Disease relevance of Cxcl1

• Cytokine-induced neutrophil chemoattractant mediates neutrophil influx in immune complex glomerulonephritis in rat [1].
• Using the rat model of anti-glomerular basement membrane (GBM) nephritis, we found that mRNA for the chemokine CINC (cytokine-induced neutrophil chemoattractant) was induced in the kidney, and the corresponding protein was elaborated by isolated inflamed glomeruli [1].
• Acute lung injury in endotoxemic rats is associated with sustained circulating IL-6 levels and intrapulmonary CINC activity and neutrophil recruitment--role of circulating TNF-alpha and IL-beta [2]?
• CINC-1 evoked a dose-dependent mechanical hypersensitivity, which was already significant 2 h after the cytokine injection, peaked 4 h after and decreased thereafter [3].
• These data suggest that CINC-1, released at sites of inflammation, mediates inflammatory hyperalgesia in rats via release of sympathomimetic amines [3].

Psychiatry related information on Cxcl1

• An inhibitory effect of cytokine-induced neutrophil chemoattractant on corticotropin-releasing factor-induced increase in locomotor activity [4].

High impact information on Cxcl1

• In slice preparations, CXCL1 inhibited embryonic oligodendrocyte precursor migration, and widespread dispersal of postnatal precursors occurred in the absence of CXCR2 signaling [5].
• TNF-alpha production, unlike CINC, was complement and leukocyte dependent [1].
• In sum, we propose that glomerular immune complex deposition/complement activation leads to cytokine production which results in CINC expression by endogenous glomerular cells [1].
• Further, dietary glycine largely prevented increases in IL-1beta and TNF-alpha in the colon 2 days after TNBS, and TNBS induction of CINC and MIP-2 in the colonic tissue also was abrogated by glycine [6].
• Further, mRNA and protein levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, cytokine-induced neutrophil chemoattractant (CINC), and macrophage inflammatory protein (MIP)-2 were detected by reverse-transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively [6].

Chemical compound and disease context of Cxcl1

• Cytokine-induced neutrophil chemoattractant in a rat model of lipopolysaccharide-induced acute lung injury [7].
• The local pre-treatment of the rats with the beta-adrenoceptor antagonist, atenolol (25 microg paw-1), but not with the cyclooxygenase inhibitor indomethacin (100 microg paw-1), inhibited (86%) the CINC-1-induced hypersensitivity [3].
• Although hepatic ischemia/reperfusion-induced increases in hepatic tissue levels of TNF-alpha, cytokine-induced neutrophil chemoattractant, and hepatic accumulation of neutrophils were inhibited by intravenously administered 30 mg/kg ranitidine, these increases were significantly enhanced by 5 mg/kg i.v. famotidine [8].
• Induction of cytokine-induced neutrophil chemoattractant in response to various stresses in rat C6 glioma cells [9].
• Chronic ethanol intoxication enhances the production of cytokine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 by hepatocytes after human immunodeficiency virus-1 glycoprotein 120 vaccination [10].

Biological context of Cxcl1

• When either MIP-2 or CINC was blocked in vivo, up-regulation of Mac-1 expression on neutrophils obtained from BAL fluids was significantly reduced [11].
• The protein, which is referred to as cytokine-induced neutrophil chemoattractant (CINC), has been shown to be a dimer of identical subunits; and the complete amino acid sequence of the subunit has been established [12].
• In vitro, treatment of cultured hepatocytes with IL-1beta led to elevated CINC-1 gene expression [13].
• Increase in the cell number was correlated with total concentrations of CINC-1 and CINC-2 [14].
• Additional studies demonstrated that acute inhalation of crocidolite fibers by rats also induced increased MIP-2 and CINC expression [15].

Anatomical context of Cxcl1

• LPS-stimulated Kupffer cell-conditioned medium enhanced an expression of CINC mRNA in hepatocytes and increased the production of CINC by hepatocytes [16].
• Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells [16].
• Identification of cytokine-induced neutrophil chemoattractants (CINC), rat GRO/CINC-2 alpha and CINC-2 beta, produced by granulation tissue in culture: purification, complete amino acid sequences and characterization [17].
• Regulation of cytokine-induced neutrophil chemoattractant in rat bone marrow-derived macrophages by inflammatory mediators [18].
• Moreover, an immunohistochemical study demonstrated the localization of CINC-1 and CINC-2 alpha primarily in alveolar macrophages and, to a much lesser extent, in bronchial epithelium of infected lung tissues, whereas CINC-2 beta and CINC-3 were not detected [19].

