Neutralization of human immunodeficiency virus type 1 (HIV-1) mediated by parotid IgA of HIV-1-infected patients.
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Infection with human immunodeficiency virus type 1 (HIV-1) has been shown to elicit a serum antibody response with neutralizing activity against T cell line-adapted HIV strains and primary HIV-1 isolates. Mucosal surfaces are the primary route of HIV-1 infection. Evidence is presented here for the presence of HIV-neutralizing antibodies in secretions. Infection of mucosal cells with HIV stimulates systemic and mucosal immune responses and results in the generation of neutralizing antibodies. Serum IgG and IgA neutralize HIV-1MN infection of susceptible T cell lines; serum IgG inhibits more effectively. Mucosal IgA purified from parotid saliva of HIV-1-seropositive individuals could neutralize both a T cell line-adapted strain and a primary isolate. The neutralizing activity of IgA was not directed against the anti-third-variable-loop or the anti-ELDKWA epitope. Thus, the specificity of mucosal IgA for HIV-1 neutralization epitopes remains to be determined and may provide insight into development of a mucosal vaccine. (+info)
Immunization with a Pseudomonas aeruginosa elastase peptide reduces severity of experimental lung infections due to P. aeruginosa Or Burkholderia cepacia.
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Pseudomonas aeruginosa and Burkholderia cepacia produce metalloproteases that effect lung injury. Two epitopes (peptides 15 and 42) previously identified on P. aeruginosa elastase induce the production of antibodies that neutralize protease activity. The effects of immunization with synthetic peptides based on these epitopes on experimental lung infections due to P. aeruginosa or B. cepacia were examined. Rats were immunized with peptides conjugated to keyhole limpet hemocyanin or tetanus toxoid before infection. Immunization with peptide 15 (pep15) resulted in a decrease in total cells and polymorphonuclear leukocytes in bronchoalveolar lavage (BAL) fluid and a 50%-70% decrease in lung histopathologic changes, compared with findings in controls. Immunization with peptide 42 decreased cells in BAL fluid but did not decrease lung pathologic changes. Immunization with pep15 alone was just as effective in protecting against lung injury as immunization with a combination of both peptides. These studies suggest that immunization with pep15 can reduce the severity of lung infections due to P. aeruginosa or B. cepacia. (+info)
Cellular aspects of selective IgA deficiency.
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Five patients with no detectable serum IgA (less than 20 mug/ml) and one patient with low serum IgA were compared to normal subjects. The number of circulating E-RFC was normal as was the lymphocyte DNA synthesis induced by PHA, Con A, and streptokinase-streptodornase. The patients had normal numbers of IgA-bearing lymphocytes and normal or increased numbers of B cells. Purified anti-immunoglobulin antibodies specific for IgG, IgA and IgM induced a normal lymphocyte DNA synthesis as did PWM. The patients' lymphocytes were able in vitro to transform into actively secreting IgA plasmocytes. This transformation was determined by counting the IgA and immunoglobulin-containing cells and then measuring the IgA and IgG secretion in the cultures. In some patients PWM was selectively suppressive in IgA B-cell transformation into IgA secreting cells; in the other patients PWM had no effect on the IgA B-cell differentiation. PWM enhanced the IgG secretion in the patients' cultures as well as IgA and IgG secretion in the normal controls. (+info)
Correlations between antibody immune responses at different mucosal effector sites are controlled by antigen type and dosage.
