Disease relevance of Il8rb

• To avoid adverse effects of steroids typically used to modify inflammation, we evaluated the effects of competitive blockade of CXCR2 in rats on neutrophil function in vitro and on neutrophil influx in vivo in hyperoxia-induced newborn lung injury, a model of bronchopulmonary dysplasia [1].
• Contrasting roles for CXCR2 during experimental colitis [2].

High impact information on Il8rb

• CXCR-2 was identified in isolated ECL cells [3].
• CXC receptor 2 (CXCR-2) expression was investigated in ECL cells by reverse-transcription polymerase chain reaction [3].
• IL-8 (or CXCL8) activates the receptors CXCR1 (IL-8RA) and CXCR2 (IL-8RB) to induce chemotaxis in leukocytes, but only CXCR1 mediates cytotoxic and cross-regulatory signals [4].
• (iii) Opioid-containing leukocytes mostly expressed CXCR2 [5].
• In summary, we have shown that TII alveolar epithelial cells produce three of the major proinflammatory CXC chemokines (GRO, CINC-2alpha, and MIP-2) and their cognate receptor CXCR2 [6].

Biological context of Il8rb

• Chemokine receptor CXCR2 activates distinct pathways for chemotaxis and calcium mobilization [7].
• Instead of upregulation like other chemokine receptors, interleukin-8 receptors, CXCR1and CXCR2, mRNA could not be detected in accord with the increase of interleukin-8 [8].
• CXCR1 and CXCR2 are receptors for ELR-positive CXC chemokines which include growth-regulated oncogene alpha (GRO-alpha) and interleukin-8 (IL-8) [9].
• Importance of the carboxy-terminus of the CXCR2 for signal transduction [10].
• In studies of the importance of phosphorylation in CXCR2 desensitization, cells expressing wild type CXCR2 lost GTP gamma S binding above basal rate after the first exposure to IL-8, while cells with the T3 mutant retained 60% of their capacity to induce GTP gamma S exchange upon a second exposure to IL-8 [10].

Anatomical context of Il8rb

• However, only one CINC receptor, CXCR2, has been found in rat neutrophils [7].
• Role of the cytoplasmic tails of CXCR1 and CXCR2 in mediating leukocyte migration, activation, and regulation [4].
• Our results suggest that IL-8 release by glial cells in vivo may activate CXCR1 and CXCR2 receptors on cholinergic septal neurons and acutely modulate their excitability by closing calcium channels [11].
• Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) revealed that CXCR1 mRNAs were expressed in the septum, striatum, hippocampus, cerebellum, and cortex (temporoparietal and entorhinal) at different levels and appeared to be regulated independently from CXCR2 during development [12].
• CXCR1 and CXCR2 transcripts were colocalized in 45% of neurons sampled and also were present in some glial fibrillary acidic protein mRNA-expressing astrocytes [12].

Associations of Il8rb with chemical compounds

• Nonpeptide CXCR2 antagonist prevents neutrophil accumulation in hyperoxia-exposed newborn rats [1].
• Signaling pathways activated by chemokine receptor CXCR2 and AMPA-type glutamate receptors and involvement in granule cells survival [13].
• The cholesterol-induced increases in CXCR2 protein and mRNA expression were significantly attenuated in OVX rats injected with estradiol-17beta (17beta-E2) (5 and 20 microg x kg(-1) x d(-1)) [14].

References