subunit vaccine in mice, can also enhance the humoral immune response when used as adjuvant of an inactivated viral vaccine, even though this effect is less marked as a result of the strong immune response elicited by the inactivated virus alone, which may also involve the contribution of endogenous IFN.

Animals↗
PubMed1983

[Effects of codeine and morphine on the primary humoral immunity of the respiratory tract].

To investigate the effects of centrally acting antitussive drugs, codeine and morphine, on the humoral immunity in the respiratory tract, male guinea pigs were immunized either systemically (i.p.) or locally (intratracheally, i.t.) with sheep red blood cells (SRBC). The development of plaque-forming cells (PFC) was determined using the spleen (S-PFC) and tracheobronchial lymph node cells (T-PFC). (I) Number of S-PFC after i.p. immunization increased to the maximum on day 5. Peak number of S-PFC and T-PFC after i.t. immunization occurred on day 6. (II) i.p. immunization: The drugs were given i.p. for 5 days before or for 4 days after immunization. Morphine (5 mg/kg) given prior to the immunization decreased spleen cellularity. Pretreatments with codeine (15 mg/kg) and morphine (5 mg/kg) also markedly inhibited the number of S-PFC. These drugs given after the immunization hardly affected the number of S-PFC. (III) i.t. immunization: The drugs were given for 5 days before or after the immunization. Codeine (15 mg/kg) given prior to the immunization inhibited the number of S-PFC. Codeine (3, 15 mg/kg) and morphine (1, 5 mg/kg) given before and after the immunization markedly inhibited the number of T-PFC, dose-dependently. These results indicate that codeine and morphine affect the humoral immunity both locally in the respiratory tract and systemically, which cautions against an easygoing use in respiratory diseases.

Animals↗
PubMed1982

Cell-mediated and humoral immune responses in guinea pigs sensitized with the thermostable antigen of human granulocytes (TSGA).

Cell-mediated and humoral immune responses are induced shortly after a single injection of the human thermostable granulocyte antigen TSGA to guinea pigs. This was proved by means of the lymphocyte transformation assay and the estimation of MIF and LIF activity in supernatants of antigen-stimulated lymph node cells as well as by immunodiffusion, immunoelectrophoresis and immunohistology. The maximum of the cellular response was observed 10 days after immunization. The antibody production appeared after a lag time and increased continuously thereafter. The antisera of guinea pig yields a strong specific fluorescence in neutrophils and a weak fluorescence in monocytes of man. The humoral immune responses of guinea pig antisera correspond to the results obtained with antisera from rabbits.

Animals↗
PubMed1999

Experimental testicular teratoma promotes formation of humoral immune responses in the host testis.

The testis is an immunologically privileged site. Very little is known about the factors regulating formation of immune responses elicited by a neoplasm in the testis. We have studied the immune response of the host testis against experimental testicular teratoma in mouse by localizing adhesion molecules (CD106, CD54, CD49d/CD29, CD44, CD18, CD8 and CD4), cytokines (IL-2, IL-4, IL-6, IL-10 and IL-12), T-cell costimulators (CD80, CD86) and the lipid antigen presenting molecule CD1d in the testis of 129/SvJ mice with and without experimental testicular teratoma. The testicular teratomas were induced by grafting male gonadal ridges from 12-day-old 129/SvJ mouse fetuses into testes of adult mice from the same strain. The tumors cultured intratesticularly for 2, 3, 4 and 8 weeks (three animals per time point) were used for immunocytochemistry. CD1d was detected in Sertoli cells and in some degenerated tubules of the host testis surrounding the graft. In the tumor, CD1d was detected in glandular epithelia, smooth muscle and in thin fibers of neural origin. IL-2 was observed in some blood vessels of the host testis and of the tumor and in occasional cell infiltrates around these vessels. Some tubular structures of the tumor were also positive for IL-2. IL-6 was detected in Sertoli cells of the normal testis and in Sertoli cells and in solitaryinterstitial cells as well as in the walls of some blood vessels of the host testis. The reaction for IL-6 was more prominent in the tubules apparently damaged by the growing tumor. In the tumor IL-6 was detected in epithelial structures, muscle cells, in thin fibers of neural origin and in some blood vessels. IL-10 was detected in individual cells in the interstitium and in degenerating tubules of the host testis. In the tumor the epithelial structures were positive for IL-10. The interstitium of the host testis was positive for CD106 and the embryonic testicular cords in the graft were also positive, but the tumor was negative. CD44 and CD18 were observed in some blood vessels and in degenerated tubules of the host testis. In the tumor CD44 and CD18 were occasionally observed in cartilage and in epithelial structures. The results of the present study suggest that cytokine microenvironment in the testis containing neoplastic tissue promotes activation of humoral immune responses. In addition, as the damaged seminiferous tubules expressed increased amounts of two cytokines promoting humoral immune responses, IL-6 and IL-10, it is possible that also in other conditions with damage to the tubules, humoral immune responses predominate.

