The aim of this study was to assess cross-sectional and longitudinal correlations between uEPX and other markers of asthma control and eosinophilic airway inflammation. <i  >Methods</i>. We measured uEPX at baseline, after 1&#x2009;year and after 2&#x2009;years in 205 atopic asthmatic children using inhaled fluticasone. At the same time points, we assessed symptom scores (2 weeks diary card), lung function (forced expiratory volume in one second (FEV<sub  >1</sub>)), airway hyperresponsiveness (AHR), and percentage eosinophils in induced sputum (&#x25; eos). <i  >Results</i>. We found negative correlations between uEPX and FEV<sub  >1</sub> at baseline (<svg     style="vertical-align:-1.59705pt;width:130.35001px;" id="M1" height="13.1625" version="1.1" viewBox="0 0 130.35001 13.1625" width="130.35001"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x1D45F" d="M393 379q-9 -16 -28 -29q-15 -10 -23 -2q-19 19 -36 19q-21 0 -52 -38q-57 -72 -82 -126l-40 -197q-23 -3 -75 -18l-7 7q49 196 74 335q7 43 -2 43q-7 0 -30 -14.5t-47 -37.5l-16 23q37 42 82 73t67 31q41 0 15 -113l-11 -50h4q41 71 85 117t77 46q29 0 45 -26&#xA;q13 -21 0 -43z" /></g><g transform="matrix(.017,-0,0,-.017,11.945,11.112)"><path id="x3D" d="M535 323h-483v50h483v-50zM535 138h-483v50h483v-50z" /></g><g transform="matrix(.017,-0,0,-.017,26.649,11.112)"><path id="x2212" d="M535 230h-483v50h483v-50z" /></g><g transform="matrix(.017,-0,0,-.017,36.627,11.112)"><path id="x30" d="M241 635q53 0 94 -28.5t63.5 -76t33.5 -102.5t11 -116q0 -58 -11 -112.5t-34 -103.5t-63.5 -78.5t-94.5 -29.5t-95 28t-64.5 75t-34.5 102.5t-11 118.5q0 58 11.5 112.5t34.5 103t64.5 78t95.5 29.5zM238 602q-32 0 -55.5 -25t-35.5 -68t-17.5 -91t-5.5 -105&#xA;q0 -76 10 -138.5t37 -107.5t69 -45q32 0 55.5 25t35.5 68.5t17.5 91.5t5.5 105t-5.5 105.5t-18 92t-36 68t-56.5 24.5z" /></g><g transform="matrix(.017,-0,0,-.017,44.786,11.112)"><path id="x2E" d="M113 -12q-24 0 -39.5 16t-15.5 42q0 24 16 40.5t40 16.5t40 -16.5t16 -40.5q0 -26 -16 -42t-41 -16z" /></g><g transform="matrix(.017,-0,0,-.017,48.662,11.112)"><path id="x31" d="M384 0h-275v27q67 5 81.5 18.5t14.5 68.5v385q0 38 -7.5 47.5t-40.5 10.5l-48 2v24q85 15 178 52v-521q0 -55 14.5 -68.5t82.5 -18.5v-27z" /></g><g transform="matrix(.017,-0,0,-.017,56.821,11.112)"><path id="x38" d="M249 635q70 0 116 -43t46 -105q0 -46 -28 -80q-22 -25 -80 -64q62 -35 97 -75t35 -99q0 -81 -63 -131t-135 -50q-83 0 -137.5 45.5t-54.5 123.5q0 52 45 95q29 28 89 64q-109 62 -109 155q0 66 50.5 115t128.5 49zM238 603q-42 0 -67.5 -31t-25.5 -72q0 -50 32.5 -79.5&#xA;t98.5 -62.5q61 48 61 124q0 59 -29.5 90t-69.5 31zM248 20q46 0 76.5 33.5t30.5 89.5q0 50 -39 85.5t-110 71.5q-81 -54 -81 -137q0 -67 35.5 -105t87.5 -38z" /></g><g transform="matrix(.017,-0,0,-.017,64.981,11.112)"><path id="x2C" d="M95 130q31 0 61 -30t30 -78q0 -53 -38 -87.5t-93 -51.5l-11 29q77 31 77 85q0 26 -17.5 43t-44.5 24q-4 0 -8.5 6.5t-4.5 17.5q0 18 15 30t34 12z" /></g><g transform="matrix(.017,-0,0,-.017,71.695,11.112)"><path id="x1D443" d="M619 482q0 -69 -40.5 -119t-96 -72.5t-118.5 -26.5h-44l-70 20l-31 -151q-14 -67 0.5 -83t89.5 -22l-5 -28h-287l8 28q65 7 81.5 22t29.5 83l79 398q12 56 0.5 70.5t-78.5 20.5l7 28h255q108 0 164 -43t56 -125zM524 478q0 141 -146 141q-25 0 -47 -8q-16 -6 -20.5 -13.5&#xA;t-10.5 -39.5l-43 -241q37 -13 83 -13q67 0 125.5 45t58.5 129z" /></g><g transform="matrix(.017,-0,0,-.017,87.215,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,101.919,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,110.078,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,113.954,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,122.114,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>), after 1 year (<svg     style="vertical-align:-1.59705pt;width:130.35001px;" id="M2" height="13.1625" version="1.1" viewBox="0 0 130.35001 13.1625" width="130.35001"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D45F"/></g><g transform="matrix(.017,-0,0,-.017,11.945,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,26.649,11.112)"><use xlink:href="#x2212"/></g><g transform="matrix(.017,-0,0,-.017,36.627,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,44.786,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,48.662,11.112)"><path id="x32" d="M412 140l28 -9q0 -2 -35 -131h-373v23q112 112 161 170q59 70 92 127t33 115q0 63 -31 98t-86 35q-75 0 -137 -93l-22 20l57 81q55 59 135 59q69 0 118.5 -46.5t49.5 -122.5q0 -62 -29.5 -114t-102.5 -130l-141 -149h186q42 0 58.5 10.5t38.5 56.5z" /></g><g transform="matrix(.017,-0,0,-.017,56.821,11.112)"><path id="x35" d="M153 550l-26 -186q79 31 111 31q90 0 141.5 -51t51.5 -119q0 -93 -89 -166q-85 -69 -173 -71q-32 0 -61.5 11.5t-41.5 23.5q-18 17 -17 34q2 16 22 33q14 9 26 -1q61 -50 124 -50q60 0 93 43.5t33 104.5q0 69 -41.5 110t-121.5 41q-53 0 -102 -20l38 305h286l6 -8&#xA;l-26 -65h-233z" /></g><g transform="matrix(.017,-0,0,-.017,64.981,11.112)"><use xlink:href="#x2C"/></g><g transform="matrix(.017,-0,0,-.017,71.695,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,87.215,11.112)"><path id="x3C" d="M512 -3l-437 233v51l437 233v-58l-378 -200v-2l378 -199v-58z" /></g><g transform="matrix(.017,-0,0,-.017,101.919,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,110.078,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,113.954,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,122.114,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>) and after 2 years (<svg     style="vertical-align:-1.59705pt;width:130.35001px;" id="M3" height="13.1625" version="1.1" viewBox="0 0 130.35001 13.1625" width="130.35001"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D45F"/></g><g transform="matrix(.017,-0,0,-.017,11.945,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,26.649,11.112)"><use xlink:href="#x2212"/></g><g transform="matrix(.017,-0,0,-.017,36.627,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,44.786,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,48.662,11.112)"><use xlink:href="#x32"/></g><g transform="matrix(.017,-0,0,-.017,56.821,11.112)"><use xlink:href="#x31"/></g><g transform="matrix(.017,-0,0,-.017,64.981,11.112)"><use xlink:href="#x2C"/></g><g transform="matrix(.017,-0,0,-.017,71.695,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,87.215,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,101.919,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,110.078,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,113.954,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,122.114,11.112)"><use xlink:href="#x32"/></g>

