Disease relevance of Csf2

• Levels of MCP-1 and GM-CSF mRNA correlated with inflammatory cytokines mRNA levels in experimental autoimmune myocarditis in rats [1].
• GM-CSF action in the CNS decreases food intake and body weight [2].
• BACKGROUND: Granulocyte-macrophage colony-stimulating factor modifies wound healing by promoting monocytopoiesis and infiltration of monocytes and macrophages into injured tissue; however, the effect of GM-CSF induction on the infarct healing process and myocardial fibrosis is unclear [3].
• Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction [3].
• OBJECTIVES: We sought to determine the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) induction on post-myocardial infarction (MI) remodeling, especially in relation to the inflammatory response and myocardial fibrosis [3].

Psychiatry related information on Csf2

• Together, these results indicate that GM-CSF treatment has previously unrecognized effects in promoting alveolar epithelial barrier integrity and that these salutary effects may be particularly relevant in the setting of chronic alcohol abuse [4].
• Granulocyte-macrophage colony-stimulating factor modulates rapid eye movement (REM) sleep and non-REM sleep in rats [5].
• RESULTS: CSF norepinephrine concentration was significantly higher in the patients with advanced Alzheimer's disease (mean = 279 pg/ml, SD = 122) than in those with mild to moderate severity (mean = 198 pg/ml, SD = 89), normal older subjects (mean = 219 pg/ml, SD = 88), or normal young subjects (mean = 154 pg/ml, SD = 53) [6].
• The concentration of sICAM-5 correlated with the performance in the immediate recall task (p = 0.013) and with the leukocyte count in the CSF (p = 0.02), especially in cases caused by herpes simplex virus (HSV) (r = 0.94; p = 0.002) [7].
• HLA DQB1*0602 positive narcoleptic subjects with cataplexy have CSF lgG reactive to rat hypothalamic protein extract [8].

High impact information on Csf2

• Granulocyte-macrophage colony-stimulating factor (GM-CSF) augments antigen presentation in a variety of cells [9].
• Idiotype/granulocyte-macrophage colony-stimulating factor fusion protein as a vaccine for B-cell lymphoma [9].
• Bilateral injections of either neurotensin (NT; 0.3, 1 or 5 micrograms in 1 microliter artificial CSF) or haloperidol (HA; 2.5 or 5 micrograms in 1 microliter 0.3% tartaric acid) into nucleus accumbens of rats markedly diminished the forward locomotion and rearing induced by d-amphetamine (AM; 2 mg per kg, IP) [10].
• Taken together, these findings demonstrate that GM-CSF signaling in the CNS can regulate energy homeostasis [2].
• Central but not peripheral administration of GM-CSF to adult rats significantly decreased food intake and body weight for at least 48 hours [2].

Chemical compound and disease context of Csf2

• As in the endotoxemia model in vivo, the effect of GM-CSF was most dramatic in the ethanol group [4].
• MATERIAL AND METHODS: Pre-established macroscopic tumours in BDIX rats were treated by intraperitoneal injections of retrovirus producing cells (FLYA13 TK, FLYA13 granulocyte macrophage-colony stimulating factor (GM-CSF), FLYA13 interleukin 12 (IL-12)) and ganciclovir (GCV) [11].
• To reconcile the autoimmune and excitotoxic hypotheses regarding the etiology of amyotrophic lateral sclerosis (ALS), we injected rats intraperitoneally with ALS immunoglobulins and monitored CSF glutamate, aspartate, glutamine, and glutathione [12].
• When artificial CSF glucose was increased from 10 to 30 mmol/L, rat optic nerves responded to anoxia in a similar manner to mouse optic nerves in 10-mmol/L glucose [13].
• Our results also suggest that vasopressin may aggravate cerebral ischemia in pathological conditions, such as subarachnoid hemorrhage, when the arteriolar response to vasopressin shifts from vasodilation to vasoconstriction due to increased vasopressin levels in plasma and CSF and impaired endothelium-derived relaxation [14].

Biological context of Csf2

• Nucleotide sequence of the Lewis rat granulocyte-macrophage colony stimulating factor [15].
• Thus, GM-CSF in Paneth cells might have an important role in mucosal immunity through increasing the expression of costimulatory molecules in epithelial cells [16].
• Scatchard analysis of equilibrium binding of 125I-GM-CSF to primary rat oligodendrocytes showed an average of 1,110 GM-CSF binding sites per cell, with a kd of 20 pmol/L [17].
• In addition, GM-CSF id, administered as a single dose with antigen, compared favorably with complete Freund's adjuvant (CFA) and alum in eliciting tt specific antibody and cellular immunity [18].
• Transfection site extracts and serum samples obtained 24 hours after gene transfer of hGM-AUGUA cDNA into mouse skin contained greater than 32 ng/mL and 650 pg/mL of GM-CSF protein, respectively, compared with 0.33 ng/mL and less than 8 pg/mL for hGM-AUUUA cDNA [19].