Animals↗
PubMed1984

Genetic control of humoral immunity to sperm acrosomal and cell surface antigens.

We have defined the nature of genetic control of humoral immunity to sperm cell surface (TSDA) and acrosome (Ac) antigens. A sperm immunization dose that distinguishes between high-responder (BALB/c) and low-responder (B10) strains of mice was identified. B10 mice were unresponsive, whereas BALB/c and F1 hybrid mice responded to sperm of both parental strains. The ratio of nonresponder to responder mice in the B10 X F1 backcross and F1 X F1 inbred generations indicates anti-TSDA or anti-Ac antibody responsiveness is controlled through more than a single gene. The significant correlation found between the anti-TSDA and anti-Ac responses is consistent with the possibility that one or more genes controls antibody responsiveness against determinants common to both the Ac and sperm cell surface. Neither anti-TSDA nor anti-Ac antibody responses were linked to the I-A subregion of the responder H-2d MHC haplotype. In addition to a genetic difference in the control of humoral immunity to sperm, a difference in sperm immunogenicity among strains was observed. Antigens of the Ac of B10 sperm are more immunogenic than those of BALB/c sperm, and this trait is linked to the B10 Y chromosome.

Acrosome↗
PubMed2006

Early epitope- and isotype-specific humoral immune responses to GAD65 in young children with genetic susceptibility to type 1 diabetes.

OBJECTIVE: The pattern of the humoral immunity to disease-associated autoantigens may reflect the severity of the autoimmune disease process. The purpose of this study was to delineate the maturation of the humoral immunity to one of the main autoantigens in type 1 diabetes (T1D), glutamic acid decarboxylase (GAD65). DESIGN AND METHODS: Serum samples were obtained for the detection of epitope- and isotype-specific antibodies sequentially with short intervals from 36 young children with HLA-conferred genetic susceptibility to T1D starting from the first appearance of GAD65Ab. During prospective observation, ten children developed T1D. Antibodies were analyzed using biotinylated anti-human immunoglobulin (Ig) antibodies and chimeric GAD molecules in radio-binding assays. RESULTS: The immune response to GAD65 started as reactivity to the middle region and spread rapidly to the C-terminal region. IgG1 antibodies dominated among the isotypes from the first appearance of GAD65Ab, while other IgG subclasses were observed to a lesser extent. IgG4 antibodies emerged clearly as the last IgG subclass. A broad initial response comprising three to four IgG subclasses and the lack of an emerging IgG4 response during follow-up was associated with increased risk for progression to clinical diabetes (P<0.05). CONCLUSIONS: The humoral response to GAD65 epitope clusters is relatively uniform in young children, whereas there is conspicuous individual variation in IgG subclass responses except for IgG1. A narrow initial IgG subclass response to GAD65 and the emergence of IgG4 antibodies were characteristic of those who remained non-diabetic over the first few years of GAD65 autoimmunity.

Antibody Formation↗
PubMed2000

Recognition and regulation of metalloproteinase activity in the haemolymph of Galleria mellonella: a new pathway mediating induction of humoral immune responses.

Proteolytic activity released within an organism by wounded tissues or invading pathogens can strongly impair the physiological homeostasis when it remains non-regulated. Thus, an efficient mechanism that enables recognition and inactivation of non-regulated proteolytic activity is essential to limit toxic effects. In larvae of the Greater wax moth Galleria mellonella we discovered that injection of bacterial thermolysin at a sublethal concentration mediates both acquired resistance against a subsequently injected lethal concentration of this metalloproteinase and stimulation of humoral immune response accompanied by the synthesis of an inducible metalloproteinase inhibitor (IMPI) which is released within the haemolymph. In search of a putative mechanism mediating recognition and regulation of released microbial metalloproteinases we determined that thermolysin-mediated hydrolysis of G. mellonella haemolymph proteins in vitro yields small (<3 kDa), heat-stable molecules which were discovered to represent potent elicitors of humoral immune responses when injected into untreated larvae. Obtained results allowed to design a model explaining for the first time regulation of released metalloproteinases within the haemolymph of insects. The determined coherence between regulation of released metalloproteinases by IMPI and the simultaneous induction of antimicrobial proteins provides a new insight into the mechanisms leading to expression of genes in course of humoral immune responses.