		
	
</svg>).  Within-patient changes of uEPX showed a negative association with FEV<sub  >1</sub> changes (at 1&#x2009;year: <svg     style="vertical-align:-1.59705pt;width:130.35001px;" id="M4" height="13.1625" version="1.1" viewBox="0 0 130.35001 13.1625" width="130.35001"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D45F"/></g><g transform="matrix(.017,-0,0,-.017,11.945,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,26.649,11.112)"><use xlink:href="#x2212"/></g><g transform="matrix(.017,-0,0,-.017,36.627,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,44.786,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,48.662,11.112)"><use xlink:href="#x32"/></g><g transform="matrix(.017,-0,0,-.017,56.821,11.112)"><path id="x34" d="M456 178h-96v-72q0 -51 12.5 -62.5t72.5 -16.5v-27h-256v27q65 5 78 17t13 62v72h-260v28q182 271 300 426h40v-407h96v-47zM280 225v295h-2q-107 -148 -196 -295h198z" /></g><g transform="matrix(.017,-0,0,-.017,64.981,11.112)"><use xlink:href="#x2C"/></g><g transform="matrix(.017,-0,0,-.017,71.695,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,87.215,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,101.919,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,110.078,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,113.954,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,122.114,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>
; at 2&#x2009;years: <svg     style="vertical-align:-1.59705pt;width:130.35001px;" id="M5" height="13.1625" version="1.1" viewBox="0 0 130.35001 13.1625" width="130.35001"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D45F"/></g><g transform="matrix(.017,-0,0,-.017,11.945,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,26.649,11.112)"><use xlink:href="#x2212"/></g><g transform="matrix(.017,-0,0,-.017,36.627,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,44.786,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,48.662,11.112)"><use xlink:href="#x32"/></g><g transform="matrix(.017,-0,0,-.017,56.821,11.112)"><use xlink:href="#x31"/></g><g transform="matrix(.017,-0,0,-.017,64.981,11.112)"><use xlink:href="#x2C"/></g><g transform="matrix(.017,-0,0,-.017,71.695,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,87.215,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,101.919,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,110.078,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,113.954,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,122.114,11.112)"><path id="x33" d="M285 378v-2q65 -13 102 -54.5t37 -97.5q0 -57 -30.5 -104.5t-74 -75t-85.5 -42t-72 -14.5q-31 0 -59.5 11t-40.5 23q-19 18 -16 36q1 16 23 33q13 10 24 0q58 -51 124 -51q55 0 88 40t33 112q0 64 -39 96.5t-88 32.5q-29 0 -64 -11l-6 29q77 25 118 57.5t41 84.5&#xA;q0 45 -26.5 69.5t-68.5 24.5q-67 0 -120 -79l-20 20l43 63q51 56 127 56h1q66 0 107 -37t41 -95q0 -42 -31 -71q-22 -23 -68 -54z" /></g>

		
	
</svg>).  Within-patient changes from baseline of uEPX correlated with changes in &#x25; eos. No relations were found between uEPX and symptoms. <i  >Conclusion</i>. In this population of children with atopic asthma, uEPX correlated with FEV<sub  >1</sub> and &#x25; eos, and within-subjects changes in uEPX correlated with changes in FEV<sub  >1</sub> and &#x25; eos. As the associations were weak and the scatter of uEPX wide, it seems unlikely that uEPX will be useful as a biomarker for monitoring asthma control in the individual child.

Marianne Nuijsink

Wim C. J. Hop

Peter J. Sterk

Eric J. Duiverman

Johan C. De Jongste

Urinary Eosinophil Protein X in Childhood Asthma: Relation with Changes in Disease Control and Eosinophilic Airway Inflammation

Mario R. Romano

John Christoforidis

Ahmed M. Abu El-Asrar

Intravitreal Inflammation: From Benchside to Bedside

<i>Background</i>. Dexamethasone (Dex) has been used to reduce inflammation in preterm infants with assistive ventilation and to prevent chronic lung diseases. However, Dex treatment results in adverse effects on the brain. Since the hippocampus contains a high density of glucocorticoid receptors (GCRs), we hypothesized that Dex affects neurogenesis in the hippocampus through inflammatory mediators. <i>Methods</i>. Albino Wistar rat pups first received a single dose of Dex (0.5&#x2009;mg/kg) on postnatal day 1 (P1) and were sacrificed on P2, P3, P5, and P7. One group of Dex-treated pups (Dex-treated D1D2) was given mifepristone (RU486, a GCR antagonist) on P1 and sacrificed on P2. Hippocampi were isolated for western blot analysis, TUNEL, cleaved-caspase 3 staining for cell counts, and morphological assessment. Control pups received normal saline (NS). <i>Results</i>. Dex reduced the developmental gain in body weight, but had no effect on brain weight. In the Dex-treated D1D2 group, apoptotic cells increased in number based on TUNEL and cleaved-caspase 3 staining. Most of the apoptotic cells expressed the neural progenitor cell marker nestin. Dex-induced apoptosis in P1 pups was markedly reduced (60&#x25;) by pretreatment with RU486, indicating the involvement of GCRs. <i>Conclusion</i>. Early administration of Dex results in apoptosis of neural progenitor cells in the hippocampus and this is mediated through GCRs.

Chun-I Sze

Yung-Chieh Lin

Yuh-Jyh Lin

Ting-Hui Hsieh

Yu Min Kuo

Chyi-Her Lin

The Role of Glucocorticoid Receptors in Dexamethasone-Induced Apoptosis of Neuroprogenitor Cells in the Hippocampus of Rat Pups

Glucagon-like peptide-1 (GLP-1) is a gut hormone produced in the intestinal epithelial endocrine L cells by differential processing of the proglucagon gene. Released in response to the nutrient ingestion, GLP-1 plays an important role in maintaining glucose homeostasis. GLP-1 has been shown to regulate blood glucose levels by stimulating glucose-dependent insulin secretion and inhibiting glucagon secretion, gastric emptying, and food intake. These antidiabetic activities highlight GLP-1 as a potential therapeutic molecule in the clinical management of type 2 diabetes, (a disease characterized by progressive decline of beta-cell function and mass, increased insulin resistance, and final hyperglycemia). Since chronic hyperglycemia contributed to the acceleration of the formation of Advanced Glycation End-Products (AGEs, a heterogeneous group of compounds derived from the nonenzymatic reaction of reducing sugars with free amino groups of proteins implicated in vascular diabetic complications), the administration of GLP-1 might directly counteract diabetes pathophysiological processes (such as pancreatic <i>&#x3b2;</i>-cell dysfunction). This paper outlines evidence on the protective role of GLP-1 in preventing the deleterious effects mediated by AGEs in type 2 diabetes.