Associations of Cxcl1 with chemical compounds

• The accumulation of CINC/gro mRNA induced by these activators was also decreased comparably by dexamethasone [20].
• Sequence determination has been achieved by automated Edman degradation of reduced and carboxymethylated CINC and of peptides generated by cleavage with cyanogen bromide and lysyl endopeptidase [12].
• The concentrations of CINC-1 and CINC-2 in the exudate during rat lipopolysaccharide (LPS)-induced inflammation were determined [14].
• Acute intratracheal instillation exposure of F344 rats to alpha quartz or titanium dioxide was shown to markedly increase steady-state levels of MIP-2 and CINC mRNA in lung tissue; a response which was associated with a significant increase in neutrophils in the bronchoalveolar lavage fluid [15].
• The results of this study show that Toki-shakuyaku-san can stimulate the secretion of 17 beta-estradiol and stimulate the ovulatory process by stimulating the production of CINC/gro, IL-1 beta and TNF alpha in vitro [21].

Regulatory relationships of Cxcl1

• These results suggest that production of CINC by hepatocytes could be regulated by IL-1 beta released from Kupffer cells, leading to neutrophil accumulation during liver injury, because this protein is a strong chemoattractant for neutrophils [16].
• In addition, carrageenin, LPS and TNF-alpha were shown to stimulate the production of immunoreactive CINC-1 in the skin of injected paws [3].
• This study was designed to determine the production of the chemokine cytokine-induced neutrophil chemoattractant (CINC) by primary rat alveolar type II (ATII) cells upon stimulation with exogenous and endogenous proinflammatory factors [22].
• CINC-3 induced enhancement of cytoplasmic calcium concentration more potently than CINC-1 and CINC-2, and desensitized calcium transients induced by CINC-1 and CINC-2, which were essentially identical to those observed in rat neutrophils [23].
• Hepatocyte growth factor stimulates the induction of cytokine-induced neutrophil chemoattractant through the activation of NF-kappaB in rat hepatocytes [24].

Other interactions of Cxcl1

• In the copresence of eotaxin, the increased levels of MIP-2 and CINC mRNAs were markedly diminished, whereas MIP-1alpha, MIP-1beta, TNF-alpha, and IL-1beta expression of mRNA and protein was not affected [25].
• On the basis of their N-terminal amino acid sequences, one of the chemokines was identical with rat GRO/cytokine-induced neutrophil chemoattractant (CINC) which we reported previously, and another was identical with rat macrophage inflammatory protein-2 (MIP-2) [17].
• Interestingly, IFN-gamma did not effect CINC-1 gene expression [13].
• In conclusion, severe ALI requires a minimum of 48 h LPS infusion in this model and is associated with high levels of circulating IL-6, increased CINC activity, and an increased percentage of PMN count in BALF [2].
• Rat cytokine-induced neutrophil chemoattractant (CINC) is an 8-kD polypeptide originally purified from media conditioned by interleukin-1 beta (IL-1 beta)-stimulated 52E, an epithelioid clone derived from the normal rat kidney (NRK) cell line [26].

Analytical, diagnostic and therapeutic context of Cxcl1

• CINC mRNA also increased as cold-ischemia time was prolonged [27].
• Instillation of recombinant MIP-2 or CINC into the lung increased the number of neutrophils recovered in bronchoalveolar lavage fluid at 4 h, and this effect was enhanced when both chemokines were administered together [28].
• The levels of CINC-1, CINC-2alpha and CINC-3 in BAL fluids were significantly higher in the LPS group than in the saline-instilled control group [7].
• Using ELISA and RT-PCR, we investigated the production and gene expression of GRO/CINC-1 in rat nasal lavage and mucosa in vivo [29].
• We examined the hypothesis that PAF may influence neutrophils by promoting the production of tumor necrosis factor alpha (TNF-alpha) and cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 (IL-8) family, and may be associated with liver and lung injury during the early phase of reperfusion after total hepatic ischemia [30].

References