Ronald P. Pelley

Abstract Spontaneous diminution of granuloma formation around schistosome eggs in chronic schistosomiasis mansoni has been demonstrated previously. In the present study these findings were confirmed by injecting schistosome eggs into the pulmonary microvasculature and removing the lungs 8 days later from mice infected for 4, 8, 12, 16, and 20 weeks; the mean area of inflammation around the eggs was then measured. At 4 weeks a primary reaction was seen, by 8 weeks a massive secondary reaction occurred, but by 12 weeks the lesion was considerably reduced in size, and at 20 weeks it was smaller than the primary reaction. Concomitant measurements of humoral hemagglutinins to soluble egg antigens (SEA) revealed no detectable antibodies at 4 and 6 weeks, relatively low levels at 8 weeks, and an exponential increase in hemagglutinins at 12 weeks and beyond. Immunodiffusion analysis revealed no precipitins at 8 weeks, 1 major band and 2 minor bands at 12 and 16 weeks, and 2 major bands and 1 minor band at 20 weeks. Spleen cells from 8-week-infected mice showed peak migration inhibitory factor (MIF) output at a concentration of 1 µg/ml of soluble egg antigens and suppression of lymphokine secretion at higher concentrations. At 12 and 16 weeks, exponentially lower antigen concentrations both stimulated and suppressed peak MIF output; at 20 weeks MIF was not detectable after stimulation over a wide range of antigen concentrations. Delayed footpad swelling to SEA reached its peak at 10 weeks and declined thereafter, but the response to PPD in tuberculin-sensitized schistosome infected mice remained constant over the period of time studied.

The biocompatibility of silicone implants has been a source of long-standing controversy. An attempt to ascertain this biocompatibility with regard to the cellular immune mechanism was undertaken. Silicone gel from a mammary prosthesis was sonicated with Freund adjuvant under aseptic conditions to produce an injectable mixture, and injected subcutaneously in 10 female guinea pigs. Control animals did not receive this initial stimulus. After four weeks each animal received a challenge silicone implant of the same product in a gel form, surgically placed intraperitoneally in the omentum. Four weeks later peritoneal exudate cells were harvested for migration inhibition studies. Site of implantation and regional lymph nodes were processed for histological and electron microscopy. The migration inhibition studies showed that the silicone environment resulted in 45% inhibition of migration of the sensitized cell population. All sites of implantation showed a marked inflammatory response with silicone inclusions in giant cells, surrounded by neutrophils, plasma cells, and lymphocytes. Electron microscopy and x-ray energy spectrograph (XES) analysis revealed cytoplasmic transference of silicone from macrophages to lymphocytes, via a cytoplasmic bridge. There was no comparable response in control animals. Although apparently inert, silicone is capable of eliciting a cellular immune response demonstrated by the migration inhibition technique. This response is comparable to that elicited by purified protein derivative and may indicate that silicone acts as a hapten-like incomplete antigen.

Abstract The therapeutic effects of Aloe vera have been examined in preventing progressive dermal ischaemia caused by burns, frostbite, electrical injury, distal dying flap and intra‐arterial drug abuse. In vivo analysis of these injuries showed that the mediator of progressive tissue damage was thromboxane A 2 (TxA 2 ). Experimentally Aloe was compared to a variety of antithromboxane agents to include U38450, a lodoxamide, a lazaroid and Carrington wound gel. In the burn injury Aloe was comparable to the lodoxamide and lazaroid with an 82% to 85% tissue survival when compared with the control and the Carrington wound gel ( p =0.05). Tissue survival in the experimental frostbite injury was 28.2% when compared with the control ( p =0.05). Similar results were obtained for the electrical injury, and intra‐arterial drug abuse. Clinically burn patients treated with Aloe healed without tissue loss as did those with frostbite ( p =0.001). In the intra‐arterial drug abuse patients Aloe reversed the tissue necrosis. This therapeutic approach was used to prevent progressive tissue loss in each injury by actively inhibiting the localized production of TxA 2 . Aloe not only acts as a TxA 2 inhibitor but maintains a homeostasis within the vascular endothelium as well as the surrounding tissue.