Alessandra Puddu

Fran&#xe7;ois Mach

Alessio Nencioni

Giorgio Luciano Viviani

Fabrizio Montecucco

An Emerging Role of Glucagon-Like Peptide-1 in Preventing Advanced-Glycation-End-Product-Mediated Damages in Diabetes

The causes of retinal hypoxia are many and varied. Under hypoxic conditions, a variety of soluble factors are secreted into the vitreous cavity including growth factors, cytokines, and chemokines. Cytokines, which usually serve as signals between neighboring cells, are involved in essentially every important biological process, including cell proliferation, inflammation, immunity, migration, fibrosis, tissue repair, and angiogenesis. Cytokines and chemokines are multifunctional mediators that can direct the recruitment of leukocytes to sites of inflammation, promote the process, enhance immune responses, and promote stem cell survival, development, and homeostasis. The modern particle-based flow cytometric analysis is more direct, stable and sensitive than the colorimetric readout of the conventional ELISA but, similar to ELISA, is influenced by vitreous hemorrhage, disruption of the blood-retina barrier, and high serum levels of a specific protein. Finding patterns in the expression of inflammatory cytokines specific to a particular disease can substantially contribute to the understanding of its basic mechanism and to the development of a targeted therapy.

Roberto dell'Omo

Francesco Semeraro

Giulio Bamonte

Francesco Cifariello

Ciro Costagliola

Vitreous Mediators in Retinal Hypoxic Diseases

Plaque rupture is the main cause of acute myocardial infarction and stroke. Atherosclerotic plaques have been described to be vulnerable and more prone to rupture when they are characterized by thin, highly inflamed, and collagen-poor fibrous caps and contain elevated levels of proteases, including metalloproteinases (MMPs). Initiation of collagen breakdown in plaques requires interstitial collagenases, a MMP subfamily consisting of MMP-1, MMP-8, and MMP-13. Previous reports demonstrated that MMP-1 and MMP-13 might be overexpressed in both human and experimental atherosclerosis. Since neutrophils have been only recently reported in atherosclerotic plaques, the role of MMP-8 (formerly known as &#x201c;neutrophil collagenase&#x201d;) was only marginally evaluated. In this paper, we will update and comment on evidence of the most relevant regulatory pathways and activities mediated by MMP-8 in atherogenesis.

S&#xe9;bastien Lenglet

Role of Matrix Metalloproteinase-8 in Atherosclerosis

Metabolic syndrome has been widely associated with an increased risk for acute cardiovascular events. Emerging evidence supports metabolic syndrome as a condition favoring an adverse cardiac remodeling, which might evolve towards heart dysfunction and failure. This pathological remodeling has been described to result from the cardiac adaptive response to clinical mechanical conditions (such as hypertension, dyslipidemia, and hyperglycemia), soluble inflammatory molecules (such as cytokines and chemokines), as well as hormones (such as insulin), characterizing the pathophysiology of metabolic syndrome. Moreover, these cardiac processes (resulting in cardiac hypertrophy and fibrosis) are also associated with the modulation of intracellular signalling pathways within cardiomyocytes. Amongst the different intracellular kinases, mitogen-activated protein kinases (MAPKs) were shown to be involved in heart damage in metabolic syndrome. However, their role remains controversial. In this paper, we will discuss and update evidence on MAPK-mediated mechanisms underlying cardiac adverse remodeling associated with metabolic syndrome.

Mohamed Asrih

Franco Dallegri

Alessandra Quercioli

Role of Mitogen-Activated Protein Kinase Pathways in Multifactorial Adverse Cardiac Remodeling Associated with Metabolic Syndrome

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<p><em>Mediators of Inflammation</em> publishes papers on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules</p>


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<p>Chief Editor, Professor Agrawal, is an Assistant Clinical Professor of the Division of Basic and Clinical Immunology. Dr. Agrawal's research focuses on the dendritic cells of the immune system in the context of aging and autoimmunity.</p>


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Mediators of Inflammation - Table of contents 2013

title

Mediators of Inflammation publishes papers on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules

Mediators of Inflammation