Serum Lipocalin-2 Research Articles

The relationship among serum lipocalin 2, bone turnover markers, and bone mineral density in outpatient women.

We aimed to investigate associations among serum levels of LCN2, bone resorption marker carboxy-terminal cross-linking telopeptide of type-1 collagen (CTx), bone formation marker osteocalcin (OCN), and bone mineral densities (BMDs) in ambulatory healthy women. This cross-sectional study analyzed 1012 previously enrolled outpatient Han Chinese women. BMDs of the lumbar spine and femoral neck were measured using dual energy X-ray absorptiometry. Serum levels of LCN2, CTx, OCN, and creatinine (Scr) were measured. Circulating LCN2 was inversely correlated with BMDs at the lumbar spine and femoral neck (Spearman's r = -0.08, P = 0.010 and r = -0.14, P < 0.001; respectively). A significant positive correlation between LCN2 and CTx (r = 0.11, P < 0.001), OCN (r = 0.06, P = 0.047), age (r = 0.21, P < 0.001), and Scr (r = 0.24, P < 0.001) was also observed. After adjusting for age and Scr, the correlation among LCN2, BMDs and OCN disappeared, but LCN2 was still positively associated with CTx (r = 0.08, P = 0.010). The circulating concentration of LCN2 showed no significant difference between subjects with and without osteoporotic fractures (43.63 (35.29, 53.66) vs. 42.25 (34.43, 51.46) ng/ml, respectively, P = 0.111). Serum CTx concentrations rose with serum LCN2 increasing from the lowest to the highest quartile (P for trend = 0.005), even after adjusting for age and Scr (P for trend = 0.040). In multivariate regression analysis, LCN2 was one of the main determinants for changes in serum CTx (standard β = 0.061, P = 0.005). In ambulatory healthy women, the relationships among serum LCN2 level, BMDs, and OCN were confounded by age and Scr. Although LCN2 was positively related with CTx, the correlation was very weak and may not be physiologically relevant.

Clinical efficacy of sublingual immunotherapy is associated with restoration of steady-state serum lipocalin 2 after SLIT: a pilot study

Background So far, only a few biomarkers in allergen immunotherapy exist that are associated with a clinical benefit. We thus investigated in a pilot study whether innate molecules such as the molecule lipocalin-2 (LCN2), with implications in immune tolerance demonstrated in other fields, may discriminate A) between allergic and non-allergic individuals, and B) between patients clinically responding or non-responding to sublingual allergen immunotherapy (SLIT) with house dust mite (HDM) extract. Moreover, we assessed haematological changes potentially correlating with allergic symptoms.Methods LCN2-concentrations were assessed in sera of healthy and allergic subjects (n = 126) as well as of house dust mite (HDM) allergics before and during HDM- sublingual immunotherapy (SLIT) in a randomized, double-blind, placebo-controlled trial for 24 weeks. Sera pre-SLIT (week 0), post-SLIT (week 24) and 9 months after SLIT were assessed for LCN2 levels and correlated with total nasal symptom scores (TNSS) obtained during chamber challenge at week 24 in patients receiving HDM- (n = 31) or placebo-SLIT (n = 10).Results Allergic individuals had significantly (p < 0.0001) lower LCN2-levels than healthy controls. HDM-allergic patients who received HDM-SLIT showed a significant increase in LCN2 9 months after termination of HDM-SLIT (p < 0.001), whereas in subjects receiving placebo no increase in LCN2 was observed. Among blood parameters a lower absolute rise in the lymphocyte population (p < 0.05) negatively correlated with symptom improvement (Pearson r 0.3395), and a lower relative increase in the neutrophils were associated with improvement in TNSS (p < 0.05). LCN2 levels 9 months after immunotherapy showed a low positive correlation with the relative improvement of symptoms (Pearson r 0.3293). LCN2-levels 9 months off-SLIT were significantly higher in patients whose symptoms improved during chamber challenge than in those whose symptoms aggravated (p < 0.01).Conclusion Serum LCN2 concentrations 9 months off-SLIT correlated with clinical reactivity in allergic patients. An increase in the LCN2 levels 9 months after HDM-SLIT was associated with a clinical benefit. Serum LCN2 may thus contribute to assess clinical reactivity in allergic patients.Trial registration Part of the data were generated from clinicaltrials.gov Identifier NCT01644617.

Exploiting bilosomes for delivering bioactive polysaccharide isolated from Enteromorpha intestinalis for hacking hepatocellular carcinoma

Bile salts containing vesicles (bilosomes) represent a portentous vesicular carrier that showed prosperous results in delivering active moieties in the gastrointestinal tract (GIT). In this study, bilosomes were exploited to deliver sulfated polysaccharide–protein complexes of Enteromorpha intestinalis (EHEM) and enhance its activity against hepatocellular carcinoma as well as resist harsh GIT conditions. Bilosomes were prepared using the sodium salt of three different bile acids (cholic, deoxycholic, taurodeoxycholic) and two different nonionic surfactants (Span 40 and 65). The effects of experimental variables were thoroughly studied to obtain an optimum formulation loading EHEM. The selected formulation (EH-Bilo-2) prepared with sodium cholate and Span 65 displayed nano-sized (181.1 ± 16.80 nm) spherical vesicles with reasonable entrapment efficiency (71.60 ± 0.25%) and controlled release properties; and thus was investigated as anti-hepatocarcinogenic candidate for in vivo studies. Treatment of hepatocellular carcinoma (HCC) bearing rats with EH-Bilo-2 experienced significant decrease in serum α-fetoprotein, endoglin, lipocalin-2, and heat shock protein 70 levels vs. the untreated counterparts. Furthermore, the photomicrographs of their liver tissue sections showed focal area of degenerated pleomorphic hepatocytes with fine fibrosis originating from the portal area. Thus, the optimized bilosomal formulation is a promising delegate for tackling hepatocellular carcinoma owing to its powerful anti-cancer and anti-angiogenic activity.

Serum lipocalin-2 concentrations and mortality of severe traumatic brain injury

BackgroundLipocalin-2 is related to acute brain injury. We assessed the prognostic value of serum lipocalin-2 in head trauma. MethodsBlood samples were collected from 115 controls and 115 patients with severe traumatic brain injury. Trauma severity was assessed by Glasgow Coma Scale (GCS) scores at baseline. Thirty-day mortality and overall survival time were recorded. ResultsCompared with the controls, serum lipocalin-2 concentrations were significantly increased in the patients. Lipocalin-2 concentrations were independently associated with GCS scores (t=−7.271, P<0.001) and serum C-reactive protein concentrations (t=4.325, P<0.001). Under receiver operating characteristic curve for 30-day mortality, sensitivity and specificity were 85.7% and 63.2% respectively for lipocalin-2 concentrations at a cutoff value of 591ng/ml. Additionally, area under curve (AUC) of lipocalin-2 concentrations [AUC, 0.825; 95% confidence interval (95% CI), 0.743–0.889] was equivalent to that of GCS scores (AUC, 0.869; 95% CI, 0.793–0.925; P=0.413). Moreover, serum lipocalin-2 concentrations >591ng/ml emerged as an independent predictor for 30-day mortality (odds ratio, 4.360; 95% CI, 1.908–12.430) and overall survival (hazard ratio, 3.820; 95% CI, 1.935–10.500). ConclusionsEnhanced serum concentration of lipocalin-2 at admission is associated with trauma severity and neuroinflammation as well as is a predictor of mortality after head trauma.

Association of lipocalin-2 level, glycemic status and obesity in type 2 diabetes mellitus