Animals↗
PubMed2006

Effects of dietary supplementation with clostridium butyricum on the growth performance and humoral immune response in Miichthys miiuy.

The effects of dietary supplementation with Clostridium butyricum on growth performance and humoral immune response in Miichthys miiuy were evaluated. One hundred and fifty Miichthys miiuy weighing approximately 200-260 g were divided into five groups and reared in 15 tanks with closed circuiting culture system. The animals were fed 5 diets: basal diet only (control) or supplemented of the basal diet with C. butyricum at doses of 10(3) (CB1), 10(5) (CB2), 10(7) (CB3) or 10(9) (CB4) CFU/g. Compared with the control, the serum phenoloxidase activity was significantly increased by the supplementation (P<0.05), acid phosphatases activity was increased significantly (P<0.05) at the doses of 10(9) CFU/g. Serum lysozyme activity peaked at dose of 10(7) CFU/g and in the skin mucus at dose of 10(9) CFU/g. Immunoglobulin M level in the serum and skin mucus was increased except at dose of 10(3) CFU/g (P<0.05). The growth at the dose of 10(9) CFU/g was higher than that of the control (P<0.05). It is concluded that supplementation of C. butyricum can mediate the humoral immune responses and improve the growth performance in Miichthys miiuy.

Animal Feed↗
PubMed2006

Bacterial adherence and humoral immune response in women with symptomatic and asymptomatic urinary tract infection.

PURPOSE: To determine the role of humoral immune response and bacterial adherence in the pathogenesis of symptomatic and asymptomatic urinary tract infection in women. METHODS: The study population consisted of 30 women with symptomatic UTI, 30 women with asymptomatic UTI and 30 healthy women as controls. Bacterial adherence to vaginal epithelial cells was studied and the concentration of serum and urine antibodies to mixed coliform antigen and clinical isolate was determined by ELISA. Surface hydrophobicity of the urine isolates was determined. Student's unpaired t test and Pearson's correlation coefficient test were used in the statistical analysis. RESULTS: Compared to asymptomatic UTI, significantly more number of bacteria adhered to the epithelial cells of women with symptomatic UTI (P< 0.001). All cases of UTI had significantly high concentration of urinary IgG antibody to mixed coliform antigens. Asymptomatic UTI cases had higher concentrations of urinary IgG, IgM and IgA antibodies to clinical isolate. Concentration of sIgA level was more in symptomatic UTI. Significant correlation was observed between urinary IgG and adherence of clinical isolate in case of asymptomatic UTI. CONCLUSIONS: The present study showed that greater receptivity of epithelial cells to bacteria may increase the susceptibility to UTI. Humoral immune response and local immunity may modify the pathogenesis of UTI.

Adolescent↗
PubMed1991

Transforming growth factor-beta and suppression of humoral immune responses in HIV infection.

We reported previously that PBMC from HIV+ patients spontaneously release increased levels of TGF beta 1, contributing to defects in cellular immune responses. This study defines the implications of TGF beta overexpression for humoral immunity in HIV infection. We found that upon Staphylococcus aureus Cowan I (SAC) stimulation of cells from HIV+ donors, B-lymphocyte proliferative responses were decreased. This deficiency correlated closely (r = 0.7, P less than 0.001) with increased TGF beta secretion by PBMC from HIV-infected donors. Conditioned medium from HIV+ PBMC and purified TGF beta 1 had similar inhibitory effects on SAC- or EBV-induced B-cell proliferation, and B cells from HIV-infected donors were as sensitive to inhibition by TGF beta as cells from normal donors. Antibodies to TGF beta 1 neutralized the inhibitory effect of HIV+ culture supernatants on normal B cells and increased low proliferative responses by HIV+ cells. Using PWM as stimulus for B cell differentiation, it was shown that activated TGF beta from HIV+ PBMC is able to significantly reduce the induction of immunoglobulins and this effect was also abrogated by anti-TGF beta. These studies support the concept that in HIV infection, TGF beta is a potent suppressor, not only of the cellular, but of the humoral immune responses as well.

