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Results for “Immunity, Humoral”

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PubMed2003

Comparison of humoral immune responses in dairy heifers vaccinated with 3 different commercial vaccines against bovine viral diarrhea virus and bovine herpesvirus-1.

A randomized clinical trial was conducted to compare the humoral immune response to 3 different commercial vaccines in dairy heifers housed in 3 different dairy farms in Quebec. All heifers were seronegative to type 1 bovine viral diarrhea virus (BVDV) (Singer strain), type 2 BVDV (NVSL 125c strain), and bovine herpesvirus-1 (BHV-1) at the beginning of the trial. In addition, control heifers in group 1 remained seronegative to the 2 viruses till the end of the trial. Significant differences in humoral immune responses occurred among the 3 commercial vaccines at 4 weeks and 6 months following vaccination. The vaccine in group 2 elicited higher mean antibody titers and seroconversion rates to both type 1 and type 2 BVDV than that in groups 3 or 4. Vaccines in groups 2 and 3 induced higher mean antibody titers to BHV-1 than did the vaccine in group 4.

Animals↗

PubMed2000

Expression of human complement receptor 2 (CR2, CD21) in Cr2-/- mice restores humoral immune function.

Complement receptor type 2 (CR2, CD21) is expressed by both human and murine B cells and has been demonstrated to play a pivotal role in the humoral immune response. We have reconstituted Cr2-/- mice with an 80-kb human genomic fragment (designated P1-5) containing the full-length human CR2 (hCR2) gene. Transfection of P1-5 into the mouse A20 B cell line confirmed that it would direct expression of the hCR2 protein in mouse B cells. Immunoprecipitation analysis in these cells revealed that hCR2 coassociates with mouse CD19. After creation of transgenic mice using P1-5, we found significant expression of hCR2 on peripheral blood and splenic B cells by flow cytometric analysis. RT-PCR analysis of tissues and purified cell populations from transgene-positive mice revealed that hCR2 expression was restricted to B cells and the spleen in a pattern that matches mouse CR2. To rigorously assess the functional capabilities of hCR2, the transgene was bred onto Cr2-/- mice, which have a notable defect in response to SRBC Ag. We found that Cr2-/- mice expressing hCR2 had a substantial restoration of the humoral immune response to SRBC as compared with nontransgenic Cr2-/- littermate controls. Overall, this study suggests that hCR2 is able to substitute for mouse CR2 in the murine immune system. Therefore, hCR2-transgenic mice offer a valuable model system to further examine immunologic roles as well as structure-function relationships important for hCR2 function in primary cells in vivo.

Animals↗

PubMed1995

Possible incorporation of an immunotoxicological functional assay for assessing humoral immunity for hazard identification purposes in rats on standard toxicology study.

The objective of this study was to examine the feasibility of conducting an immunotoxicological assay for assessing humoral immunity in rats on standard toxicology study. Male CD rats were untreated or dosed intraperitoneally daily for 30 or 90 days, excluding weekends, with vehicle or 2 mg/kg cyclophosphamide (CY). Six days prior to sacrifice, selected rats were injected intravenously with sheep red blood cells (SRBC). One day prior to necropsy, blood samples for hematological and clinical chemical measurements were collected from each rat. On the day of necropsy standard protocol tissues were collected, weighed, processed to slides, and examined microscopically. One-half of each spleen was used to prepare a single cell suspension in order to assess spleen cell numbers. Serum was analyzed for anti-SRBC IgM antibody using an enzyme-linked immunosorbent assay. A second set of studies was performed to examine further the effect of SRBC administration on lymphoid organ weights using 30- and 90-day study age-equivalent naive male CD rats. Exposure of animals to 2 mg/kg CY for 30 or 90 days resulted in a 28% and 61% decrease, respectively, in SRBC-specific serum IgM levels. CY treatment also caused mild alterations in some leukocytic parameters, with significant decreases of 35% and 33% in white blood cell and lymphocyte counts, respectively, observed in 30-day CY-treated animals receiving SRBC. Injection of SRBC alone did not alter hematological or clinical chemistry parameters. With the expected exception of the spleen (increased number and size of germinal centers), administration of SRBC did not significantly alter the weights or morphology of routine protocol tissues. Furthermore, administration of SRBC did not mask the immunosuppressive effects of CY treatment under the conditions of this study. Based on our preliminary findings, a functional assay for assessing humoral immunity may be conducted in animals on standard toxicology study.

Animals↗

PubMed1987

Suppression of the vitro humoral immune response of mouse splenocytes by benzo(a)pyrene metabolites and inhibition of benzo(a)pyrene-induced immunosuppression by alpha-naphthoflavone.

Several investigators have demonstrated that the humoral immune response of mice and splenocyte cultures was suppressed with benzo(a)pyrene [B(a)P] exposure. The mechanism of the B(a)P immunosuppression, however, has not been established. Since reactive metabolites of B(a)P, rather than the parent compound, have been shown to mediate the carcinogenic effects of B(a)P, it was hypothesized that the immunosuppression produced by B(a)P may also be mediated by its reactive metabolites. The objective of this investigation was to examine the role of B(a)P metabolism in the B(a)P-induced suppression of the in vitro humoral immune response. This was addressed by first determining if various B(a)P metabolites are capable of inhibiting the generation of antibody-forming cells (AFC) of splenocyte cultures. Addition of B(a)P or B(a)P-7,8-diol (2 X 10(-5) M) to splenocyte cultures produced a similar dose-dependent suppression of the in vitro T-dependent AFC response to sheep red blood cells. In contrast, decreases in the AFC response and cell viability of cultures exposed to the 4,5-diol or 9,10-diol were only observed at 2 X 10(-5) M. Exposure of cultures to 3-hydroxy-B(a)P resulted in a significant decrease in the AFC response at 2 X 10(-6) and 2 X 10(-5) M. Slight decreases in the AFC response were observed with the addition of B(a)P-4,5-epoxide or B(a)P-6,12-dione at 2 X 10(-6) M, whereas a dramatic decrease in the AFC response, as well as a 45% decrease in cell viability, was obtained at 2 X 10(-5) M. The second objective was to examine the effects of the cytochrome P-450 inhibitor, alpha-naphthoflavone (ANF), on the B(a)P- and B(a)P-7,8-diol-induced suppression of the in vitro AFC response. Exposure of splenocyte cultures to 2 X 10(-5) M ANF did not affect the AFC response. Coincubation of splenocytes with ANF was observed to attenuate the suppressive effects of B(a)P and B(a)P-7,8-diol. This concentration of ANF was observed to inhibit the metabolism of [3H]B(a)P by splenocyte cultures to water soluble metabolites. Moreover, B(a)P metabolism by splenic microsomal preparations of untreated mice was inhibited by ANF. These findings suggest that the B(a)P-induced suppression of the in vitro AFC response is mediated by B(a)P metabolites generated by cytochrome P-450 present within splenocytes.

Animals↗

PubMed2002

Humoral immunity and bronchiectasis.

Bronchiectasis is a common complication of primary antibody deficiency but the incidence of antibody deficiency as an underlying cause of bronchiectasis is largely undefined. In this study the humoral immune status of a cohort of bronchiectatic patients was investigated to detect the frequency of significant antibody deficiency and to determine the extent of immunological investigation which is appropriate for routine assessment of bronchiectasis patients. Fifty-six out-patients (with a mean age of 59.6 years) had serum immunoglobulins, IgG subclasses and specific antibodies to capsular polysaccharides of Haemophilus influenzae and Streptococcus pneumoniae measured. Where specific antibody -levels were low, where possible, appropriate immunization with pneumococcal or conjugated Haemophilus polysaccharide vaccines was offered and the responses quantified. Three of 56 patients had low total serum IgG levels. Thirteen of 56 had deficiencies of either a single IgG subclass or combinations of two or more subclasses, with IgG4 being most frequently implicated (9/56). Twenty-nine of 56 had low basal specific polysaccharide antibody levels. Test immunization, where performed, produced satisfactory responses in all cases except one, where a specific defect of responsiveness to pneumococcal polysaccharide was identified. This study indicates that antibody deficiency is an uncommon aetiological/underlying factor in the causation of bronchiectasis beyond the fourth decade and that detailed investigation of humoral immune status as a routine in bronchiectasis patients, at least at this age, is not generally justified.

Adult↗

PubMed1979

Stimulation of humoral immunity by peptidoglycan monomer from Brevibacterium divaricatum.