BackgroundManagement of type 2 diabetes mellitus aims to maintain a normal glycemic status, which if not, it may lead to acute and/or chronic diabetic complications. Earlier studies found Lipocalin-2 elevated in complications associated with type 2 diabetes mellitus such as ischemic heart disease. These lipocalin-2 changes had been linked to obesity and uncontrolled diabetes. So, it could be useful to understand the effect of glycemic control and obesity on lipocalin-2.MethodsThis was a case control study. Fifty-seven patients with type 2 diabetes and 30 non-diabetic controls participated after getting a written consent. Weight (kg), height (m) and waist circumference (cm) were measured then the body mass index (kg/m2) was determined. Blood samples were collected after an overnight fasting. HbA1c, lipid profile and serum creatinine were measured using enzymatic methods. Lipocalin-2 was measured using sandwich ELISA.ResultsLipocalin-2 was found significantly higher in patients with type 2 diabetes (P = 0.001). However, it had no significant correlation with any of the studied variables. Females had elevated BMI compared to males in the patients group (P < 0.001). HbA1c, serum creatinine, LDL and total cholesterol were elevated in patients with diabetes (P < 0.02). HDL was lower in the patients (P = 0.002). Significant elevation in HbA1c was found in male patients (P = 0.028) compared to female patients. Patients were further classified into controlled, uncontrolled diabetics, obese and non-obese. There was a significant elevation in waist circumference in uncontrolled diabetics compared to controlled ones. Lipocalin-2 had no significant changes between controlled and uncontrolled diabetics nor non-obese and obese patients.ConclusionPatients with type 2 diabetes mellitus have elevated level of serum lipocalin-2. There was no significant association found between lipocalin-2 and glycemic control nor obesity.

EFFECT OF TESTOSTERONE ON SERUM LIPOCALIN-2 IN ORCHIDECTOMIZED ADULT MALE ALBINO RATS

Background: Lipocalin-2 (Lcn2) was initially identified as a protein secreted from human neutrophils. It has been implicated in many functions as inflammation, cell survival, innate immunity and biology of the genitourinary system as a developmental and a protective factor. The effect of testosterone on the circulating lipocalin-2 level in adult male rats is still unknown. Objective: To explore the effect of testosterone on serum lipocalin-2 levels in orchidectomized adult male albino rats. Material and Methods: The present study was conducted on 32 adult male albino Wistar rats divided into 4 equal groups: group (I): Sham operated control group; group (II): Orchidectomized group; group (III): Orchidectomized with subcutaneous physiologic testosterone replacement therapy; group (IV): Orchidectomized with subcutaneous supra-physiologic dose of testosterone. Results: In group (II) and group (III), serum lipocalin-2 level significantly decreased compared to control group. In group (IV), there was further significant reduction in serum lipocalin-2 when compared with control group, group II and group III with a significant negative correlation with serum testosterone level. Conclusion: Normal physiologic levels of testosterone are needed for normal lipocalin-2 expression. Disturbance of testosterone level (either by decrease or increase) significantly decreased lipocalin-2 level.

Impact of terlipressin infusion during and after live donor liver transplantation on incidence of acute kidney injury and neutrophil gelatinase-associated lipocalin serum levels: A randomized controlled trial.

Acute kidney injury (AKI) with liver transplantation (LT) is not uncommon. Impact of terlipressin infusion on AKI, hemodynamics, and plasma concentration of neutrophil gelatinase-associated lipocalin (NGAL) was studied. Patients (n=50) were randomized (NCT02059460, USA) into two equal groups: terlipressin vs Controls. Terlipressin (1-4μg/kg/h) was administrated for 5days. Intraoperative transesophageal Doppler for hemodynamic management. Renal functions, peak portal vein blood flow velocity (PPV), and hepatic artery resistive index (HARI) were recorded. Plasma NGAL (pNGAL) was measured baseline, 2 and 24hours postreperfusion. Hepatitis C virus (HCV) was the main etiology. Age, sex, model of end-stage liver disease (MELD), and renal functions were comparable. Postoperative AKI incidence and NGAL concentrations were comparable (P>.05) between terlipressin and controls groups (44% vs 48% and 112.5±9 vs 93.1±8ng/mL), respectively, but intraoperative NGAL in both groups increased significantly 2hours postreperfusion (P<.05). The three NGAL readings were comparable (P>.05) between AKI (n=23) and non-AKI developers (n=27). Mean arterial blood pressure (MAP) was maintained in both groups with less systemic vascular resistance (SVR) fluctuations with terlipressin. Median norepinephrine consumption was lower in terlipressin vs controls (8 vs 12mg; P=.04). The PPV and HARI were not affected by terlipressin at any stage (P>.05). Postliver transplant AKI was not prevented by terlipressin use nor predicted by NGAL levels.

