Disease relevance of Ccl4

• Role of CC chemokines (macrophage inflammatory protein-1 beta, monocyte chemoattractant protein-1, RANTES) in acute lung injury in rats [1].
• The initial expression of the chemokines closely correlated with the appearance of inflammatory cells in the injured CNS, suggesting that RANTES and MIP-1 beta may play a role in the inflammatory events of traumatic brain injury [2].
• Identification of cell types producing RANTES, MIP-1 alpha and MIP-1 beta in rat experimental autoimmune encephalomyelitis by in situ hybridization [3].
• Using a stab wound model for mechanical injury, we studied the expression of two other beta chemokines: RANTES (Regulated on Activation, Normal T cell Expressed and Secreted) and MIP-1 beta (macrophage inflammatory protein-1 beta) in the rat brain [2].
• Furthermore we induced compensatory cirrhosis by application of CCL4 and biochemical analysis of sera was carried out after a 30-min occlusion [4].

High impact information on Ccl4

• Furthermore, dexamethasone failed to inhibit the increase in expression of mRNAs for tumor necrosis factor alpha, macrophage inflammatory protein 1 beta, interleukin 6, and mob-1, which occurs in the CNS of animals infected with BDV [5].
• Conversely, exogenously MIP-1 beta, but not RANTES or MCP-1, caused enhancement of the lung vascular leak [1].
• Treatment of rats with anti-MIP-1 beta Ab significantly decreased vascular permeability by 37% (p = 0.012), reduced neutrophil recruitment into lung by 65% (p = 0.047), and suppressed levels of TNF-alpha in bronchoalveolar lavage fluids by 61% (p = 0.008) [1].
• 2. The concurrent microinjection of 25 pg MIP-1 alpha and 25 pg MIP-1 beta into the AHPOA attenuated the effects on Tb of either cytokine alone [6].
• Microinjection of 25 pg MIP-1 beta into the AHPOA induced a fever of rapid onset, whereas 5.0 pg MIP-1 beta did not alter body temperature (Tb) significantly [6].

Chemical compound and disease context of Ccl4

• Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver [7].
• The purpose of this study was 2-fold: (i) to determine whether the potent doublet of this cytokine, MIP-1beta, is actually produced in the brain in response to a pyrogenic dose of a lipopolysaccharide of Escherichia coli and (ii) to determine the anatomical site of synthesis of this cytokine in the brain [8].
• The purpose of this study was to examine the action of an inhibitor of protein synthesis, anisomycin, on the pyrexia which follows intrahypothalamic injection of MIP-1 beta [9].
• The results showed that anti-MIP-1beta failed to alter the PGE2 hyperthermia [10].
• Micronodular cirrhosis was present in CCL4-treated rats with elevated AST and alkaline phosphatase levels [11].

Biological context of Ccl4

• The kinetics of RANTES, MIP-1 alpha and MIP-1 beta expression paralleled those of the recruitment of infiltrating inflammatory cells and disease severity [3].
• The effects of a single exposure, by gastric intubation or inhalation, to carbon tetrachloride (CCL4) on rat lungs were assessed [12].
• These data thus demonstrate that MIP-1beta is sequestered in diencephalic structures underlying thermoregulation even though it is not involved in PGE2 hyperthermia [10].
• Differentiation of necrotic cell death with or without lysosomal activation: application of acute liver injury models induced by carbon tetrachloride (CCL4) and dimethylnitrosamine (DMN) [13].
• D-003 protected against the histological changes characteristic of CCL4-induced hepatic injury in rats, in which the process of lipid peroxidation plays the main role [14].

Anatomical context of Ccl4

• This study also demonstrates for the first time MIP-1 beta expression in reactive astrocytes following trauma to the rat CNS [2].
• In addition, MIP-1 beta staining was also detected on macrophages at the site of injury [2].
• The chemokines RANTES, macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta are members of the beta-family of chemokines and potent chemoattractants for lymphocytes and monocytes [3].
• Most of the MIP-1 alpha- and MIP-1 beta-positive mononuclear cells were located around blood vessels [3].
• The mRNA induction for the beta-chemokines macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, and RANTES preceded the expression of markers for lymphocytes [cluster of differentiation (CD)4, CD8], microglia/macrophages (MHC I), and natural killer cells in the infarct area [15].

Associations of Ccl4 with chemical compounds

• Following the intense fever produced by intraperitoneal administration of lipopolysaccharide in the unrestrained rat, MIP-1beta immunoreactivity was identified post mortem in two regions of the brain implicated in fever: the organum vasculosum laminae terminalis (OVLT) and the anterior hypothalamic, preoptic area (AH/POA) [8].
• When 10 mg/kg anisomycin was administered subcutaneously, the febrile response to 25 pg MIP-1 beta injected in the AH/POA was significantly suppressed [9].
• After 3 to 7 weeks, the rats were injected with CCL4 (ip) and ethane was collected for 9 hours [16].
• This dissociation supports the viewpoint that at least two distinct systems exist in the brain which underlie a febrile response: MIP-1beta underlies one component whereas PGE2 comprises the other [10].
• Pyrazole treatment of rats potentiates CCL4-but not CHCL3-hepatotoxicity [17].

Other interactions of Ccl4

• MIP-1 alpha and MIP-1 beta mRNA-positive cells appeared around day 10, increased further on days 12-13 and then gradually decreased [3].
• In order of potency, the magnitude of the febrile response induced by RANTES was greater than that produced with equipotent doses of either macrophage inflammatory protein-1beta or interleukin-6 [18].
• Effect of mu-selective opioid antagonists on MIP-1 beta and IL-1 beta-induced fever [19].

Analytical, diagnostic and therapeutic context of Ccl4

• The rats of model group and treatment group were given small dosage of CCL4 combined with a fat-rich diet, and those of control group were given normal diet [20].
• Alteration of hepatic ethanol metabolism in CCL4-intoxicated rats: analysis using isolated liver perfusion system [21].
• Intracellular structures of hepatocytes were studied in rats intoxicated with carbon tetrachloride (CCL4) by scanning electron microscopy (SEM) [22].

References