The enhancement of avian NK cell cytotoxicity by thymulin is not mediated by the regulation of IFN-gamma production.

Preincubation with either thymulin or IFN-gamma can enhance NK activity. In addition, overnight in vitro pre-treatment with thymulin and IFN-gamma increases NK activity further than either treatment alone. It has been hypothesized that thymulin increases the responsiveness of immune cells to IFN-gamma by either increasing the expression of IFN-gammaR or by increasing the production and/or secretion of IFN-gamma. The effects of thymulin on IFN-gamma production and secretion were examined in this study. While an overnight incubation with the polyclonal activator Con A increased the number of cells positive for intracellular IFN-gamma, a similar incubation with thymulin produced no change in the percentages of cells labeling positive for intracellular IFN-gamma when compared to the media control cells. In addition, IFN-gamma was not secreted by splenocytes following an overnight incubation with thymulin, but increased secretion was induced by Con A stimulation. Taken together, these results suggest that thymulin does not increase IFN-gamma production or induce IFN-gamma secretion by avian splenocytes.

The effects of triodothyronine and thymulin on avian NK cytolytic activity.

The effects of triiodothyronine (T3), thymulin, and recombinant chicken interferon-y (ChIFN-gamma) on natural killer (NK) cell cytotoxicity was investigated using the euthyroid control K and the T3-deficient sex-linked dwarf (SLD) chicken strains. Factorial design experiments were used to investigate the effects of T3 treatments where animals of both strains received either 0 or 0.1 ppm T3 supplementation to the standard chick starter diet. The ChIFN-gamma treatments were administered in vitro by incubation with effector cells overnight prior to the addition of the RP9 lymphoblastoma target cell line. All cytotoxicity assays were run at 50:1 and 25:1 effector/target (E/T) ratios. Treatments were begun at hatching and continued through 7 weeks. NK cells for these assays were enriched by separation of splenocytes over ficoll. Splenocyte preparations from untreated K strain consistently had significantly higher NK-mediated cytolysis than did samples from the untreated SLD at both E/T ratios. T3 treatment alone had no effect on NK activity in cell preparations from the K strain but did significantly enhance that activity in the T3-deficient SLD whereas IFN treatment alone enhanced NK activity in both strains. The combined T3 and IFN treatments resulted in a greater enhancement of NK cytolytic activity in both strains than any separate treatment and resulted in an elimination of differences in NK cell responsiveness between the K and SLD strains. Similar results were obtained when NK cell cultures were incubated in vitro with thymulin prior to assessing cytotoxicity. In vitro thymulin treatments alone significantly enhanced cytolytic activity for NK cells for both K and SLD strains. The greatest effect of in vitro thymulin exposure was to increase the responsiveness to NK cells to ChIFN-gamma stimulation.

Evidence for the direct action of thymulin on avian NK cells.

The ability of thymulin to directly enhance NK cell-mediated cytotoxicity was examined. Specific cell population depletions were done in K and SLD chicken splenocyte preparations using anti-CD3, CD4, and CD8 monoclonal antibodies and secondary complement-fixing polyclonal antibodies. The remaining cells were incubated overnight with in vitro treatments of thymulin and IFN-gamma, either separately or together, followed by an assay for cytotoxicity. Although the control K-strain had higher overall NK cell-mediated cytotoxicity than the thymulin-deficient SLD-strain, the following trends were seen in both strains. Thymulin continued to enhance NK activity following CD4 or CD3 cell depletion, but not after CD8 or CD8 and CD4 cell depletion. Since avian NK cells express CD8 alpha, but not CD3 or CD4 on their surface, these results suggest that the ability of in vitro thymulin treatments to enhance NK activity is not mediated by T-cells but may be due to direct effects on NK cells.

Minor oral injuries in children.

Traumatic injuries involving the oral cavity in children often result from falls or collisions with stationary objects. Repair of lacerations involving the soft tissue structures within the oral cavity is described. These injuries often can be managed by emergency department personnel, with referral to an oral and maxillofacial surgeon for follow-up care. Initial management of more extensive injuries such as dentoalveolar fractures, penetrating injuries and burns is also described. Immediate consultation with the appropriate specialist is suggested, because significant deformity and/or morbidity may result from minor oral injuries.