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Humoral immune response of foals to experimental infection with Rhodococcus equi.

Humoral immune response to Rhodococcus equi in experimentally infected foals was studied with the enzyme-linked immunosorbent assay (ELISA) method. Class-specific antibodies were measured by ELISA in the sera of foals after intratracheal or oral inoculation with R. equi ATCC 6939 or T 48 and in the lung washings of a foal after intratracheal inoculation or of normal horses. After intratracheal or oral inoculation with R. equi, serum antibodies were first detected in immunoglobulin G (IgG) followed by IgM and IgA classes, but significant levels of IgM and IgA developed only in the foal infected intratracheally with R. equi T 48. Only the foal infected intratracheally with T 48 developed pneumonia. Anti-R. equi IgG and IgA antibodies appeared in lung washings of the intratracheally infected foal. There were differences in the antibody response to R. equi among the intratracheally infected foals, the orally infected foal and the naturally infected foal. These results suggest that the humoral immune response to R. equi may be affected by the type of R. equi strain and the route and extent of R. equi exposure.

Actinomycetales Infections↗

Duration and specificity of humoral immune responses in mice vaccinated with the Alzheimer's disease-associated beta-amyloid 1-42 peptide.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by overproduction of beta-amyloid (Abeta), which is formed from amyloid precursor protein (APP), with the subsequent pathologic deposition of Abeta in regions of the brain important for memory and cognition. Recently, vaccination of murine models of AD that exhibit Abeta deposition has halted or delayed the usual progression of the pathology of AD. Our group has demonstrated that vaccination of a doubly transgenic mouse model (expressing mutant APP and presenilin-1) with the Abeta 1-42 peptide protects these mice from the memory deficits they would ordinarily develop. This report further characterizes the Abeta 1-42 peptide vaccine in mice. Anti-Abeta response time course analysis indicated that at least three vaccinations (each 100 microg) were necessary to elicit a significant anti-Abeta titer. Subsequent vaccinations resulted in half-maximal antibody titers of at least 10,000, and these titers were maintained for at least 5 months after the final boost. Peptide binding competition studies indicated that the highest humoral responses are generated against the N terminus of the Abeta peptide. Also, measurement of specific murine Ig isotypes in Abeta-vaccinated mice demonstrated a predominant IgG(1) and IgG(2b) response, suggesting a type 2 (Th2) T-helper cell immune response, which drives humoral immunity. Finally, lymphocyte proliferation assay experiments using Abeta peptides and splenocytes from vaccinated mice demonstrated that the vaccine specifically stimulates T-cell epitopes present within the Abeta peptide.

Amino Acid Sequence↗

Gene complementation in biological crosses for humoral immune response to glutamic acid-alanine-tyrosine.

Level of humoral immune response to GAT has been associated with the MHC of chickens. Matings between two unrelated lines of chickens with low antibody response to GAT (G-B1 and S1 Line B19L) resulted in progeny that were higher responders to GAT challenge (P < .05) than either of the parental lines. Progeny of matings between two related sublines that are low responders to GAT (S1 Lines B19L and B1L) had antibody responses to GAT that were not higher than the parental lines. Progeny of the between-line cross were backcrossed to S1 B19L and G-B1 (B13) parental lines, as well as mated inter se. These matings produced F2 progeny whose GAT response was significantly associated (P < .05) with their MHC (Ea-B) type. The progeny were of three MHC types (B19B19, B19B13, and B13B13) that bound 66.6, 71.9, and 4.6%, respectively, of the GAT in a radioimmunoassay. The results from these matings suggest that MHC or MHC-linked genes, as well as genes not linked to the MHC, contribute to control of humoral immune response to GAT in the lines of chicken tested.

Amino Acid Sequence↗

[Cellular and humoral immune responses in calves after experimental infection with bovine herpesvirus 1].

