Levels Of Antibody Responses Research Articles

The ability of the enzyme-linked immunosorbent assay to detect antibody against Staphylococcus aureus in milk following experimental intramammary infection.

Changes in the milk antibody levels against Staphylococcus aureus were measured at the start of an experimental intramammary instillation of either S. aureus (Study I) or Staphylococcus hyicus (Study II). A commercial enzyme-linked immunosorbent assay system was used. Twenty-one Holstein cows were enrolled in Study I and 15 Holstein cows were used in Study II. Pathogen instillation began 21 days before the start of the non-lactating period. Cows received intramammary antibiotic treatment in all quarters immediately after the last milking, the start of the non-lactating period. Lacteal secretions were collected before the start of the non-lactating period, and during the immediate postpartum period in both studies, and during the non-lactating period in Study I. Milk was cultured for mastitis pathogens and S. aureus antibody levels and somatic cell counts were determined from all samples. There was an approximate 2-week delay in the elevation in antibody levels in response to the instillation of S. aureus. Antibody levels remained elevated in cows with S. aureus intramammary infections postpartum, but were below threshold in cows where intramammary infections were cured during the non-lactating period. Antibody levels were elevated by S. hyicus intramammary infections, remained elevated for the first 12 days postpartum, but were below threshold by day 21 postpartum. Cows with incipient intramammary S. aureus infections might be misclassified as false negatives by the antibody test. However, results suggest that cows with S. hyicus intramammary infections that were not cured would not be misclassified if milk is withheld from test for the first 30 days postpartum, as recommended by the manufacturer of the test.

Collagen-induced arthritis in nonhuman primates: multiple epitopes of type II collagen can induce autoimmune-mediated arthritis in outbred cynomolgus monkeys.

To define which regions of the type II collagen (CII) molecule result in anticollagen antibody production and the subsequent development of autoantibodies in a collagen-induced arthritis (CIA) nonhuman primate model. Male and female cynomolgus monkeys (2-6 of each sex per group) were immunized with either chicken (Ch), human, or monkey (Mk) CII, or with cyanogen bromide (CB)-generated peptide fragments of ChCII emulsified in Freund's complete adjuvant. Monkeys were observed for the development of arthritis, and sera were collected and analyzed for anticollagen antibody specificity by enzyme-linked immunosorbent assay. Overt arthritis developed in all groups of monkeys immunized with intact CII and with all major CB peptide fragments of ChCII except CB8. Onset and severity of arthritis correlated best with serum anti-MkCII antibody levels. The levels of IgG autoantibody to MkCII were a result of the cross-reactivity rate of anti-heterologous CII antibodies with MkCII, which was based on the genetic background of individual monkeys rather than on sex differences. CII from several species and disparate regions of the CII molecule were able to induce autoantibody-mediated arthritis in outbred cynomolgus monkeys. The strong anti-MkCII response suggests that epitope spreading or induction of broad-based CII cross-reactivity occurred in these animals. Autoantibody levels to MkCII were higher in CIA-susceptible monkeys than in resistant monkeys, despite comparable antibody levels in response to the various immunizations of CII. These results closely parallel the type of anticollagen responses found in sera from rheumatoid arthritis patients. Perhaps this can be accounted for by similar major histocompatibility complex heterogenicity associated with an outbred population, or maybe this is a primate-specific pattern of reactivity to CII.

Collagen‐induced arthritis in nonhuman primates: Multiple epitopes of type I collagen can induce autoimmune‐mediated arthritis in outbred cynomolgus monkeys

Objective To define which regions of the type II collagen (CII) molecule result in anticollagen antibody production and the subsequent development of autoantibodies in a collagen-induced arthritis (CIA) nonhuman primate model. Methods Male and female cynomolgus monkeys (2-6 of each sex per group) were immunized with either chicken (Ch), human, or monkey (Mk) CII, or with cyanogen bromide (CB)-generated peptide fragments of ChCII emulsified in Freund's complete adjuvant. Monkeys were observed for the development of arthritis, and sera were collected and analyzed for anticollagen antibody specificity by enzyme-linked immunosorbent assay. Results Overt arthritis developed in all groups of monkeys immunized with intact CII and with all major CB peptide fragments of ChCII except CB8. Onset and severity of arthritis correlated best with serum anti-MkCII antibody levels. The levels of IgG autoantibody to MkCII were a result of the cross-reactivity rate of anti-heterologous CII antibodies with MkCII, which was based on the genetic background of individual monkeys rather than on sex differences. Conclusion CII from several species and disparate regions of the CII molecule were able to induce autoantibody-mediated arthritis in outbred cynomolgus monkeys. The strong anti-MkCII response suggests that epitope spreading or induction of broad-based CII cross-reactivity occurred in these animals. Autoantibody levels to MkCII were higher in CIA-susceptible monkeys than in resistant monkeys, despite comparable antibody levels in response to the various immunizations of CII. These results closely parallel the type of anticollagen responses found in sera from rheumatoid arthritis patients. Perhaps this can be accounted for by similar major histocompatibility complex heterogenicity associated with an outbred population, or maybe this is a primate-specific pattern of reactivity to CII.

Two cases of acute anti-GM1 antibody elevations in response to exogenous GM1 without neurological symptoms

During a study evaluating GM1 ganglioside as a possible treatment for Alzheimer's disease, two patients suffered immune responses that appeared to be limited to localized inflammation at the sites of the intramuscular GM1 injections. We determined that one patient's anti-GM1 IgM antibody titer rose from 1:400 to 1:3200 and her anti-GM1 IgG titer from 1:50 to 1:400 000 during the immune response. The second patient's titers rose from <1:50 to 1:3200 IgM and from 1:3200 to 1:400 000 IgG. These findings document that patients may experience acute rises in their anti-GM1 antibody levels in response to GM1 and that such rises may not necessarily cause significant acute clinical neuronal injury.