Anatomical context of Csf2

• These findings suggest that elevated MCP-1 and GM-CSF may associate with the migration and proliferation of monocytes/macrophages in EAM [1].
• Thus, we evaluated levels of MCP-1 and GM-CSF mRNA in the myocardium of EAM in rats using a real time quantitative PCR method [1].
• Thus, in neonate rats and, to a lesser extent, in adult rats, cultured CP stroma cells form large colonies of macrophages, in response to M-CSF or GM-CSF, while, under the same conditions, peripheral blood monocytes do not [20].
• In addition, under GM-CSF treatment, free-floating colonies of CD11c(+) monocytic cells are generated which, when restimulated with GM-CSF and IL-4, differentiate into OX62(+)/MHC class II(+) dendritic cells [20].
• Peritoneal macrophages (PM) also migrated in response to AEC-CM and each of the recombinant cytokines; however, AM were much more sensitive to AEC-CM, RANTES, and GM-CSF than were PM [21].

Associations of Csf2 with chemical compounds

• The MI animals were randomized to receive GM-CSF inducer (romurtide 200 microg/kg/day for 7 consecutive days) (MI/Ro) or saline (MI/C) [3].
• In this study, we determined that recombinant rat GM-CSF improved lung liquid clearance (as reflected by lung tissue wet:dry ratios) in ethanol-fed rats anesthetized and then challenged with 2 ml of saline via a tracheostomy tube [4].
• METHODS: Anaesthetized (sodium thiopental 70 mg/kg, i.p.) Wistar rats were injected subcutaneously with 1 microg/kg of hr GM-CSF [22].
• In three tests of dopaminergic antagonism--elevation of levels of CSF homovanillic acid in monkeys, striatal dihydroxyphenylacetic acid in rats, and prolactin in man--as well as in a clinical trial of neuroleptic efficacy in schizophrenics, thiethylperazine was fully active and approximately three times as potent as chlorpromazine [23].
• Adding glutamine at CSF concentration prevented the loss of aspartate and glutamate and revealed an enhancement of aspartate in the terminals at moderate depolarization [24].

Regulatory relationships of Csf2

• These findings indicated that centrally administered GM-CSF stimulates SRIF release through activation of the NO system in the hypothalamus [5].
• Kinetic analysis indicated that GM-CSF stimulated IL-6 expression early (1.5 h), with maximal effect observed at 24 h and up to 5 days thereafter [25].
• In addition, GM-CSF induced Jak2, STAT5A, and STAT5B in BV-2 cells, as it does in monocytes and macrophages [26].
• After ingestion of apoptotic cells, only previously unstimulated, but not GM-CSF-differentiated microglial cells decreased their T cell-activating potential as measured by IFN-gamma secretion in antigen-activated MBP-specific T cells [27].
• The addition of recombinant erythropoietin promotes a rise in the number of megakaryocytes and a shift in ploidy to higher values while recombinant murine granulocyte-macrophage colony stimulating factor is without effect on the cultured megakaryocytes [28].

Other interactions of Csf2

• Thus, MCP-1 and GM-CSF may play an important role in the progression of EAM [1].
• Fibroblasts under basal culture conditions express much higher levels of IL-6 and GM-CSF compared with AMs [29].
• AMs isolated after intratracheal instillation of silica up-regulated mRNA levels of four additional genes [granulocyte/macrophage-colony stimulating factor (GM-CSF), IL-1beta, IL-10, and inducible nitric oxide synthase] [29].
• Direct injection of 5 pmol ET-1 into the SFO resulted in a 20 +/- 3 mm Hg increase in mean arterial pressure (MAP) (+/- SE) and a 14.1 +/- 0.3 pg/ml increase in the mean plasma AVP level (+/- SE) (P < 0.001 vs. artificial CSF) that was blocked by selective ET(A) inhibition [30].
• Electron microscopic examination established that a significant proportion of fibroblastic cell in GM-CSF-, IL-1-alpha- or TGF-beta-treated animals were typical myofibroblasts [31].

Analytical, diagnostic and therapeutic context of Csf2

• Neutralizing antibodies to RANTES and to MCP-1 and immunoprecipitation of GM-CSF decreased the chemotactic activity of AEC-CM by 58%, 29%, and 47%, respectively [21].
• RESULTS: After 10 days of treatment with GM-CSF, the number of small preantral and large preantral follicles was significantly increased compared with the control group (P < 0.05) [32].
• Identification of GM-CSF in Paneth cells using single-cell RT-PCR [16].
• We identified the exclusive expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in Paneth cells using single-cell reverse transcription-polymerase chain reaction and cDNA array [16].
• GM-CSF and IL-2 vaccine therapy and pretreatment with gammaIFN represent effective strategies in reducing hepatic tumor [33].

References