Peptidoglycan monomer (PGM), a water soluble and nontoxic disaccharide pentapeptide unit obtained from Brevibacterium divaricatum, was administered intravenously into mice, and the humoral immune response to sheep erythrocytes was assayed by means of Jerne's technique for plaque-forming cells (PFC) in the spleen. The PFC response was evidently stimulated. The counts were increased to practically the same extent over a great range of doses of PGM (from 25 to 1600 microgram per animal), and the effect was present in the mice immunised with optimal, as well as in those immunised with suboptimal, doses of antigen. The magnitude of the immunostimulation depend only on the timing of PGM administration: it was maximal if PGM was injected 1 or 2 days after the antigen. In vitro, in a 4-day culture of spleen cells, PGM did not stimulate PFC formation. We conclude that stimulation of the humoral immune response to sheep red blood cell antigens by PGM probably occurs without cell multiplication and probably involves more than simply a contact of immunocompetent cells with PGM.

Adjuvants, Immunologic↗

PubMed1999

Humoral immune responses induced by Gymnorhynchus gigas extracts in BALB/c mice.

The aim of this study was to determine if the plerocercoid larvae of Gymnorhynchus gigas, a common cestode of the ray's bream (Brama raii), possess antigenic compounds potentially capable of provoking anaphylactic episodes. A murine experimental model, using BALB/c mice, was developed to study the humoral immune response induced by G. gigas extracts. A highly specific humoral immune response was detected and cross-reactions were not observed between parasite and host antigens. The presence of IgM and IgG3 levels suggest the presence of thymus-independent antigens in the parasitic extract. The IgG antibody class showed the highest levels, with the IgG1 the predominant subclass. These IgG1 levels are in accordance with the supposed presence of a type I allergic reaction after the ingestion of G. gigas plerocercoids parasitizing fish, as well as inducing anaphylaxia in fish. These results indicate that somatic products released from ingested larvae of G. gigas could induce the development of a Th2 response capable of causing allergic disorders.

Anaphylaxis↗

PubMed2002

The effects of ochratoxin/aluminosilicate interaction on the tissues and humoral immune response of broilers.

This study aimed to evaluate the effect of dietary ochratoxin, in the presence or absence of aluminosilicate, on the histology of the bursa of Fabricius, liver and kidneys, and on the humoral immune response of broilers vaccinated against Newcastle disease virus. The exposure of birds to 2 p.p.m. ochratoxin, in the presence or absence of aluminosilicate, reduced their humoral immune response and the number of mitotic cells in the bursa. The relative weight of the livers of the birds exposed to this toxin was increased and, microscopically, there was hepatocyte vacuolation and megalocytosis with accompanying hyperplasia of the biliary epithelium. The kidneys showed hypertrophy of the renal proximal tubular epithelium, with thickening of the glomerular basement membrane. Aluminosilicate did not ameliorate the deleterious effects of the ochratoxin.

Aluminum Silicates↗

PubMed1982

Progressive myoclonus epilepsy is not accompanied by humoral immune response within the central nervous system.

CSF and serum from five patients with progressive myoclonus epilepsy taken on two occasions with about one month's interval were examined for intrathecal humoral immune response. The CSF IgG and IgA index values were normal, and no oligoclonal bands were detectable by agarose electrophoresis or polyacrylamide isoelectric focusing (IEF). Immunofixation of IEF separated IgG with four different viruses as possible antigens, and autoradiography did not reveal any intrathecal antibody production. In contradiction to previous reports, no evidence was obtained for a local humoral immune response in progressive myoclonus epilepsy.

Adult↗

PubMed1988

Humoral immune responses within the lung of bone marrow transplant recipients studied by bronchoalveolar lavage.

We investigated 20 bone marrow transplant recipients with pneumonitis using bronchoalveolar lavage (BAL) to assess the humoral immune response in the lung. We measured the levels of total IgG, IgM and IgA in bronchoalveolar lavage fluid and serum, and albumin measurements were used to correct for simple diffusion of immunoglobulins from serum into the lung. We found evidence for the local production of immunoglobulins G, M and A in 15 patients. This was independent of the cause of the pneumonitis. We also found that, although seven patients who recovered from their pulmonary problem had evidence of considerable local production of immunoglobulin, eight patients who died were also producing immunoglobulins in the lung. Death due to pneumonitis in BMT recipients cannot, therefore, be ascribed to a failure of the local humoral immune response.

Adolescent↗

PubMed2006

Evaluation of the humoral immune response in BALB/c mice immunized with a naked DNA vaccine anti-methicillin-resistant Staphylococcus aureus.