Studied were some of the humoral and cellular factors of immunity with calves experimentally infected with Herpes virus 1. The clinical signs manifested by the infected calves were followed up for 10 to 12 days. The shedding of the virus through the nasal mucosa was demonstrated up to the eighth day, the peak values reached being between the 3rd and 5th day of infection. Demonstrated was blastic transformation in vitro with a phytohemagglutinin of the lymphocytes obtained from the peripheral blood prior to infection; the same phenomenon was observed also with each sample taken from the peripheral blood of the controls. Blastic transformation of lymphocytes was demonstrated also with the use of a specific antigen with the group infected from the 6th to the 15th day, with highest indices between the eighth and tenth day. This spoke of the presence of an immune response. The humoral immune response, followed up in its dynamics, was manifested by the presence of local antibodies in the infected calves first on the eighth day, and of serum antibodies on the 12th day. The results obtained point to the importance of both components of immunity with calves. It is of interest to note that the peak of the cell response set in on the eighth to ninth day of infection which coincided with the cease of virus shedding. On the other hand, the serum antibodies were demonstrated later--between the eighth and the twelfth day. This data showed that cellular immunity played a greater part in the recovery of calves in the case of a primary Herpes virus 1 infection.

Animals↗

Immunological studies with aortic and venous tissue antigens. III. Examination of cell-mediated and humoral immune response induced by human vascular antigens.

The effects of human vascular antigens on the cell-mediated and the humoral immune response were studied in guinea pigs. In animals immunized with buffer extracts of aortic and venous wall a well measurable cell-mediated and humoral immune response were developed. Between the two kinds of vascular extracts in the skin tests, migration inhibition tests and antibody-production tests a cross-reactivity was observed, whereas the induction of desoxyribonucleic acid-synthesis proved to be specific. No cellular or humoral immune response to vascular extracts was detectable in the control animals. Analysing the time-kinetics of the cell-mediated and humoral immune response it was found, that with the increased production of antibodies the cellular immune reactions did not cease until the ninth week.

Animals↗

Nucleotide actions on humoral immune responses.

Previous studies indicate the importance of dietary nucleotides in maintaining optimal cellular immunity. Our studies using murine spleen cells showed that polynucleotides significantly increase in vitro antibody production in response to T-cell-dependent antigen. They seem to exert actions on T-helper cells at antigen presentation, perhaps during cognitive cell-cell interactions. They do not augment the actions of cloned, antigen-specific, activated T-helper cells, nor do they increase antibody production in response to T-cell-independent antigen or polyclonal B-cell activation. Polynucleotides increase in vitro human immunoglobulin production in response to T-cell-dependent stimuli and antigen. Humoral immune responses to T-cell-dependent antigen were depressed in mice fed a nucleotide-free diet, but were restored by a mononucleotide-nucleoside mixture. Responses to T-cell-independent antigen remained intact in these mice. The mononucleotide-nucleoside mixture had no effect on in vitro antibody production and did not further increase humoral immune responses in mice fed regular lab chow. These results suggest that the in vivo actions of polynucleotides on humoral immune responses may reflect local immune responses, perhaps at the site of inflammation. Mononucleotides and nucleosides may be incorporated into the tissue nucleotide pool fairly rapidly in a state of relative nucleotide deficiency and help restore T-cell-dependent humoral immune responses. Our findings may further support the importance of dietary nucleotides.

Animals↗

Etiopathogenetic aspects of hepatitis A II. Specific and nonspecific humoral immune response during the course of infection.

The anti-HAV humoral immune response in the IgM, IgA, and IgG classes was analyzed weekly in 35 patients with clinically overt hepatitis A during the time of their hospitalization and 2-3 years afterward. In parallel, the dynamics of total immunoglobulins and complement C3 component (C3) levels were determined. The results suggest that the appearance of class-specific anti-HAV is compatible with the course of primary humoral immune response, with IgM and IgA anti-HAV, providing immunity in the early and intermediate phases of the infection, and IgG anti-HAV, providing immunity in the later phase. The overall appearance of anti-HAV, total immunoglobulins, and C3, do not support the view that liver injury is mediated by the humoral immune mechanisms. Instead, the hepatocyte damage is probably caused by direct viral cytotoxicity. This hypothesis is supported by a case of hepatitis A in a patient under immunosuppressive treatment.

