%0 Journal Article
%T Hypothermia Induced by Adenosine -Monophosphate Attenuates Acute Lung Injury Induced by LPS in Rats
%A Zhimin Miao
%A Shulai Lu
%A Na Du
%A Weiting Guo
%A Jidong Zhang
%A Yu Song
%A Xuefeng Wang
%A Wei Ren
%A Yunlong Wang
%A Tao Jiang
%J Mediators of Inflammation
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/459617
%X We have built a rat¡¯s model to investigate whether the hypothermia induced by adenosine 5¡ä-monophosphate (5¡ä-AMP) (AIH) could attenuate acute lung injury induced by LPS in rats. We detected the inflammatory cytokine levels in the plasma and bronchoalveolar lavage fluid samples, and we analyzed the pathological changes in the lungs. We have found that AIH can effectively inhibit acute inflammatory reactions and protect the lung from acute injury induced by LPS in rats. 1. Introduction Lipopolysaccharides (LPSs) are the main components of the outer membrane of gram-negative bacteria and act as basic mediators that host the inflammatory sequelae after a gram-negative bacterial infection. Consisting of four different parts, including lipid A, the inner core, the outer core, and the O antigen [1], LPS is nontoxic when it functions as a component of the bacterial cell wall. However, it becomes the opposite when it is released from the cell wall as the cells multiply or die due to its toxic component, lipid A [1]. After the host¡¯s immune system is exposed to lipid A, an inflammatory response is evoked. Upon binding with LPS-binding protein (LBP) in the plasma, the LPS-LBP complex integrates into the cell surface and activates the CD14 receptor, where LPS is then delivered to the transmembrane signaling receptor toll-like receptor 4 [1]. Following the infection, endotoxemia or endotoxic shock is induced, which are characterized by a cascade of cytokines that are expressed and released, such as tumor necrosis factor-¦Á (TNF-¦Á), interleukin-1¦Â (IL-1¦Â), and IL-6, followed by an anti-inflammatory response with the production of anti-inflammatory cytokines, such as IL-10 [2, 3]. Both endotoxins and cytokines contribute to the pathophysiology of endotoxic shock and the development of organ injury in endotoxemia, such as acute lung injury [4, 5]. It has been shown that hypothermia can reduce the mortality in the murine endotoxic shock model [6]. One of the possible mechanisms for this reduction may be decreased oxygen demand, which can contribute to organ preservation. Another possibility is a decrease in the levels of proinflammatory cytokines and an increase in the levels of anti-inflammatory cytokines in the plasma [4, 5, 7]. 5¡ä-AMP, a biomolecule that was recently discovered, allows nonhibernating mammals to enter a rapid and safe severe hypothermia. It is the first endogenous biomolecule found to have this effect [8]. In mice, 5¡ä-AMP can induce torpor when their core body temperature falls to 31.8¡ãC or below [9¨C11]. The torpor duration also appears to be dependent
%U http://www.hindawi.com/journals/mi/2012/459617/