Serum lipocalin-2 is a potential biomarker for pruritus in patients with psoriasis

Serum lipocalin-2 is a potential biomarker for pruritus in patients with psoriasis

Effect of curcumin on inhibiting atherogenesis by down-regulating lipocalin-2expression in apolipoprotein E knockoutmice.

Curcumin possesses significant anti-atherosclerosis properties. Lipocalin-2 (LCN2) is already known as one of the most promising biomarkers of atherosclerosis. However, research on the effect of curcumin on regulating LCN2 expression in atherogenesis is very limited. The aim of the study was to investigate whether curcumin could alleviate atherosclerosis in ApoE-/- mice by down-regulating LCN2 expression. Fifty apolipoprotein E knockout (ApoE-/-) mice were fed with a western diet for 12 weeks and randomly divided into five groups: model group (Mod), positive control group (Lov, with 30mg/kg/d lovastatin), three curcumin groups (CurL, CurM and CurH, with 40, 60 and 80mg/kg/d curcumin), while 10 C57BL/6J mice were fed with a standard mouse chow diet as a control group (Con). LCN2 in serum and aorta, biomarkers of serum lipid and inflammation were determined and the plaque area of the atherosclerosis lesions was quantified. CurM and CurH group were significantly lower than Mod group in terms of serum LCN2, lipid and inflammatory cytokine levels, plaque area and LCN2 expression in atherosclerotic lesions, similar to lovastatin treatment. Our findings indicate that dietary curcumin ameliorates western diet-induced atherosclerosis in ApoE-/- mice, which is related to LCN2 down-regulation, anti-hyperlipidemia effect as well as the inhibition of inflammation.

Lipocalin-2 expression and serum levels as early predictors of type 2 diabetes mellitus in obese women.

Obesity and diabetes are increasing in epidemic proportions globally. Lipocalin-2 (LCN-2) is an inflammatory adipocytokine and obesity-related marker of low-grade inflammation. We aimed to investigate, for first time, the possible role of LCN-2 expression and serum levels in prediction of impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) among obese Egyptian women. This study included 188 obese women and 180 controls. Obese women were subdivided into three subgroups according to their fasting blood glucose, normal glucose tolerance (NGT), IGT and T2DM. Circulating LCN-2 expression levels were determined by real time polymerase chain reaction. Serum LCN-2 concentrations were assessed by ELISA. Our findings revealed that LCN-2 expression and serum levels were higher in obese women compared to lean controls. They were higher in IGT and T2DM obese cases than in NGT obese women. Receiver operating characteristic analyses revealed that LCN-2 expression level was a useful biomarker discriminating IGT from NGT and T2DM from IGT obese women (AUC were 0.735 and 0.740, respectively). It was an independent predictor of IGT and T2DM among obese women. Serum LCN-2 level was a useful biomarker discriminating IGT from NGT and T2DM from IGT obese women (AUC were 0.705 and 0.728, respectively). It was independent predictor of T2DM without predicting IGT among obese women. The power of combined LCN-2 serum levels and expression in discriminating between IGT from NGT and T2DM from IGT obese women was high (AUC = 0.717 and 0.741, respectively). In conclusion, LCN-2 expression and serum levels could discriminate IGT from NGT and T2DM from IGT obese women and early predicting T2DM among obese women. While, LCN-2 expression level was the independent predictor of IGT in obese women. Combination of both LCN-2 expression and serum levels improved their diagnostic value in early detection of IGT and T2DM among obese women. © 2017 IUBMB Life, 69(2):88-97, 2017.