Conjunctival scarring in trachoma is associated with depressed cell-mediated immune responses to chlamydial antigens.

In vitro responses of peripheral blood mononuclear cells (PBMC) were measured to antigens of Chlamydia trachomatis in 29 subjects with severe conjunctival scarring and compared with responses from 29 age-, sex-, and location-matched controls from a trachoma-endemic area in The Gambia. Proliferative and interferon-gamma responses were measured against chlamydial elementary bodies, recombinant major outer membrane protein, and affinity-purified recombinant chlamydial heat shock protein 60. Serum antibody levels in response to these antigens were also compared between the two groups, and the presence of ocular chlamydial antigen and DNA was assessed. PBMC from donors with conjunctival scarring had reduced proliferative responses to chlamydial antigens but not control antigens or mitogens compared with matched controls. By contrast, subjects with scarring had significantly higher levels of anti-chlamydial IgG antibody compared with matched controls and were more likely to be harboring ocular chlamydial antigen or DNA (or both).

An investigation of the relationship between adrenal activity, social rank and immunocompetence in pregnant sows kept in different housing conditions

Measures of immune system function are important indicators of welfare. As high adrenal activity can have immunosuppressive effects, the relationships between measures of adrenal activity and immunological responses are of particular interest. In two studies of pregnant sows, adrenal activity was assessed by measuring cortisol production in response to an injection of adrenocorticotrophic hormone (ACTH). In addition, cortisol suppression following an injection with dexamethasone was examined. Immune system function was assessed by measuring serum and colostrum antibody levels in response to injection with an antigen. In 31 stall-housed sows, adrenal activity was not correlated with levels of serum antibody to tetanus toxoid. However, sows which showed the highest adrenal response to ACTH had the lowest levels of

IMMUNE RESPONSE OF MALLARD DUCKS TREATED WITH IMMUNOSUPPRESSIVE AGENTS: ANTIBODY RESPONSE TO ERYTHROCYTES AND IN VIVO RESPONSE TO PHYTOHEMAGGLUTININ-P

The ability of two in vivo tests to assay immune competence of mallard ducks (Anas platyrhynchos) treated with various immunomodulatory agents was examined. Skin responses to phytohemagglutinin-P (PHA-P) injected intradermally and serum antibody levels produced in response to sheep red blood cells (SRBC) were measured. As measured by the skin response to PHA-P, ducks injected intramuscularly with cyclophosphamide or cyclosporine did not respond differently from control-injected ducks. Dexamethasone injected intramuscularly significantly suppressed the skin response to PHA-P. As measured by antibody levels in response to SRBC, ducks injected intramuscularly with cyclophosphamide responded with antibody titers similar to controls. Cyclosporine injected intramuscularly reduced the level of immunoglobulin (Ig) G significantly in one of two experiments. Dexamethasone injected intramuscularly reduced peak total and IgG titers. These experiments provide information on the viability of these two in vivo tests to reflect immune competence of mallard ducks.

Fluctuations in crevicular and salivary anti-A. viscosus antibody levels in response to treatment of gingivitis.

Experimental gingivitis studies support a pathogenic rôle for Actinomyces viscosus because of its numerical predominance in disease-associated plaques. The aims of the present investigation were to quantify specific crevicular IgG against A. viscosus before and after conventional gingivitis treatment and to determine whether salivary IgA and IgG against A. viscosus and A. naeslundii would be affected concomitantly. 6 subjects with generalized gingivitis were selected. Examinations were made before and after treatment and included collection of unstimulated saliva, paraffin-stimulated saliva and crevicular material as well as measurements of clinical parameters. The immunoglobulins were estimated by an ELISA assay using whole bacterial cells as antigen. Crevicular IgG against A. viscosus WVU 627 was demonstrated in pre- and post-treatment samples with a tendency towards increased values in the post-treatment samples. Salivary IgA and IgG against A. viscosus were also demonstrated in pre- and post-treatment samples. There were tendencies towards increased IgA values for paraffin-stimulated saliva and increased IgG values for unstimulated saliva in the post-treatment samples. Salivary IgA and IgG values against A. naeslundii ATCC 12104 were either not detected or barely detectable in both pre- and post-treatment samples. A. naeslundii B 74 IgG values were also rather low. As for A. viscosus WVU 627, anti-B 74 IgA values demonstrated a post-treatment increase for most subjects, especially for unstimulated saliva for which all post-treatment values were elevated. It is interesting to note that saliva samples showed changes similar to crevicular material, considering that salivary IgA is most likely derived from a different source. Together, elevated crevicular and salivary antibody concentrations might account for some of the beneficial effects of periodontal therapy by scaling.

Assessment of antibody production in sex-linked and autosomal dwarf chickens

The humoral immune response was examined in two dwarf and one control strain of Single Comb White Leghorn chicks. Circulating antibody levels in response to immunization with varying concentrations of sheep erythrocytes were determined following primary immunization and again following a secondary antigen challenge. The males of the sex-linked dwarf strain produced significantly less antibody to lower antigen dosages in both the primary and secondary response but as antigen dose was increased the humoral response was no longer depressed below that of the controls. The antibody response of females carrying the dw gene was not significantly impaired over the entire antigen dose range nor was that of either sex of the autosomal dwarf strain. Similar results were obtained when the numbers of splenic plaque-forming cells (PFC's) were examined. However, in this assay both the males and females of the sex-linked dwarf strain demonstrated significantly impaired plaque-forming activity. No differences were found between the control and autosomal dwarf strains in their ability to generate PFC's.