Antibody Formation↗
PubMed2005

Virus infection-associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF-alpha/LTalpha.

We previously showed that influenza virus infection of mice induces a depletion of bone marrow B lineage cells due to apoptosis of early B cells mediated by a mechanism involving TNF-alpha/LTalpha. Here we demonstrate that this effect is also observed with acute lymphocytic choriomeningitis virus (LCMV) infection and resulted in a deficiency of both splenic transitional B cells and mature follicular B cells. To determine whether there was an associated impairment of humoral immunity, we infected mice with LCMV and 10 days later at the peak of the B cell depletion, inoculated them with influenza virus. We found that influenza virus-specific antibody titers were dramatically reduced in mice recovering from LCMV infection compared to those in mice infected with influenza virus alone. Further, we showed that there was no reduction of the influenza virus-specific antibody response in LCMV-infected TNF-alpha/LTalpha-deficient mice, suggesting that TNF-alpha/LTalpha-mediated effects on bone marrow and/or peripheral lymphocytes were responsible for the observed impairment in humoral immunity. These results show that the TNF-alpha/LTalpha production induced following infection with diverse viruses has detrimental effects on early B cells in the bone marrow, and may be among the factors that lead to the severely compromised humoral immunity observed to subsequent heterologous infections.

Animals↗
PubMed2004

Intranasal immunization with liposome-encapsulated plasmid DNA encoding influenza virus hemagglutinin elicits mucosal, cellular and humoral immune responses.

BACKGROUND: Influenza viral infections are a significant global public health concern due to the morbidity and mortality associated with acute respiratory disease, associated secondary complications and pandemic threat. Currently, the most effective preventative measure is an annual intramuscular (i.m.) injection of a trivalent vaccine. Intramuscular immunization induces strong systemic humoral responses but not mucosal immune responses which are important in the first line of defense against influenza. OBJECTIVES: A plasmid encoding influenza A/PR/8/34 (H1N1) hemagglutinin (HA; pCI-HA10) was evaluated with respect to the mucosal, cellular and humoral immune responses generated and to its efficacy in protection against a challenge with a lethal dose of influenza. STUDY DESIGN: BALB/c mice were immunized with pCI-HA10 DNA or liposome-encapsulated pCI-HA10 by either an intranasal (i.n.) or i.m. route. Sera and bronchoalveolar lavage (BAL) fluid were collected at various times and evaluated for HA-specific IgG and IgA antibodies and T cells, isolated from draining lymph nodes and spleens, were analyzed for their proliferative ability. Immunized mice were challenged with a lethal dose (5LD(50)) of influenza and monitored for survival. RESULTS AND CONCLUSIONS: Intranasal immunization with liposome-encapsulated pCI-HA10 stimulated both IgG and IgA humoral responses and increased IgA titers in BAL fluid, whereas immunization with naked pCI-HA10 had no effect on the antibody response. Intramuscular immunization with both naked and liposome-encapsulated pCI-HA10 elevated serum IgG levels, but had no effect on IgA levels in either the serum or BAL fluid. Both i.n. and i.m. administration of HA vaccine (naked and liposome-encapsulated) elicited T cell proliferative responses. These results suggest that i.n. administration of liposome-encapsulated HA-encoding DNA is effective at eliciting mucosal, cellular and humoral immune responses. Mice immunized i.n. were able to withstand a lethal challenge of influenza virus, confirming that the immune responses mediated by the vaccine were protective.

Administration, Intranasal↗
PubMed1991

[Interrelations of cellular and humoral immune response and different doses of sheep erythrocytes in mice].

In experiments on CBA and C57BL/6 mice the generation of antibody-forming cells respectively either in the popliteal lymph nodes or spleen as well as a rate of delayed type hypersensitivity response (DTHR) on the background of subcutaneous (into foot) or intraperitoneal injection of different doses of sheep erythrocytes (from 10(4) to 10(8)) have been studied. In so doing two types of immune response can be isolated on the dependence upon the sensitivity threshold to antigen of DTHR and humoral immunity. Thus in C57BL/6 mice the antigen threshold for DTHR is of one time (in intraperitoneal immunization) or of a two times (in subcutaneous) lower order than for antibody response. In CBA line mice under subcutaneous immunization there can be seen quite an opposite picture while intraperitoneal immunization causes exact correlation of antigen threshold for cellular and humoral immune response.

Animals↗