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Intestinal epithelial cells secrete a spectrum of chemoattractant and proinflammatory cytokines after invasion by bacteria. We suggest the novel concept that epithelial cells not only act as a mechanical barrier to invasive bacteria, but that they also signal the presence of invasive pathogens to the mucosal immune and inflammatory cells.
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Heat-labile opsonins to pneumococci in normal mammalian sera, unlike antibodies, fail to interact with the bacteria at 0 degrees C and require Ca(++) and/or Mg(++). They are readily removed from serum by antigen-antibody complexes that fix complement (C) and are inhibited by reagents that inactivate various C components. The principal heat-labile opsonin to pneumococci is activated C3 (C3(b)), but a slight enhancing effect is exerted by one or more of the late-reacting components of the hemolytic complement system (C5-C9). Since heat-labile opsonins are immunologically polyspecific, they presumably play a broad protective role in the early (preantibody) phase of acute bacterial infections.
Recent studies have shown that the sialic acid content of Sindbis virus influences both its ability to active the alternative pathway in vitro and its susceptibility to complement dependent clearance from the bloodstream in vivo. Other studies have shown that the sialic acid content of Sindbis virus is determined by the host in which it is propagated. Because individuals vary in their cell surface sialic acid content, it is possible they also vary in their ability to defend themselves against Sindbis virus infection by virtue of their ability to modify the virus sialic acid content and thereby the capacity of the virus to activate the alternative pathway. To test this hypothesis, outbred Swiss mice were injected subcutaneously with Sindbis virus. There was a significant positive correlation between the level of viremia 18 hr after infection and the sialic acid content of the host's erythrocytes. In addition, animals with erythrocyte sialic acid levels equal to or greater than the mean had a higher level of viremia than animals with erythrocyte sialic acid levels less than the mean. Finally, animals that had muscle sialic acid levels equal to or greater than the mean had a higher incidence of viremia than animals with muscle sialic acid levels less than the mean. These studies suggest that the amount of tissue sialic acid in an individual host influences its ability to resist Sindbis virus infection.
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BACKGROUND: The capacity to generate (interferon-gamma) IFN-gamma, a potent immunoregulatory and inflammatory cytokine, is low in neonates and deficient in patients with food allergy. METHODS: We investigated the effect of IFN-gamma on antigen transport in the gut. In experiment I rat pups were randomized into two groups at the age of 14 days i.e., before gut maturation: Group IFN was given intraperitoneally recombinant rat IFN-gamma on days 14, 16, 18, 20. In experiment II, rats were randomized into two groups at the age of 26 days, i.e., after gut maturation: Group IFN received the IFN-gamma treatment on days 26, 28, 30, 32. Controls in both experiments received sterile saline. The absorption of horseradish peroxidase (HRP) across jejunal segments with and without Peyer's patches was studied in Ussing chambers on days 21 and 33 for experiments I and II, respectively. RESULTS: In experiment I, the absorption of intact HRP across both types of segments was significantly increased in Group IFN compared to controls. The mean (95% confidence interval) rate of degraded HRP absorption across patch-containing segments in Group IFN was significantly greater than in controls, 4420 (3162-6179) ng.h-1.cm-2 in comparison to 1550 (633-3790) ng.h-1.cm-2; F = 8.96, p = 0.009. CONCLUSION: IFN-gamma increases macromolecular transport before gut maturation particularly across Peyer's patches. This Peyer's patch-targeted effect can be important eliciting mucosal immune responses against dietary antigens early in life and aiding their immune exclusion.
BACKGROUND AND OBJECTIVES: Despite a successful outcome of the anti-D prophylaxis programme, alloimmunization still occurs. The aim of this study was to estimate the frequency of Rh-specific B lymphocytes in the peripheral blood of nine Rh-alloimmunized individuals at different time intervals after parturition. MATERIALS AND METHODS: The donors' B lymphocytes were transformed with Epstein-Barr virus (EBV) and cultured at different cell densities over a feeder of human fetal fibroblasts. Culture supernatants were screened for human immunoglobulin by enzyme-linked immunosorbent assay (ELISA) and for anti-Rh antibody by using a direct haemagglutination technique. The percentage of CD19+ B lymphocytes in peripheral blood was determined by flow cytometry, and the frequency of Rh-specific B lymphocytes was estimated by limiting-dilution assay (LDA). RESULTS: The frequency of Rh-specific B lymphocytes varied from 1 : 150 to 1 : 27,850 in different donors. There was a decrease in this frequency and level of anti-Rh antibody with increase in time interval between bleeding and last exposure to the antigen. Furthermore, a positive correlation was observed between the titre of Rh-specific antibody and frequency of Rh-specific B cells in each of three subjects bled at multiple time-points postdelivery. CONCLUSIONS: The magnitude of the specific antibody response to Rh antigens varies greatly in Rh-alloimmunized women, which partly reflects the difference in frequency of specific B cells in these individuals.
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Humoral immune response to ectropic leukemia viruses in AKR and C57BL/6 mice was controlled by a gene that mapped in linkage group IX. Mice of the AKR strain had an immune nonresponsive allele of this gene, whereas mice of the C57BL/6 strain had an immune responsive allele. Antibody against murine leukemia virus (MuLV) reacted primarily with p15 protein of the viral envelope. It was concluded that the failure to find antibody production in AKR mice was the result of a genetic immunological defect, rather than the result of immunological tolerance that was induced by the persistent viremia of endogenous MuLV.
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