Adolescent↗

Humoral immune response during filarial fever in Bancroftian filariasis.

Humoral immune responses against filarial parasitic infection were studied in 62 cases of acute filarial disease presenting with filarial fever with adenolymphangitis, in a community where Bancroftian filariasis was endemic, during and about one month before and after the febrile episode. Their total leucocyte and differential peripheral blood cell counts and anti-streptolysin O titre were determined and compared. Polymorphonuclear cellular responses and anti-streptolysin O titre did not show any significant alteration during and after fever. Three of 53 previously amicrofilaraemic subjects (9 of whom were initially microfilaraemic) had microfilaria in their circulation during fever, with a significant increase in their geometric mean microfilaria count. Titres of specific immunoglobulin (Ig) G and IgG4 antibody to Wuchereria bancrofti microfilarial excretory/secretory antigens (measured by enzyme-linked immunosorbent assay) decreased significantly during the fever and the lower levels were maintained one month after fever. The mean circulating immune complex level increased significantly during fever, and a significant percentage of cases demonstrated circulating filarial antigen during fever, which declined after one month, suggesting the release of filarial antigen into the circulation during fever which bound to antibodies to form immune complexes. These observations do not support the suggestion that bacterial infection is the aetiology of filarial fever. It is postulated that antigens released from parasites into the circulation during parturition by adult worms may evoke an allergic response in the host, causing periodic febrile episodes.

Animals↗

Influence of supplemental selenium on humoral immune responses in weaned beef calves.

Influence of supplemental Se on humoral immune response was measured in 60 weaned beef calves with marginal blood Se status. Calves were fed a Se-deficient diet consisting of corn silage, corn grain, and soybean meal. Blood Se concentrations, primary and secondary humoral immune responses to hen egg lysozyme inoculation, and weight gain were determined in a 70-day trial. Calves fed 20 mg of Se/kg of mineral mixture ad libitum had lower antibody responses (P less than 0.02), compared with calves fed 20 mg of Se/kg of mineral mixture and given 0.1 mg of Se and 0.22 IU of vitamin E/kg of body weight, IM, or with calves fed 80, 120, 160, or 200 mg of Se/kg of mineral mixture. Calves fed 80, 120, 160, or 200 mg of Se/kg of mineral mixture had higher (P less than 0.001) blood Se concentrations on day 70, compared with calves fed 20 mg of Se/kg of mineral mixture and given 0.1 mg of Se and 0.22 IU of vitamin E/kg of body weight, IM. Selenium supplementation had no effect on weight gain.

Administration, Oral↗

Detection of humoral immune response to Gnathostoma spinigerum in mice.

The humoral immune response to early third stage larvae (EL3) and advanced third stage larvae (AL3) of Gnathostoma spinigerum infection was studied in mice by Ouchterlony gel diffusion technique. The antibodies was detected at week 3 in mice infected with EL3 and remained up to week 10 after infection. Highest positive sample of sera were demonstrated at week 4 to week 7. Similar results were obtained from AL3 infected sera except the antibodies was found and disappeared earlier (week 2 to week 6). G. spinigerum larvae recovery from mice in both groups showed that the number of advanced third stage larvae located in muscle correlated to the peak of positive sera. No cross reaction was observed on positive sera of G. spinigerum and antigens of A. cantonensis, P. siamensis, T. spiralis, O. viverrini and A. ceylanicum. Cross reaction was shown on the G. spinigerum antigen against rat sera with angiostrongyliasis and bandicoot sera with paragonimiasis.

Animals↗

The T-dependent and T-independent humoral immune response in cobra venom treated mice.

The humoral immune response to T-dependent antigens (SRBC, DNP5BSA, DNP50BSA, DNP-KLH) and T-independent antigens (SIII, Levan, DNP-SIII, DNP-Levan) was studied by hemolytic plaque assay in mice depleted of C3 by Cobra venom treatment. Suppression of the immune response in C3 depleted animals was not restricted only to T-dependent response and also the response to some T-dependent antigens (DNP50-BSA, DNP-KLH) was not suppressed under conditions of the experiment. Results are discussed in relation to postulated exclusive role of C3 in the induction of T-dependent immune response.

