The Journal of allergy and clinical immunology
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J. Allergy Clin. Immunol. · Jan 2007
Clinical TrialChildhood Asthma Management Program: lessons learned.
The National Heart, Lung, and Blood Institute Childhood Asthma Management Program was initiated in 1991 and is now the largest and most comprehensive study of long-term intervention with anti-inflammatory therapy in children with mild to moderate asthma. The purpose of this perspective is to review key findings of the study and lessons learned in conducting research in more than 1000 children with persistent asthma for more than 10 years. A key lesson was absence of a continued effect of inhaled corticosteroid on lung growth during long-term follow-up even as symptoms and airway responsiveness remained improved.
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J. Allergy Clin. Immunol. · Jan 2007
History of serious asthma exacerbations should be included in guidelines of asthma severity.
It is unclear whether asthma severity measured with consensus guidelines is better than a history of a serious asthma exacerbation in predicting current disease activity and future clinical course. ⋯ Adding a history of a serious asthma exacerbation to the consensus guidelines for asthma severity is likely to improve the ability of these clinical tools to predict current disease activity and future clinical course.
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J. Allergy Clin. Immunol. · Jan 2007
Comparative StudyJMF2-1, a lidocaine derivative acting on airways spasm and lung allergic inflammation in rats.
Prior reports show that nebulized lidocaine might be an effective treatment for asthma. ⋯ Nebulized JMF2-1 might be a means of achieving the antiasthmatic effects of lidocaine without the anesthetic effects.
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J. Allergy Clin. Immunol. · Jan 2007
S100A12 provokes mast cell activation: a potential amplification pathway in asthma and innate immunity.
The calcium-binding protein S100A12 might provoke inflammation and monocyte recruitment through the receptor for advanced glycation end products. ⋯ MC activation by S100A12 might exacerbate allergic inflammation and asthma. S100A12 might provide a novel marker for eosinophilic asthma.
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J. Allergy Clin. Immunol. · Dec 2006
Case ReportsInterleukin receptor-associated kinase-4 deficiency impairs Toll-like receptor-dependent innate antiviral immune responses.
Engagement of all known Toll-like receptors (TLRs) causes the production of inflammatory cytokines, including TNF-alpha, whereas in humans, engagement of TLRs 3, 7, 8, and 9 also induces type I IFNs. IRAK-4 is a critical effector in signaling by TLRs and the IL-1 receptor, which share homology in their intracellular domain and recruit IRAK-4 via the adaptor myeloid differentiation factor 88 (MyD88). Patients with IRAK-4 deficiency are susceptible to invasive bacterial infections but have so far not been reported to be susceptible to viral infection. Blood cells from these patients are impaired in their ability to make TNF-alpha in response to activation by TLRs. A recent report has described concomitant impairment of type I IFN production after activation of TLRs 7, 8, and 9, but not TLR3. ⋯ IRAK-4 may play a broader role in human innate antiviral immunity than previously appreciated.