Altered Systemic Adipokines in Patients with Chronic Urticaria

Background: Increasing evidence suggests that adipokines affect immune responses and chronic urticaria (CU) is associated with an altered immune response related to chronic systemic inflammation. Our objectives were to investigate whether adipokines are involved in CU pathogenesis and to outline relationships between adipokines and urticaria severity and quality of life. Methods: Serum adiponectin, leptin, lipocalin-2 (LCN2), interleukin (IL)-10, IL-6, and tumor necrosis factor (TNF)-α concentrations were measured by enzyme-linked immunosorbent assays in 191 CU patients and 89 healthy controls. The effect of LCN2 on N-formyl-methionine-leucine-phenylalanine (fMLP)-induced neutrophil chemotaxis was assessed using migration assays. CU severity was assessed based on the urticaria activity score (UAS). To explore relationships between adipokines and UAS and the chronic urticaria-specific quality of life (CU-QoL) questionnaire, a structural equation model was used. Results: Mean levels of serum LCN2, TNF-α, IL-6, and IL-10 were significantly higher in CU patients than in controls. Adiponectin levels were significantly lower in patients with CU than in controls. While serum IL-6 levels were significantly higher in refractory CU patients, compared to responsive CU individuals, LCN2 levels were significantly lower. LCN2 inhibited fMLP-induced neutrophil migration. LCN2 showed a direct relationship with UAS (β = -0.274, p < 0.001), and UAS was found to contribute to CU-QoL (β = 0.417, p < 0.001). Conclusions: Our results highlighted an imbalance in pro- and anti-inflammatory adipokines in CU patients. We suggest that LCN2 could be a differential marker for disease activity and the clinical responses to antihistamine treatment in CU patients. Modulation of systemic inflammation may be a therapeutic strategy for treating severe, refractory CU.

Lipocalin 2 over-expression facilitates progress of castration-resistant prostate cancer via improving androgen receptor transcriptional activity.

BackgroundCastration-resistant prostate cancer (CRPC) is the lethal phenotype of prostate cancer. Lipocalin 2 (LCN2) is aberrantly expressed in many cancers including primary prostate cancer (PCa), but its role in CRPC has not been reported.ResultsLCN2 expression was upregulated in human primary PCa and CRPC tissues. Overexpression of LCN2 promoted C4-2B and 22RV1 cell proliferation while knockdown of LCN2 markedly inhibited C4-2B and 22RV1 cell growth. LCN2 overexpression led to increased AR downstream gene SLC45A3 without upregulating AR expression. In the xenograft model, overexpression of LCN2 significantly promoted tumor growth.MethodsLCN2 expression was detected in primary PCa and CRPC tissues and cell lines C4-2B and 22RV1 using immunohistochemistry and western blotting, respectively. Serum LCN2 level was detected vi ELISA. Lentiviruses-mediated over-expression of LCN2 and LCN2 knockdown were performed in CRPC cell lines. Expressions of androgen receptor (AR) downstream genes was examined in cell lines, in CRPC tissues, and in animal models.ConclusionLCN2 could facilitate cell proliferation of CRPC via AR transcriptional activity. LCN2 could be a novel target in CRPC.

Cerebrospinal fluid lipocalin 2 in patients with clinically isolated syndromes and early multiple sclerosis

Background: Lipocalin 2 (LCN2) may be involved in the immunopathogenesis of multiple sclerosis (MS) and might further impact on iron homoeostasis. Brain iron accumulates in MS; however, the association to iron-related proteins is still unsolved. Objective: To investigate cerebrospinal fluid (CSF) and serum LCN2, transferrin (Trf) and ferritin in early MS in relation to disease evolution and longitudinal brain iron accumulation. Methods: We analysed CSF and serum LCN2 by enzyme-linked immunosorbent assay (ELISA) and Trf and ferritin by nephelometry in 55 patients (45 clinically isolated syndrome (CIS), 10 MS, median clinical follow-up 4.8 years) and 63 controls. In patients, we assessed sub-cortical grey matter iron by 3T magnetic resonance imaging (MRI) R2* relaxometry (median imaging follow-up 2.2 years). Results: Compared to controls serum (p < 0.01), CSF (p < 0.001) LCN2 and CSF Trf (p < 0.001) levels were reduced in the patients. CSF LCN2 correlated with CSF Trf (r = 0.5, p < 0.001). In clinically stable patients, CSF LCN2 levels correlated with basal ganglia iron accumulation (r = 0.5, p < 0.05). In CIS, higher CSF LCN2 levels were associated with conversion to clinically definite MS (p < 0.05). Conclusion: We demonstrate altered LCN2 regulation in early MS and provide first evidence for this to be possibly linked to both clinical MS activity and iron accumulation in the basal ganglia.

Serum lipocalin-2 levels are positively associated with not only total body fat but also visceral fat area in Chinese men.

Serum lipocalin-2 (LCN2) plays an important role in the regulation of the obesity-associated dysmetabolic state and cardiovascular disease. However, relatively little is known about the relationship between serum LCN2 levels and body fat content and distribution. We examined the associations of total body fat content and abdominal fat distribution with serum LCN2 levels in Chinese men.The study was based on a cross-sectional analysis of data for 1203 Chinese men aged 22 to 78 years from the Shanghai Obesity Study. Body fat percentage (fat%) was assessed by bioelectrical impedance analysis, and magnetic resonance imaging was adopted to quantify the visceral fat area (VFA) and subcutaneous fat area (SFA). Serum levels of LCN2 were measured with a standard enzyme-linked immunosorbent assay method.Subjects with a high fat% had higher serum LCN2 levels than those with a normal fat% regardless of their body mass index category (<25 and ≥25 kg/m2). The frequency of isolated high VFA was increased with increasing quintiles of serum LCN2 levels (P < 0.001), but the frequency of isolated high SFA did not differ between quintiles of serum LCN2 levels. A trend of increasing VFA was observed with increasing serum LCN2 levels (P < 0.001). Multiple stepwise regression analysis showed that VFA was positively associated with serum LCN2 levels, independent of overall obesity and other confounding factors (standardized β = 0.082, P = 0.008).Serum LCN2 levels are positively correlated with body fat content and independently associated with VFA in Chinese men.

Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

Lipocalin 2 (LCN2) is induced in the injured liver and associated with inflammation. Aim of the present study was to evaluate whether serum LCN2 is a non-invasive marker to assess hepatic steatosis in patients with non-alcoholic fatty liver disease (NAFLD) or residual liver function in patients with liver cirrhosis. Therefore, LCN2 was measured by ELISA in serum of 32 randomly selected patients without fatty liver (controls), 24 patients with ultrasound diagnosed NAFLD and 42 patients with liver cirrhosis mainly due to alcohol. Systemic LCN2 was comparable in patients with liver steatosis, those with liver cirrhosis and controls. LCN2 negatively correlated with bilirubin in both cohorts. In cirrhosis, LCN2 was not associated with more advanced liver injury defined by the CHILD-PUGH score and model for end-stage liver disease score. Resistin but not C-reactive protein or chemerin positively correlated with LCN2. LCN2 levels were not increased in patients with ascites or patients with esophageal varices. Consequently, reduction of portal pressure by transjugular intrahepatic portosystemic shunt did not affect LCN2 levels. Hepatic venous blood (HVS), portal venous blood and systemic venous blood levels of LCN2 were similar. HVS LCN2 was unchanged in patients with end-stage liver cirrhosis compared to those with well-compensated disease arguing against increased hepatic release. Current data exclude that serum LCN2 is of any value as steatosis marker in patients with NAFLD and indicator of liver function in patients with alcoholic liver cirrhosis.

Effect of psoriasis activity and topical treatment on serum lipocalin-2 levels

Objective: Psoriasis has been considered as systemic disorder. Lipocalin-2 might be a link between psoriasis and its comorbidities. Aim of the study was to investigate the associations between serum lipocalin-2 levels and the disease activity, markers of inflammation or metabolic disturbances and changes after topical treatment in psoriatic patients. Methods: Thirty-seven individuals with active plaque-type psoriasis and 15 healthy controls were recruited. Blood samples were collected before and after 14 days of therapy. Serum lipocalin-2 concentrations were examined by enzyme-linked immunosorbent assay. The results were correlated with Psoriasis Area and Severity Index (PASI), body mass index (BMI), inflammatory and biochemical markers, lipid profile and with effectiveness of topical treatment.Results: Lipocalin-2 serum levels were significantly increased in psoriatic patients in comparison to the controls (p = 0.023). No significant correlations with indicators of inflammation, nor BMI or PASI were noted. A statistical association between lipocalin-2 and low-density lipoprotein-cholesterol was shown. After topical treatment serum lipocalin-2 level did not significantly change (p = 0.9), still remaining higher than in the controls, despite clinical improvement.Conclusions: Lipocalin-2 might be a marker of psoriasis and convey cardiovascular or metabolic risk in psoriatic patients, but may not be a reliable indicator of inflammation, severity of psoriasis nor efficacy of antipsoriatic treatment.

Induction of Lipocalin2 in a Rat Model of Lung Irradiation.

Previously, we showed that lipocalin2 (LCN2) serum levels increased after liver irradiation and during acute-phase conditions. Here, we evaluate LCN2 expression and serum levels after single-dose lung irradiation with 25 Gy, percutaneously administered to the lung of randomly-paired male Wistar rats. Due to the concave anatomy of the lung recesses, the irradiation field included the upper part of the liver. No rat died due to irradiation. In control tissue, lung immunohistochemistry showed a high constitutive expression of LCN2+ granulocytes. LCN2 mRNA levels in lung tissue increased up to 24 h (9 ± 2.3-fold) after irradiation. However, serum LCN2 levels remained undetectable after lung irradiation. LCN2 expression in the upper part of the liver increased up to 4.2-fold after lung irradiation, but the lower liver showed an early decrease. Acute-phase cytokines (IL-1β and TNF-α) showed a significant increase on transcript level in both lung and upper liver, whilst the lower liver did not show any considerable increase. In conclusion, constitutive expression of LCN2 in local immune cells demonstrates its local role during stress conditions in the lung. The absence of LCN2 in the serum strengthens our previous findings that the liver is the key player in secreting LCN2 during stress conditions with liver involvement.

Giant unilamellar vesicles containing Rhodamine 6G as a marker for immunoassay of bovine serum albumin and lipocalin-2

Functionalized giant unilamellar vesicles (GUVs) containing a fluorescence dye Rhodamine 6G is proposed as a marker in sandwich-type immunoassay for bovine serum albumin (BSA) and lipocalin-2 (LCN2). The GUVs were prepared by the electroformation method and functionalized with anti-BSA antibody and anti-LCN2 antibody, respectively. The purification of antibody-modified GUVs was achieved by conventional centrifugation and a washing step in a flow system. To antigen on an antibody slip, antibody-modified GUVs were added as a marker and incubated. After wash-out of excess reagents and lysis of the bound GUVs with Triton X-100, the fluorescence image was captured. The fluorometric immunoassays for BSA and LCN2 exhibited lower detection limits of 4 and 80 fg ml−1, respectively.

Effect of psoriasis activity and topical treatment on serum lipocalin-2 levels

Effect of psoriasis activity and topical treatment on serum lipocalin-2 levels

SERUM LIPOCALIN-2 PREDICTS CARDIOVASCULAR MORBIDITY RISKS IN SUBCLINICAL HYPOTHYROID RAT MODEL

Background: Subclinical hypothyroidism (SCH) and its associations with cardiovascular disease (CVD) remain controversial. Previous studies revealed that lipocalin -2 (LCN2) associated with increased cardiovascular mortality risk. Objective: Evaluation of the serum level of LCN2 and its association with some cardiovascular risk factors in SCH rat model. Material and methods: Twenty four adult male albino rats weighing 150-170 g were used and divided into two equal groups: control euthyroid group and SCH-induced group where SCH was induced by administration of methimazole (MMI) (10 mg/kg body weight) by gavage once daily for 3 months. Groups were compared for body mass index (BMI), serum thyroid-stimulating hormone (TSH), triiodothyronine (T3) thyroxin (T4), glucose, insulin, lipid profiles, C reactive protein (CRP), LCN2 ,Homeostasis model assessment of insulin resistance (HOMA-IR), atherogenic index ,systolic (SBP) and diastolic blood pressure (DBP). Results: SCH induced group showed significantly higher mean serum levels of TSH, LCN2, insulin, total cholesterol, low density lipoprotein - cholesterol (LDL- C), triglycerides (TG), CRP than that of control. Also, BMI, calculated HOMA, atherogenic index, SBP and DBP were significantly higher than that of control and all these parameters were positively correlated to LCN2. However, high density lipoproteins- cholesterol (HDL- c) levels were significantly lower than that of control group and negatively correlated with serum LCN2 levels. Conclusion: Serum lipocalin-2 may be associated and can predict cardiovascular risk factors in SCH.