title: Effects of bilateral adrenalectomy on the innate immune responses  following trauma in rats.
abstract: BACKGROUND
  The regulation of neuroendocrine hormones on the innate immune responses in trauma has not been fully understood. Previous studies have shown that the neuroendocrine hormones are important factors in their effects on immune parameters, depending on their concentration and timing instead of the simple suppressive effects.
  
  
  METHODS
  A total of 144 Sprague–Dawley rats were divided randomly into sham, pulmonary blast injury (BI) and adrenalectomy plus pulmonary BI groups. Bilateral adrenalectomy was performed on rats, which were then subjected to blast injury. Following this, peripheral leucocyte responsiveness to lipopolysaccharide (LPS) stimulation, phagocytosis activities of macrophages and bacteria translocation (BT) were examined. Tumour necrosis factor-a (TNF-a) levels and the expression levels of scavenger receptor (SR) A, CD14, Toll-like receptor (TLR) 4 and MD2 were assayed with enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction, respectively.
  
  
  RESULTS
  In adrenalectomised rats after pulmonary BI, the number of peripheral leucocytes was increased and the phagocytosis of peritoneal and splenic macrophages was decreased as compared to the BI group. Simultaneously, the gut-derived BT and TNF-a secretion in lung tissues were elevated, whilst the LPS-stimulated TNF-a synthesis by peripheral leucocyte responsiveness was reduced. Furthermore, the mRNA levels of SR-A, CD14, TLR4 and MD2 in lung tissues of adrenalectomised rats decreased. Adrenalectomised rats showed enhancement of inflammatory responses and severe tissue injuries in trauma.
  
  
  CONCLUSIONS
  Release of adrenal hormones might enhance, rather than inhibit, the innate immune functions, particularly in the early stages of trauma.
authors.affiliation: State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Changjiang Zhilu, Daping, Chongqing, China.
authors.forename: Ce
authors.initials: C
authors.lastname: Yang
authors.forename: Jun
authors.initials: J
authors.lastname: Yan
authors.forename: Hai-yan
authors.initials: HY
authors.lastname: Wang
authors.forename: Lin-lin
authors.initials: LL
authors.lastname: Zhou
authors.forename: Jian-yun
authors.initials: JY
authors.lastname: Zhou
authors.forename: Zheng-guo
authors.initials: ZG
authors.lastname: Wang
authors.forename: Jian-xin
authors.initials: JX
authors.lastname: Jiang
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D018988:Bacterial Translocation; D001753:Blast Injuries / Q000276:immunology* / Q000601:surgery; D002452:Cell Count; D004797:Enzyme-Linked Immunosorbent Assay; D007113:Immunity, Innate / Q000502:physiology*; D007962:Leukocytes; D008070:Lipopolysaccharides / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D055370:Lung Injury / Q000276:immunology* / Q000601:surgery; D008198:Lymph Nodes / Q000378:metabolism; D008264:Macrophages / Q000502:physiology; D008297:Male; D010587:Phagocytosis; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011971:Receptors, Immunologic / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D008070:Lipopolysaccharides; D012333:RNA, Messenger; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha