Abnormal in vitro CXCR2 modulation and defective cationic ion transporter expression on polymorphonuclear neutrophils responsible for hyporesponsiveness to IL-8 stimulation in patients with active systemic lupus erythematosus

Rheumatology
S-C HsiehC-L Yu

Abstract

To elucidate the molecular basis of hyporesponsiveness of polymorphonuclear neutrophils (PMN) to interleukin-8 (IL-8) stimulation in patients with active SLE. PMN obtained from active SLE and well-matched healthy individuals were studied. The expression of two IL-8 receptors, CXCR1 and CXCR2, in PMN were detected by flow cytometry and reverse transcriptase-polymerase chain reaction. The binding affinity of PMN with IL-8 was calculated by Scatchard plotting. Soluble CXCR2 level in IL-8-stimulated PMN culture supernatant was measured by sandwich enzyme-linked immunosorbent assay. The resting and IL-8-stimulated membrane potential (MP) changes, and membrane expression of cationic ion transporters including Na+-K+-ATPase, renal epithelial Na+ channel (ENaC) and renal outer medullary epithelial K+ channel 1 (ROMK1) on PMN were detected by flow cytometry. Compared with normal PMN, decreased CXCR2 gene expression, but normal IL-8-binding affinity of SLE-PMN, was found. For exploring the molecular basis of the defect, the modulation of CXCR2 in SLE-PMN was intensively investigated. We found that increased cytosolic CXCR2 expression in SLE-PMN was due to defective surface translocation, increased spontaneous internalization and/or incre...Continue Reading

Citations

Sep 29, 2011·Nature Reviews. Rheumatology·Mariana J Kaplan
Nov 12, 2014·International Reviews of Immunology·Margherita Sisto, Sabrina Lisi
Jan 15, 2008·Autoimmunity Reviews·José C Crispín, George C Tsokos
Apr 3, 2020·Cellular & Molecular Immunology·Mieke MetzemaekersPaul Proost

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