Serum TGF-beta in thermally injured rats

Citation
M. Varedi et al., Serum TGF-beta in thermally injured rats, SHOCK, 16(5), 2001, pp. 380-382
Citations number
35
Categorie Soggetti
Aneshtesia & Intensive Care","Cardiovascular & Hematology Research
Journal title
SHOCK
ISSN journal
10732322 → ACNP
Volume
16
Issue
5
Year of publication
2001
Pages
380 - 382
Database
ISI
SICI code
1073-2322(200111)16:5<380:STITIR>2.0.ZU;2-W
Abstract
A severe thermal injury is commonly associated with immune suppression and increased susceptibility to sepsis, frequently leading to multiple organ fa ilure. Transforming growth factor-beta (TGF-beta) is a potent immunosuppres sive cytokine involved in complications associated with major trauma. Inter leukin-4 (IL-4) is thought to synergize the immunosuppressive activity of T GF-beta by promoting naive lymphocytes to differentiate and generate TGF-be ta secreting cells. This study examines the alterations in serum levels of TGF-beta and IL-4 after a thermal injury. Male Sprague-Dawley rats (300-400 g) were anesthetized and received a 50% total body surface area full-thick ness scald burn followed by fluid resuscitation and analgesia. Control rats were given the same treatment, but were immersed in water at room temperat ure. Rats were sacrificed from 1 h to 8 days after injury. Blood samples we re collected aseptically from the inferior caval vein. Serum levels of TGF- beta and IL-4 were measured by enzyme linked immunosorbent assay, Rats in t he control and thermal injury groups showed similar increases in serum TGF- beta1 h after injury. A progressive increase in serum TGF-beta was observed in burned animals compared to control animals starting on day 3 and contin ued through day 8 (P<0.01). Serum IL-4 levels in control and thermally inju red animals remained undetectable (<15.6 pg/mL) throughout the experiment. Thermal injury induces a significant increase in serum TGF-beta, which may contribute to post-burn immunosuppression with an increased susceptibility to sepsis.