Animals↗

[Effect of trypsin on the development of a humoral immune response and of delayed hypersensitivity].

Trypsin was found to stimulate the development of humoral immune response to the thymus-dependent antigen when administered simultaneously with immunization and to exert no influence on this form of immune response being injected 4 days after immunization. Trypsin fails to affect the development of humoral immune response induced by the thymus-independent antigen. Trypsin was shown to enhance the development of hypersensitivity of delayed type at administration simultaneously with the sensitizing or resolving dose of the antigen. Trypsin appeared to attenuate the antigen-specific immunosuppressing effect of lymphocytes of the hyperimmunized animal spleen.

Animals↗

Oral administration of type-II collagen peptide 250-270 suppresses specific cellular and humoral immune response in collagen-induced arthritis.

Oral antigen is an attractive approach for the treatment of autoimmune and inflammatory diseases. Establishment of immune markers and methods in evaluating the effects of antigen-specific cellular and humoral immune responses will help the application of oral tolerance in the treatment of human diseases. The present article observed the effects of chicken collagen II (CII), the recombinant polymerized human collagen II 250-270 (rhCII 250-270) peptide and synthesized human CII 250-270 (syCII 250-270) peptide on the induction of antigen-specific autoimmune response in rheumatoid arthritis (RA) peripheral blood mononuclear cells (PBMC) and on the specific cellular and humoral immune response in collagen-induced arthritis (CIA) and mice fed with CII (250-270) prior to immunization with CII. In the study, proliferation, activation and intracellular cytokine production of antigen-specific T lymphocytes were simultaneously analyzed by bromodeoxyuridine (BrdU) incorporation and flow cytometry at the single-cell level. The antigen-specific antibody and antibody-forming cells were detected by ELISA and ELISPOT, respectively. CII (250-270) was found to have stimulated the response of specific lymphocytes in PBMC from RA patients, including the increase expression of surface activation antigen marker CD69 and CD25, and DNA synthesis. Mice, fed with CII (250-270) before CII immunization, had significantly lower arthritic scores than the mice immunized with CII alone, and the body weight of the former increased during the study period. Furthermore, the specific T cell activity, proliferation and secretion of interferon (IFN)-gamma in spleen cells were actively suppressed in CII (250-270)-fed mice, and the serum anti-CII, anti-CII (250-270) antibody activities and the frequency of specific antibody-forming spleen cells were significantly lower in CII (250-270)-fed mice than in mice immunized with CII alone. These observations suggest that oral administration of CII (250-270) can suppress the cellular and humoral immune response in collagen-induced arthritis, and the simultaneous analysis of antigen-specific cellular and humoral immune responses at single-cell level will help the understanding of the oral tolerance mechanisms in CIA and the development of innovative therapeutic intervention for RA.

Administration, Oral↗

[The effects of ciprofloxacin and ofloxacin on the cellular and humoral immune response in mice].

The effects of a 7 days chemotherapy with ciprofloxacin or ofloxacin on the cellular and humoral immune responses in albino mice were studied. The non-toxic doses of the drugs (10 or 30 mg/kg/day) were used. The delayed-type hypersensitivity reaction to sheep blood cells and skin biopsy were evaluated for cellular immune response. The complement fixation method was applied for the determination of the humoral immune response. Both drugs increased the cellular and humoral immune responses.

Animals↗

Use of an adsorption enzyme immunoassay to evaluate the Haemophilus ducreyi specific and cross-reactive humoral immune response of humans.

