Passive immunization involving the delivery of antibodies specific to pathogens of infectious diseases to the host has been an attractive approach to establish protective immunity against a variety of microbial pathogens, including Streptococcus mutans, which is the principal etiologic agent of dental caries in humans. The overall purpose of the present study was to determine the effectiveness of a mouth rinse containing antibodies to S. mutans in preventing the establishment of this bacterium in dental plaque of humans. The antibodies were derived from egg yolks obtained from hens immunized with whole cells of S. mutans grown in sucrose-containing medium. The immunoglobulin derived from the yolks (IgY) of immunized hens was characterized in vitro and in vivo in human volunteers. Cross-reactivity tests showed that immune IgY reacted with every serotype, except serotype b, which had lost its GTase activity, when the bacteria were cultured in sucrose-containing medium. Immune IgY inhibited S. mutans adherence to saliva-coated hydroxyapatite discs by 59.2%, while control IgY caused an inhibition of only 8.2%. In the short-term (4-hour) test using a mouth rinse containing 10% sucrose, immune IgY decreased the ratio of the percentage of S. mutans per total streptococci in saliva. In the long-term (7-day) test using a mouth rinse without sucrose, the ratio in saliva was not significantly reduced in the volunteers using the immune IgY due to the large standard deviation. However, comparing the ratios of the percentage of S. mutans per total streptococci in plaque of individual subjects, there was a tendency for a reduction of the ratios in the volunteers receiving the mouth rinse containing immune IgY These results support the effectiveness of IgY with specificity to S. mutans grown in the presence of sucrose as an efficient method to control the colonization of mutans streptococci in the oral cavity of humans.

SUMMARYPassive immunity against gastrointestinal infections has recently been successfully applied as prophylaxis and therapy in patients in a variety of virally and bacterially induced infections. Campylobacter jejuni is frequently associated with acute diarrhoea in humans, and several species of animals have been shown to transmit the disease, although birds have been implicated as the main source of infection. We used bovine and chicken immunoglobulin preparations from the milk and eggs, respectively, of immunized animals for prophylactic and therapeutic treatment of chickens infected with C. jejuni. A marked prophylactic effect (a >99% decrease in the number of bacteria) was noted using either antibody preparation, whereas the therapeutic efficacy, i.e. when antibodies were given after the infection was established, was distinctly lower (80-95%) as judged by faecal bacterial counts. These observations may serve as a starting point for experiments aimed at elimination of the infection in an industrial or farm setting. It may also encourage future attempts to treat, prophylactically or therapeutically, patients with Campylobacter-induced diarrhoea.

Inhibitors of differentiation (Id) play an essential role in the neurogenesis of the central nervous system. However, the expression and function of Id in the development of cochlear sensory epithelial cells have yet to be elucidated. In this study, we demonstrate the Id1 gene was expressed in the rapidly growing otocyst on embryonic day 12 (E12) and in the organ of Corti, spiral ganglions, and stria vascularis on postnatal day 1 (P1) by cellular and molecular biologic techniques. Knockdown of the Id1 gene with short interfering RNA (siRNA) in a cochlear sensory epithelial cell line (OC1) significantly reduced its proliferation, whereas overexpression of Id1 in OC1 significantly increased the proliferation of OC1, suggesting a role of Id1 in the development of cochlear sensory epithelial cells. The proliferative action of Id1 on OC1 was mediated by nuclear factor-kappaB (NF-kappaB) and cyclin D1 (a downstream molecule of NF-kappaB). Blockage of the NF-kappaB activity with pyrrolidine dithiocarbamate (PDTC) or enhancement of the NF-kappaB activity with p65 (a subunit of NF-kappaB) in OC1 significantly inhibited or increased, respectively, the cell proliferation and transcription of cyclin D1 induced by Id1. Truncation of the NF-kappaB binding site in the cyclin D1 promoter fully abrogated the transcription of cyclin D1, suggesting that the cyclin D1 transcription is dependent on NF-kappaB. We concluded from this study that Id1 induces the proliferation of OC1 via the NF-kappaB/cyclin D1 pathway.

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PDGFs and their receptors may play a role in the proliferation of developing cochlear hair cells.