Stress hormone secretion and gut signal transducer (STAT) proteins after burn injury in rats.

A burn injury triggers traumatic reactions characteristic of a stress. Here we investigated the early responses of prolactin (PRL), corticosterone (CS), and signal transducer and activator of transcription 5 (Stat5) in male Sprague-Dawley rats after burn injury. PRL and CS levels were determined in blood serum. Stat5 and phospho-Stat5 levels were determined in jejunum total protein extracts. The results confirmed an expected increase of CS between 4 and 6 hours following the burn injury. Unexpectedly, PRL secretion was suppressed during the same time frame. These hormone levels returned to normal 6 to 8 hours after burn injury. Stat5 was increased in the jejunum after burn injury, and its phosphorylation was increased between 8 and 11 hours after burn injury. These changes in Stat5 were not temporally correlated with either the hormone changes that we observed, or with previously documented changes of the gut function following burns

The serum concentration of prolactin is suppressed and corticosterone is elevated in male rats following sublethal burn injury

To improve the current clinical protocols used after a burn injury, injections of anabolic hormones like growth hormone (GH) or prolactin (PRL), which are also known to be immunostimulators has been suggested (Knox et al., 1995). Glucocorticoids, GH and PRL are considered stress hormones because their secretion is strongly altered by exposure to environmental stressors. Consistent with this concept, previous studies have suggested that the circulating levels of each of these hormones is increased by 24 h after a burn injury. However, the patterns of their secretion during the first hours after the burn injury is less well known. Working on male Sprague-Dawley rats, we have investigated the levels of corticosterone (CS) and PRL in the first hours after burn injury. Male rats were divided in three groups: 1) no treatment and no handling before execution (this allowed us to monitor the normal circadian cycle of the hormones); 2) rats are anesthesised using pentobarbitol, shaved and prepared for the burn, but not burned (sham-treated animals); 3) rats anesthesised and burned at 8AM. The rats were thereafter sacrified at specific times (day 1: 9AM, 10AM, 12PM, 4PM, 7PM; day 2: 8AM, 9AM, 10AM, 4PM, 7PM). Plasma was collected and the serum levels of CS and PRL were measured by ELISA and RIA, respectively. The circadian cycle of CS showed the predicted nadir at 10AM, and peak at 4PM. CS levels were elevated 6-fold by 1h after burn injury, reaching a maximum at 600ng/ml at 10AM. The concentration was progressively reduced to normal levels by 6 h after the burn injury, and followed the normal pattern thereafter. In sham-treated animals, CS concentration was similar to the burned animals, but the maximum elevation was only 3-4-fold, and the return to normal concentration was faster, after only 4 hours. The normal circadian cycle of PRL peaked at 8AM (110ng/ml) at 8AM. In contrast to CS, serum PRL fell dramatically following burn injury to less than 20ng/ml, and stayed low for 4h folowing the burn injury. In sham-treated animals, the changes in PRL were similar, but less dramatic than in the burned animals. In conclusion anesthesia and burn stress have similar effects on hormone secretion, but burn represents a stronger stressor. In the immediate hours following burn injury the animal physiology is dominated by high levels of secretion of an immunosuppressor (CS) and low levels of a potential immunostimulator (PRL)

Effects of prolactin deficiency on myelopoiesis and splenic T lymphocyte proliferation in thermally injured mice.

The importance of prolactin (PRL) in mammopoiesis and milk production is undisputed. However, previous studies investigating the role of PRL in immune function have yielded inconsistencies. These inconsistencies have led to our hypothesis that the immunomodulatory effects of PRL are only manifest under conditions in which the organism is subjected to stress. Thermal injury is a well-known stressor. The goal of this study was to determine whether the lack of PRL enhanced the negative effects of thermal injury-induced immune alterations utilizing a mouse model in which the PRL gene had been disrupted. Mice received either sham or burn treatment, and were sacrificed 4 days later. The immune parameters studied were the capacity of bone marrow cells to form granulocyte-macrophage colony forming units (GM-CFU) in the presence of granulocyte-macrophage colony stimulating factor, and the ability of the splenic T lymphocytes to proliferate in response to phytohemagglutin (PHA). As shown by others, our results reveal that burn increased the number of GM-CFU compared to sham controls; however, this elevation was only significant in the PRL-/- mice. Thermal injury increased PHA-stimulated proliferation of splenic T lymphocytes, however this increase was only significant in the PRL+/- group. We conclude that under conditions of a controlled stress event (thermal injury) [a] the increase in the GM-CFU is exaggerated in the absence of PRL, and [b] the enhancement of PHA-induced proliferation of splenic lymphocytes required PRL. This study supports the hypothesis that the immunomodulatory effects of PRL are manifest when the organism is subjected to stress