Effects of prolactin level on burn-induced aberrations in myelopoiesis

被引:11
作者
Dugan, AL
Schwemberger, S
Babcock, GF
Buckley, D
Buckley, AR
Ogle, CK
Horseman, ND [1 ]
机构
[1] Univ Cincinnati, Dept Mol & Cellular Physiol, Cincinnati, OH 45267 USA
[2] Univ Cincinnati, Coll Pharm, Cincinnati, OH 45267 USA
[3] Shriners Hosp Children, Cincinnati, OH 45229 USA
来源
SHOCK | 2004年 / 21卷 / 02期
关键词
thermal injury; interleukin; 12; monocyte chemoattractant protein-1; 6; bone marrow; colony formation;
D O I
10.1097/01.shk.0000108401.56565.e2
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
In this study, we sought to determine if prolactin (PRL) had any influence on burn-induced alterations in myelopoiesis and serum IL-6, IL-10, IL-12, IFN-gamma, TNF-alpha, and MCP-1 levels. To do this, we used mice that were PRL normal, PRL deficient, or hyperprolactinemic and had received a 15% total body surface area burn, sham treatment, or no treatment. We performed clonogenic assays of bone marrow cells, and we found that sham treatment significantly decreased monocyte/macrophage (M) colony formation relative to the control group in the PRL-deficient and PRL-normal mice (P < 0.01). Hyperprolactinemia attenuated the sham-induced decrease in M colony formation. Burn injury significantly increased M colony formation relative to the sham group with an equal significance in the PRL-deficient and PRL-normal mice (P < 0.05). We also showed that burn led to a significant increase in GM colony formation relative to the sham group. This burn-induced increase was significant in the PRL-normal (P < 0.05) and the PRL-deficient (P < 0.01) mice. In the PRL-normal mice, burn injury caused a 2.1-fold increase in the GM colony number, whereas in the PRL-deficient mice burn led to a 2.6-fold increase in GM colony number. When comparing the effects of burn injury on colony formation to the control groups, there were no significant differences seen, irrespective of the PRL level. We observed that all of the cytokines studied, with the exception of IL-10, were influenced by either sham treatment, burn injury, or both forms of stress. This stress-induced response occurred most often in animals that were either hypo- or hyperprolactinemic. We conclude that the PRL level was able to influence the sham-induced and burn-induced alterations in GM and M colony formation. Under euprolactinemic conditions, mice exhibited less often with stress-induced serum cytokine level alterations. We did not find any significant correlations with any of the serum cytokine levels and the ability to form colonies. Importantly, the sham treatment led to immune alterations independent of, and sometimes opposite of burn-induced effects.
引用
收藏
页码:151 / 159
页数:9
相关论文
共 37 条
[21]   Protective effects of early interleukin 10 antagonism on injury-induced immune dysfunction [J].
Lyons, A ;
Goebel, A ;
Mannick, JA ;
Lederer, JA .
ARCHIVES OF SURGERY, 1999, 134 (12) :1317-1323
[22]   Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL-12 [J].
Majumder, B ;
Biswas, R ;
Chattopadhyay, U .
INTERNATIONAL JOURNAL OF CANCER, 2002, 97 (04) :493-500
[23]   Interleukin-12 protects thermally injured mice from herpes simplex virus type 1 infection [J].
Matsuo, R ;
Kobayashi, M ;
Herndon, DN ;
Pollard, RB ;
Suzuki, F .
JOURNAL OF LEUKOCYTE BIOLOGY, 1996, 59 (05) :623-630
[24]  
POJDA Z, 1992, EXP HEMATOL, V20, P874
[25]   PROLACTIN RECEPTORS IN RAT-LIVER - POSSIBLE INDUCTION BY PROLACTIN [J].
POSNER, BI ;
KELLY, PA ;
FRIESEN, HG .
SCIENCE, 1975, 188 (4183) :57-59
[26]  
Sacco S, 1997, BLOOD, V90, P4473
[27]   Myeloid commitment shifts toward monocytopoiesis after thermal injury and sepsis [J].
Santangelo, S ;
Gamelli, RL ;
Shankar, R .
ANNALS OF SURGERY, 2001, 233 (01) :97-106
[28]   COMPARATIVE-ANALYSIS OF TRANSCRIPTION AND PROTEIN RELEASE OF THE INFLAMMATORY CYTOKINES INTERLEUKIN-1-BETA (IL-1-BETA) AND INTERLEUKIN-8 (IL-8) FOLLOWING MAJOR BURN AND MECHANICAL TRAUMA [J].
SCHINKEL, C ;
ZIMMER, S ;
KREMER, JP ;
WALZ, A ;
RORDORFADAM, C ;
VONDONNERSMARCK, GH ;
FAIST, E .
SHOCK, 1995, 4 (04) :241-246
[29]   Does burn wound excision after thermal injury attenuate subsequent macrophage hyperactivity and immunosuppression? [J].
Schwacha, MG ;
Knöferl, MW ;
Chaudry, IH .
SHOCK, 2000, 14 (06) :623-628
[30]   Mechanisms of neutropenia involving myeloid maturation arrest in burn sepsis [J].
Shoup, M ;
Weisenberger, JM ;
Wang, JL ;
Pyle, JM ;
Gamelli, RL ;
Shankar, R .
ANNALS OF SURGERY, 1998, 228 (01) :112-122