Alexandros Alexis1, Dionyssia-Pinelopi Carrer2, Dionyssia-Irini Droggiti3, Konstantinos Louis4, Aikaterini Pistiki5, Mihai G Netea6, Yota Kapessidou7, Evangelos J Giamarellos-Bourboulis8. 1. 4th Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Str., 12462 Athens, Greece; Anesthesiology and Reanimation Department, Hospital Saint-Pierre, Université Libre de Bruxelles, 322 rue Haute, 1000 Brussels, Belgium. Electronic address: alexandrosalexis@hotmail.com. 2. 4th Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Str., 12462 Athens, Greece. Electronic address: n_carrer@hotmail.com. 3. 4th Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Str., 12462 Athens, Greece. Electronic address: stonecityndr@hotmail.com. 4. 4th Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Str., 12462 Athens, Greece. Electronic address: kostaslouiss@hotmail.com. 5. 4th Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Str., 12462 Athens, Greece. Electronic address: aipistiki@gmail.com. 6. Department of Medicine and Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. Electronic address: M.Netea@aig.umcn.nl. 7. Anesthesiology and Reanimation Department, Hospital Saint-Pierre, Université Libre de Bruxelles, 322 rue Haute, 1000 Brussels, Belgium; Institut for Medical immunology (IMI), 8 Adrienne Bolland str., 6041, Gosselies, Belgium. Electronic address: Panayota_KAPESSIDOU@stpierre-bru.be. 8. 4th Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Str., 12462 Athens, Greece. Electronic address: egiamarel@med.uoa.gr.
Abstract
BACKGROUND: Thermal injuries are followed by a complex immune response, but the relationship between the severity of burn injury and the time exposure to the thermal injury on the extent of the immune response is still not known. OBJECTIVE: This study focuses on characterising the effect of temperature and time exposure on the post-burn immune response. METHODS: We used 120 C57BL/6 male mice divided equally in 5 burn groups and one sham operated group (groups A-E and sham). Ten mice per group were sacrificed at 24 and 48 h after burn injury and whole blood was collected; specimens of liver, lung, spleen, kidney and bowel were excised. Apoptosis and TREM-1 expression on circulating blood cells were measured. Splenocytes were isolated and stimulated for cytokine production; the rate of apoptosis of splenocytes was also measured. RESULTS: Production of IL-17 from splenocytes of mice group D was enhanced. Considerable effects were shown on the apoptosis of circulating lymphocytes and of spleen cells. The apoptotic rates varied between groups and also evolved after 24 and 48 h. To examine the origin of this differential response, quantitative bacterial cultures of liver, lung and kidney were made but no differences were observed compared with sham-operated animals. LIMITATIONS: This study was based on an experimental murine model. CONCLUSION: There is a unique response for each type of injury depending on the temperature of the thermal source and the exposure time.
BACKGROUND: Thermal injuries are followed by a complex immune response, but the relationship between the severity of burn injury and the time exposure to the thermal injury on the extent of the immune response is still not known. OBJECTIVE: This study focuses on characterising the effect of temperature and time exposure on the post-burn immune response. METHODS: We used 120 C57BL/6 male mice divided equally in 5 burn groups and one sham operated group (groups A-E and sham). Ten mice per group were sacrificed at 24 and 48 h after burn injury and whole blood was collected; specimens of liver, lung, spleen, kidney and bowel were excised. Apoptosis and TREM-1 expression on circulating blood cells were measured. Splenocytes were isolated and stimulated for cytokine production; the rate of apoptosis of splenocytes was also measured. RESULTS: Production of IL-17 from splenocytes of mice group D was enhanced. Considerable effects were shown on the apoptosis of circulating lymphocytes and of spleen cells. The apoptotic rates varied between groups and also evolved after 24 and 48 h. To examine the origin of this differential response, quantitative bacterial cultures of liver, lung and kidney were made but no differences were observed compared with sham-operated animals. LIMITATIONS: This study was based on an experimental murine model. CONCLUSION: There is a unique response for each type of injury depending on the temperature of the thermal source and the exposure time.
Authors: Laurel B Kartchner; Cindy J Gode; Julia L M Dunn; Lindsey I Glenn; Danté N Duncan; Matthew C Wolfgang; Bruce A Cairns; Robert Maile Journal: Burns Date: 2019-03-02 Impact factor: 2.744