کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6155909 | 1247883 | 2015 | 47 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The sickle cell mouse lung: proinflammatory and primed for allergic inflammation
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کلمات کلیدی
PBSType 2 helper T cellTNFHLNTh2CXCLTregCCLGM-CSFS1PTLRBALi.p.OVAAHRBCASCDAADSACBSA - BSAbovine serum albumin - آلبومین سرم گاوSphingosine-1-phosphate - اسپینگسین-1-فسفاتperiodic acid–Schiff - اسید فسفریک SchiffOvalbumin - اوبلبومینimmunoglobulin - ایمونوگلوبولینinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینbicinchoninic acid - بیسینکنینیک اسیدallergic airway disease - بیماری آلرژیک هواییSickle cell disease - بیماری سلول داسی شکلTumor-necrosis factor - تومور-نکروز فاکتورToll-like receptor - تیالآرintraperitoneal - داخل صفاقیRegulatory T cell - سلول T تنظیم کنندهgranulocyte-macrophage colony-stimulating factor - عامل گرانولوسیت-ماکروفاژ colony-stimulating factorSacrifice - قربانیbronchoalveolar lavage - لارو برونکلو آلوئولارchemokine (C-C motif) ligand - لیموج کوموکین (C-C motif)chemokine (C-X-C motif) ligand - لیکوئید کوموکین (C-X-C motif)Phosphate-buffered saline - محلول نمک فسفات با خاصیت بافریenhanced pause - مکث طولانیPAS - نهairway hyper-responsiveness - پاسخ سریع هواپیماPenh - پناه
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
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چکیده انگلیسی
Comorbid asthma in sickle cell disease (SCD) confers higher rates of vaso-occlusive pain and mortality, yet the physiological link between these two distinct diseases remains puzzling. We used a mouse model of SCD to study pulmonary immunology and physiology before and after the induction of allergic airway disease (AAD). SCD mice were sensitized with ovalbumin (OVA) and aluminum hydroxide by the intraperitoneal route followed by daily, nose-only OVA-aerosol challenge to induce AAD. The lungs of naive SCD mice showed signs of inflammatory and immune processes: (1) histologic and cytochemical evidence of airway inflammation compared with naive wild-type mice; (2) bronchoalveolar lavage (BAL) fluid contained increased total lymphocytes, %CD8+ T cells, granulocyte-colony stimulating factor, interleukin 5 (IL-5), IL-7, and chemokine (C-X-C motif) ligand (CXCL)1; and (3) lung tissue and hilar lymph node (HLN) had increased CD4+, CD8+, and regulatory T (Treg) cells. Furthermore, SCD mice at AAD demonstrated significant changes compared with the naive state: (1) BAL fluid with increased %CD4+ T cells and Treg cells, lower %CD8+ T cells, and decreased interferon gamma, CXCL10, chemokine (C-C motif) ligand 2, and IL-17; (2) serum with increased OVA-specific immunoglobulin E, IL-6, and IL-13, and decreased IL-1α and CXCL10; (3) no increase in Treg cells in the lung tissue or HLN; and (4) hyporesponsiveness to methacholine challenge. In conclusion, SCD mice have an altered immunologic pulmonary milieu and physiological responsiveness. These findings suggest that the clinical phenotype of AAD in SCD mice differs from that of wild-type mice and that individuals with SCD may also have a unique, divergent phenotype perhaps amenable to a different therapeutic approach.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 166, Issue 3, September 2015, Pages 254-268
Journal: Translational Research - Volume 166, Issue 3, September 2015, Pages 254-268
نویسندگان
Biree Andemariam, Alexander J. Adami, Anurag Singh, Jeffrey T. McNamara, Eric R. Secor, Linda A. Guernsey, Roger S. Thrall,