Methicillin-resistant Staphylococcus aureus (MRSA) is the major pathogen involved in nosocomial infections, leading to high rates of morbidity and mortality in hospitals worldwide. The methicillin resistance occurs due to the presence of an additional penicillin-binding protein, PBP2a, which has low affinity for beta-lactam antibiotics. In the past few years, vancomycin has been the only antibiotic option for treatment of infections caused by multiresistant MRSA; however, reports of vancomycin-resistant strains have generated great concerns regarding the treatment to overcome these infections. In the present study, we report preliminary results regarding the humoral immune response generated in BALB/c mice by two different doses of naked DNA vaccine containing an internal region, comprising the serine-protease domain, of the PBP2a of MRSA. The immunization procedure consisted of four immunizations given intramuscularly within 15-day intervals. Blood was collect weekly and anti-PBP2a-specific antibodies were screened by ELISA. BALB/c mice immunized with DNA vaccine anti-PBP2a have shown higher antibody titers mainly after the fourth immunization, and intriguingly, no correlation between the humoral immune response and DNA dose was observed. Our results suggest that the DNA vaccine anti-PBP2a induced an immune response by production of specific antibodies anti-MRSA in a non-dose-dependent manner, and it could represent a new and valuable approach to produce specific antibodies for passive immunization to overcome MRSA infections.

Animals↗

PubMed2002

Humoral immune response to recombinant adenovirus and adeno-associated virus after in utero administration of viral vectors in mice.

Adenovirus and adeno-associated virus vector-mediated gene delivery is limited by the induction of a humoral immune response that prevents readministration. To determine whether viral delivery in the "preimmune" fetus would produce dose- or time-dependent tolerance, we evaluated the humoral immune response after sequential pre- and postnatal virus administration. We evaluated six injection route and viral dose combinations of adenovirus (intra-amniotic, intrahepatic, and intramuscular injection at 4 x 10(8) and 2 x 10(9) particles/fetus) at d 15 postconception (p.c.); three route and dose combinations at d 13 p.c. (intramuscular injection at 1 x 10(8), 3 x 10(8), and 5 x 10(8) particles/fetus); and one route and dose combination of adeno-associated virus (intramuscular at 2.5 x 10(10) genome copies/fetus) at d 15 p.c. In utero injection of either viral vector at any route and dose combination resulted in the production of low titers of neutralizing antivirus and antitransgene (beta-galactosidase) antibodies. This primary immune response only partially blocked transgene expression after the readministration of viral vectors postnatally. However, delivery of the virus postnatally triggered an immune response that completely blocked transgene expression after a third viral injection. Together, these results suggest that, for B6/129 F1 mice, in utero injection of recombinant adenovirus or adeno-associated virus between d 13 and 15 p.c. does not induce tolerance to the viral vector or transgene product.

Adenoviridae↗

PubMed2001

Human and murine humoral immune recognition of multiple peptides from Schistosoma mansoni glyceraldehyde 3-P dehydrogenase is associated with resistance to Schistosomiasis.

Schistosoma mansoni glyceraldehyde 3-phosphate dehydrogenase (SG3PDH) is a target of cellular and humoral immune responses of Brazilian and Egyptian subjects putatively resistant to reinfection with S. mansoni. In an aim to develop a safe, stable and effective vaccine based on this promising molecule, six peptides derived from its primary sequence were selected based on the lowest homology to human G3PDH. The synthetic peptides were tested by ELISA against plasma of humans putatively susceptible or resistant to reinfection with S. mansoni or S. haematobium following chemotherapeutic cure of previous infection. Repeat experiments indicated that the six peptides bear human B-cell epitopes that bind immunoglobulin (Ig)M, IgG1 and IgG3 antibodies. Resistance to reinfection appeared to be significantly associated with humoral immune responses to multiple peptides. This contention was supported by studies in the murine model, whereby we examined the B cell immune responses of Swiss and inbred BALB/c and C57BL/6 mice immunized with recombinant SG3PDH (rSG3PDH) to the six SG3PDH-derived peptides. The serum antibodies of rSG3PDH-immunized Swiss mice were directed to only one of the six peptides tested by ELISA. Antibodies from rSG3PDH-immunized C57BL/6 and BALB/c mice bound, respectively, to four and six out of six peptides. In contrast to Swiss mice, immunization of C57BL/6 and BALB/c mice with rSG3PDH induced protection against challenge cercariae which reached the level of significance (P < 0.05) for BALB/c mice. The data together indicate that host recognition of multiple peptides of a candidate vaccine antigen is necessary for the expression of its ability to contribute to protective immunity against Schistosomiasis.

