Biomedical subjects

T S Kupper

Publications and source records attributed to T S Kupper.

95 records · Page 6Linked to original sources

PubMed1984

Reversal of postburn immunosuppression by the administration of vitamin A.

The effect of high doses of vitamin A was evaluated on the suppression of cellular immunity after a 30% body surface area experimental scald burn in a mouse model. Male CBA/J mice were treated postburn with daily intraperitoneal injections of either 3000 IU of vitamin A or an equal volume of 0.9N saline. Similar groups of unburned mice were also studied as controls. At the seventh postburn day, one-way mixed lymphocyte reactions were tested for each group with whole spleen cells of CBA/J mice used as responders and mitomycin C-treated whole spleen cells of C57 BL/6 mice used as stimulators. When results were expressed as mean percentage of the values of control animals, no significant difference was observed between the saline-injected unburned control group (taken as 100%) and the vitamin A-treated unburned control groups (89%). The burned animals treated with saline showed suppression to 21% of the control values. However, the burned animals treated postburn with vitamin A improved the response rate dramatically to 52% of control values. This improvement over the untreated burned animals was significant in all experiments performed (p less than 0.02). This study suggests that vitamin A may be an effective agent in the reversal of cellular immunosuppression after burns.

Animals↗

PubMed1984

Immunoregulation after thermal injury: sequential appearance of I-J+, Ly-1 T suppressor inducer cells and Ly-2 T suppressor effector cells following thermal trauma in mice.

Immunoregulation as a consequence of thermal injury was investigated by using a murine model involving a 30% surface area full thickness burn. Both allogeneic mixed lymphocyte reaction (MLR) and in vitro anti-SRBC responses were depressed from days 3 to 25 post-burn. Suppressor T cells could be identified in both systems between days 5 and 15. On day 5 post-burn, an Ly-1+,2-, I-J+ T cell is responsible for the majority of the suppression observed. This cell behaves like a T suppressor inducer T cell in that it must interact with an Ly-2+ cyclophosphamide-sensitive cell to manifest suppression. On day 7 post-burn, only Ly-1-,2+ suppressor T cells are found which can directly suppress the activity of Ly-1+,2- helper T cells. Thus, these cells behave as T suppressor effector cells. We suggest that feedback suppression is in operation after thermal injury, with functional suppressor inducer cells appearing on day 5 post-burn, leading to the appearance of T suppressor effector cells by 7 days post-burn. Recovery from post-burn immunosuppression occurs by day 25 post-burn and is associated with the appearance of V. villosa-adherent T cells, whose activity antagonizes that of the day 7 post-burn suppressor effector. These cells may represent contrasuppressor T cells, which could play a role in the restoration of immunocompetence after burn injury.

Animals↗

PubMed1982

Impairment of reticuloendothelial function following thermal injury and its restoration with ATP-MgCl2 administration.

It is well known that reticuloendothelial system (RES) function is depressed following thermal injury. Since previous studies have shown that adenosine triphosphate (ATP)-MgCl2 restored the depressed RES function following hepatic ischemia, the present study was undertaken to determine whether administration of ATP-MgCl2 following thermal injury would have any beneficial effects on the RES function. Thermal injury in rats was produced by immersing 30% of the skin surface area in 95 degrees C H2O for 12 sec. Immediately following this, the rats received saline s.c. and 0.25 ml of ATP-MgCl2 (12.5 mumol each) or an equivalent volume of saline i.p. RES function was evaluated by measuring the intravascular clearance of 131I-triolein-labeled gelatinized test lipid emulsion. The intravascular half-time (t/2) in the burned saline-treated rats was double that of control rats at 1 and 3 days post-burn, suggesting that significant depression in RES function occurred following thermal injury. At 5 days post-burn, although the t/2 was lower than at 3 days post-burn, it was still significantly higher than controls. Administration of ATP-MgCl2 following burn injury resulted in a t/2 and phagocytic index values similar to controls, indicating the impairment of phagocytic activity of the RES function following thermal injury was reversed with treatment.

Adenosine Triphosphate↗

PubMedDate not supplied

Immunologic alterations following excisional wounding and immediate repair with syngeneic or allogeneic skin grafts.

Immunosuppression and its associated infectious complications have long been recognized as consequences of major thermal trauma, though the factors that mediate this suppression remain unclear. A murine split-thickness skin graft model was developed to investigate the role of a large surface area wound in the initiation of immunosuppression in the absence of burn injury. Significant T cell-mediated immunosuppression was demonstrated following wounding and immediate repair with either syngeneic or allogeneic split-thickness skin grafts. These results are consistent with previous experiments in a murine burn model treated by escharectomy and resurfacing with syngeneic composite full-thickness skin. Data also supports the concept that mediators of inflammation at the wound site play an important role in postburn immunosuppression. Furthermore, these results suggest that the use of skin allografts during the early postburn period does not adversely affect cell-mediated immunity in any way that could be abrogated by primary autografting.

Animals↗

PubMedDate not supplied

Interleukin-1 and T cell function following injury.

Sepsis is responsible for 75% of late deaths after major thermal or traumatic injury. In the clinical setting, efforts to prevent or control sepsis, or both, should include an understanding of normal host resistance, proper resuscitation techniques, and nutritional support. Previous studies have identified T suppressor cell abnormalities following thermal injury and have suggested macrophage defects after traumatic injury. Although major thermal injury is easier to quantify than mechanical trauma, both insults can stress patients' host resistance to a maximal degree, leading to profound and often fatal immunosuppression. Recent studies summarized in this paper have suggested that the macrophage and the interleukin system may play a major role in initiating some of these immune abnormalities following injury.

Animals↗