Measuring eosinophiluria, urinary eosinophil cationic protein and urinary interleukin-5 in patients with Lupus Nephritis

Abstract

BackgroundUrine is increasingly becoming an attractive biological fluid in clinical practice due to being an easily obtained, non-invasive sampling method, containing proteins and peptides. The aim of this study was to investigate eosinophiluria, urinary eosinophil cationic protein (uECP) and urinary IL-5 (uIL-5) in patients with Lupus Nephritis.MethodsSeventy-four patients with SLE—20 with clinical and laboratory evidence of lupus nephritis (LN group) and 54 without evidence of renal involvement (non-LN group)—were analyzed regarding eosinophiluria, uECP and uIL-5. Eosinophiluria was observed by Hansel's stain, ECP by fluoroenzymeimmunoassay and uIL-5 by quantitative sandwich enzyme immunoassay. Both uECP and urinary IL-5 (uIL-5) were corrected by urinary creatinine. Eosinophiluria and uECP were compared with glomerular erythrocyturia, protein/creatinine ratio (Pr/Cr ratio), serum creatinine, estimated glomerular filtration rate (eGFR), anti-double-stranded DNA (anti-dsDNA), serum levels of complement (C3 and C4), uIL-5/Cr ratio, and SLE disease activity index.ResultsPatients of the LN group had higher eosinophiluria, uECP, uECP/Cr ratio levels, and uIL-5 than patients of the non-LN group (p<0.001 for all). These variables showed a statistically significant correlation with glomerular erythrocyturia, casts, Pr/Cr ratio, serum creatinine, eGFR, anti-dsDNA, uIL-5/Cr, and SLE disease activity index (all p<0.05).ConclusionThese results provide evidence of increased urinary eosinophils, ECP and IL-5 in patients with SLE and LN; uECP/Cr ratio showed better correlation with markers of renal function and SLE disease activity.

PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia

“…IL-5 is the most specific to the eosinophil lineage and is responsible for selective differentiation, regulating growth, activation, and survival of eosinophils (Brito et al, 2014). IL-13 is the major cytokine-induced striking asthmalike tissue and physiologic responses including airway hyperreactivity, goblet cell hyperplasia, eosinophilic inflammation in mice (Grünig et al, 1998;Wills-Karp et al, 1998;Zhu et al, 1999).…”

Deep Phenotyping of Urinary Leukocytes by Mass Cytometry Reveals a Leukocyte Signature for Early and Non-Invasive Prediction of Response to Treatment in Active Lupus Nephritis

“…Although the cellular composition of the urine sediment has already been analyzed in several studies (13)(14)(15)(20)(21)(22)(23), these commonly fluorescence-based flow cytometric analyses were restricted by methodological limitations, such as limited number of parameters necessary for deep and comprehensive profiling of leukocyte subsets, issues emerging from autofluorescence of cells present in the urine, and how these can be appropriately compensated for when spilled over in the fluorescence channels of interest. As mass cytometry eliminates these technical limitations, we have used it for a deep comparative profiling of blood and urinary leukocytes.…”

“…: pauci-immune. (20), most studies conducted so far focused on mononuclear cell subsets, although they account for only 20% of total cells detectable in urine of LN patients (21). Several recent publications indicate that granulocytes (neutrophils, basophils, and eosinophils) play an important role in SLE pathogenesis by promoting innate and adaptive aberrant autoimmune responses and enhancing tissue damage (25).…”

Role of iron and oxidative stress in the exacerbation of allergic inflammation in murine lungs caused by urban particulate matter <2.5 μm and desert dust

“…T‐helper (Th)2 cytokine IL‐5 causes eosinophil infiltration into the airways submucosa and airways hyper‐responsiveness (Ok, Kim, Kim, Lee, & Lee, ), selective differentiation, regulating growth, activation and survival of eosinophils (Brito et al, ). Th2 cytokine IL‐13 causes airways hyper‐reactivity, goblet cell proliferation and eotaxin production (Grünig et al, ; Wills‐Karp et al, ; Zhu et al, ).…”

“…OVA + ASD + LPS + DFO markedly suppressed the infiltration of these inflammatory cells ( Figure 7F). (Brito et al, 2014). Th2 cytokine IL-13 causes airways hyper-reactivity, goblet cell proliferation and eotaxin production (Grünig et al, 1998;Wills-Karp et al, 1998;Zhu et al, 1999).…”