Adult↗

PubMed2002

Induced humoral immunity and vaccination against major human fungal pathogens.

Protection against fungal pathogens can theoretically be elicited by vaccines that stimulate humoral or cellular immunity, or both. There is conclusive evidence that humoral immunity can modify the course of infection against certain pathogenic fungi such as Candida albicans and Cryptococcus neoformans. However, for other fungi, such as Aspergillus fumigatus, the notion that humoral immunity contributes to host defence is unproven. Attempts to evaluate the potential efficacy of humoral immunity using immune sera are often inconclusive, whereas consistent results can be obtained with monoclonal antibodies. Protective monoclonal antibodies can be used to identify antigens that induce useful humoral responses.

Animals↗

PubMed2000

Mucosal humoral immune response to CagA shows a high prevalence in patients with gastric MALT-type lymphoma.

In the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT)-type lymphoma, CagA-positive Helicobacter pylori strains have been suspected of making a significant contribution. To investigate this hypothesis in more detail, the mucosal humoral immune response of 15 patients with gastric MALT-type lymphoma was examined in the tumor and in the tumor-free gastritis of the same patient. Mononuclear cells from different sites (antrum, corpus, lymphoma) were cultured. Culture supernatant and serum of the same patient were used for immunodetection of CagA. All patients displayed an immune response to CagA in the tissue-culture supernatants. Although the humoral immune response in the tumor was restricted to a very few H. pylori antigens, antibodies directed against CagA protein were found in most patients. The immune response to CagA in nearly all lymphoma patients--not only in the serum, but also in the mucosa, including the tumor site--support the hypothesis that CagA is involved in the pathogenesis of gastric MALT-type lymphoma.

Antibody Formation↗

PubMed2004

Humoral immune response elicited by plasmid DNA containing HGV E2 gene fragment.

In order to study the feasibility of E2 gene fragment of hepatitis virus G(HGV) as a component of DNA vaccine against the hepatitis virus G infection, a 559bp DNA fragment encoding HGV E2 was cloned into plasmid pCMV-S from pThioHis-E2 in the same reading frame with HBsAg gene to form a recombinant plasmid named pCMV-S-E2. BALB/c mice of Kunming strain were immunized with purified plasmid DNA of pCMV-S-E2 by intra-muscularly inoculation. The immunizations were boosted twice at an interval of 14 days. The whole blood was collected from mice orbit on the day-8 after the last boost. Mice sera were screened by ELISA to determine the humoral immune response using E2-GST fusion protein as the immobilized antigen and the sera from mice immunized with pCMV-S as control. The result indicated that the immunization with plasmid DNA of pCMV-S-E2 could induce quite strong humoral immune response.

Animals↗

PubMed1984

Derangement of humoral immune system in nondialyzed uremic patients.

To evaluate the humoral immune system in patients with chronic renal failure, a cytological approach was taken. The uremic lymphocytes and their subsets in the peripheral blood were quantitated and their functions studied. In order to exclude the possible effects of extra-uremic factors, the lymphocytes were obtained from the uremic patients with serum creatinine levels of 8 mg/dl or more, and who had been submitted neither to blood transfusions nor dialysis therapy. Absolute numbers of PBL, T cells, B cells, null cells and double marker cells were decreased in uremic patients compared to healthy controls (p less than 0.001), although the percentages of each cell subset of the patients were the same as with the healthy controls. In vitro plaque forming cell responses and DNA synthesis by uremic lymphocytes, stimulated with pokeweed mitogen, were significantly lower than those of the healthy controls. These data point to B lymphocyte as well as T lymphocyte dysfunction in uremia, which may be causally related to the uremic state itself.

Adult↗

PubMed1991

Humoral immune response of normal rhesus monkeys during primaquine administration.

Humoral immune response of normal rhesus monkeys was studied after giving a standard dose of primaquine. The drug did not effect the level of complement (C3) and its haemolytic activity. Levels of Immunoglobulin i.e. IgG, IgM & IgA and number of immunoglobulin secreting cells also remained unaffected. Results of this study suggested that primaquine did not suppress the immune status of the host and could be given safely to the malaria patients.

Animals↗