Serodiagnosis of chancroid is limited by the cross-reactivity of Haemophilus ducreyi with Haemophilus influenzae and Haemophilus parainfluenzae. This research describes an adsorption enzyme immunoassay (EIA) that assesses the humoral immune response of North Americans and Africans to H. ducreyi. Adsorption effectively removed anti-H. influenzae and anti-H. parainfluenzae antibodies, revealing that North American control sera had no residual anti-H. ducreyi reactivity. However, African control sera still had a residual anti-H. ducreyi response. Assessment of the duration of the humoral immune response in sera from African patients with chancroid showed that the humoral antibodies persisted for up to 8 months after the diagnosis. This may explain the lack of specificity of the adsorption EIA in areas where chancroid is endemic. The detection of the humoral immune response was affected by the strain of H. ducreyi used, with indigent strains being most useful. Using H. ducreyi 35000 for Canadian sera, the sensitivity of the adsorption EIA was 100% and the specificity was 88%. For African sera, H. ducreyi strain R018 was used, and the adsorption EIA had a sensitivity of 81% and a specificity of only 23%. These data reveal that the existing humoral response in a country where chancroid is endemic differs from that in a country where it is not, and that care must be used interpreting unadsorbed humoral immune responses. The adsorption EIA approach may prove useful as an epidemiologic tool for definition of existing (past and present) levels of exposure to H. ducreyi.

Adolescent↗

[Humoral immune response in hepatic and intestinal amebiasis in children].

The various classes of immunoglobulins with antibody function against E. histolytica were studied in 8 children with amebic liver abscess and in 7 with acute intestinal amebiasis. The predominant fraction was IgG in 7 patients from the first group and in 1 from the second; this suggests a secondary type humoral immune response which implies a previous experience with E. histolytica antigens. A definitive predominance of IgM was shown in a patient with amebic liver abscess, the same as in primary humoral immune response. Humoral antibodies did not develop in the remaining 6 patients with acute intestinal amebiasis. The disparateness of the humoral immune response found in these cases make it difficult to speculate on the role of immunoglobulins in the pathogenesis or in immunologic protection in amebiasis. Possibly, the most important is the participation of cellular immunity.

Child↗

The effect of environmental temperature on immune response and metabolism of the young chicken. 3. Effect of environmental temperature on the humoral immune response following injection of sheep red blood cells.

The effect of environmental temperature on the humoral immune response of pullets following injection of sheep red blood cells (SRBC) was investigated. For this purpose four experiments were performed in two climate respiration chambers. In each experiment a standard temperature regimen of constant 25 C was maintained in one chamber. The temperature regimens in the other chamber were as follows: a constant temperature of 15 C (Experiment 1) and 35 C (Experiment 3) and a temperature, which fluctuated between 10 to 20 C (Experiment 2) and between 30 to 40 C (Experiment 4). Total haemagglutinin anti-SRBC antibody titers at Day 5 after injection were increased significantly (P less than .01) at 10 to 20 C, 35 C, and 30 to 40 C compared to the antibody titers of pullets at 25 C. 2-Mercapto-ethanol resistant antibody titers at Day 5 after injection were increased significantly (P less than .05) at 35 C and 30 to 40 C. The effect of feeding level and thermal acclimation on antibody titers was investigated within each temperature regimen. Restricted feeding at low or high temperatures increased antibody titers at Day 5 after injection. Exchange of pullets, just before injection, to low or high temperatures decreased total antibody titers at Day 5 after injection.

Acclimatization↗

Effects of dimethyl sulfoxide on humoral immune responses to acetylcholine receptors in the rat.

The effects of dimethyl sulfoxide (DMSO) on the humoral immune responses to acetylcholine receptors (AChR) were studied in rats with experimental autoimmune myasthenia gravis. DMSO was administered during primary, ongoing, and secondary phases of the immune response to AChR. Anti-AChR antibody titers were measured to determine the effect of the treatment. DMSO had pronounced effects on the humoral immune response, which differed depending on the stage of the response and the strength of antigenic stimulation. When given during an ongoing immune response, DMSO suppressed anti-AChR antibody levels by an average of 53-76%. This effect was similar whether DMSO was given by oral, rectal, or intraperitoneal routes. DMSO treatment also suppressed the anti-AChR antibody response to a weak primary antigenic stimulus to a similar extent. In contrast, when administered during a secondary or a strong primary immunization, DMSO enhanced the anti-AChR antibody response 1.7- to 2.8-fold. These results show that DMSO may either enhance or suppress humoral immune responses. Further studies will be required to analyze the cellular mechanisms underlying the actions of DMSO.

Animals↗