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Monitoring specific secretory immunoglobulin A (IgA) responses in the intestines after mucosal immunization or infection is impeded by the fact that sampling of small intestinal secretions requires invasive methods not feasible for routine diagnostics. Since IgA plasma cells generated after intragastric immunization are known to populate remote mucosal sites as well, secretory IgA responses at other mucosal surfaces may correlate to those in the intestines and could serve as proxy measures for IgA secretion in the gut. To evaluate the practicability of this approach, mice were immunized intragastrically with 0.2, 2, and 20 mg of ovalbumin plus 10 microg of cholera toxin, and the antigen-specific local secretory IgA responses in duodenal, ileal, jejunal, rectal, and vaginal secretions, saliva, urine, and feces, as well as serum IgG and IgA responses were analyzed by enzyme-linked immunosorbent assay. Correlation analysis revealed significant relationships between serum IgG and IgA, urinary IgA, salivary IgA, and secretory IgA in duodenal, jejunal, ileal, and rectal secretions for the 0.2-mg but not for the 20-mg ovalbumin dose. Fecal samples were poor predictors for intestinal antiovalbumin IgA responses, and no correlations could be established for cholera toxin, neither between local anti-cholera toxin levels nor to the antiovalbumin responses. Thus, specific IgA in serum, saliva, or urine can serve as a predictor of the release of specific IgA at intestinal surfaces after intragastric immunization, but the lack of correlations for high ovalbumin doses and for cholera toxin indicates a strong dependency on antigen type and dosage for these relationships. (+info)
We have previously shown that Salmonella enterica serovar Typhimurium expressing the hagB hemagglutinin gene from Porphyromonas gingivalis can induce primary and recall immune responses in serum and secretions in mice; however, the longevity of memory induced by oral Salmonella carriers has not been adequately demonstrated. In this study, we examined the capacity of mice to mount a recall response 52 weeks after primary immunization. Recall responses were seen in serum immunoglobulin G (IgG) and IgA following boosting at week 52, and in most cases, they were equal to or greater than the primary responses. Significant mucosal IgA recall responses in saliva and vaginal wash were also detected following boosting at week 52. In addition, there was a considerable residual response in secretions at week 51, prior to boosting. These results indicate that oral Salmonella vectors can induce long-term memory to recombinant HagB and are particularly effective at inducing long-lasting mucosal responses as well as at inducing the capacity for mucosal recall responses. (+info)
A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria.
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The immunoglobulin A (IgA) is produced to defend mucosal surfaces from environmental organisms, but host defenses against the very heavy load of intestinal commensal microorganisms are poorly understood. The IgA against intestinal commensal bacterial antigens was analyzed; it was not simply "natural antibody" but was specifically induced and responded to antigenic changes within an established gut flora. In contrast to IgA responses against exotoxins, a significant proportion of this specific anti-commensal IgA induction was through a pathway that was independent of T cell help and of follicular lymphoid tissue organization, which may reflect an evolutionarily primitive form of specific immune defense. (+info)
Practolol and ocular toxicity. Antibodies in serum and tears.
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Serological studies in 22 patients presenting with ocular disease attributable to dosage with the beta-blocking agent practolol revealed a raised incidence of antinuclear antibodies. There was also a marginal increase in the incidence of antibodies to smooth muscle in the more severely affected individuals but the incidence of ther autoantibodies and levels of IgG, IgA, and IgM were within normal limits. Semi-quantitative analysis of tears from 14 of the patients showed absence or near absence in the more severely affected patients of secretory IgA, which is indicative of damage to the lacrimal gland. Other immunological parameters in the tears were normal. (+info)
Poliovirus-specific intestinal antibody responses coincide with decline of poliovirus excretion.
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Antibody responses to poliovirus type 3 were studied in fecal samples of 66 children immunized with 3 doses of enhanced-potency inactivated poliovirus vaccine (E-IPV), followed by 1 dose of monovalent oral poliovirus vaccine (OPV, type 3 Sabin). One fecal sample taken before OPV vaccination and 9 collected thereafter were tested for neutralizing antibodies by a microneutralization assay and for class-specific responses by heavy chain-capture radioimmunoassays. Both neutralizing antibody and IgA responses usually occurred during the second week and coincided with ceasing of virus excretion or a decrease in the excreted virus titer. Half of the vaccinees had received a trypsin-modified E-IPV, but their responses did not differ from those of children immunized with the regular E-IPV. These results are in agreement with the view that an intestinal antibody response, mainly consisting of IgA, may be involved in the ceasing of a primary poliovirus excretion. (+info)