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History of the World Allergy Organization: Reflective Recollections of the WAO Presidency, 2010-2011
Richard F Lockey
World Allergy Organization Journal , 2012, DOI: 10.1097/wox.0b013e318249715a
Abstract:
Aspirin-Exacerbated Asthma
Mathew Varghese, Richard F Lockey
Allergy, Asthma & Clinical Immunology , 2008, DOI: 10.1186/1710-1492-4-2-75
Abstract: Acetylsalicylic acid (aspirin) is one of the most prescribed and frequently used over-the-counter medications of all time. Aspirin-exacerbated asthma (AEA) was first reported 84 years ago after severe bronchospasm in an individual with asthma was observed following aspirin ingestion and is characterized by eosinophilic rhinosinusitis, nasal polyposis, aspirin sensitivity, and asthma[1,2]. All cyclooxygenase-1 (COX-1) inhibiting nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, induce bronchospasm, rhinorrhea, and nasal obstruction in these subjects [2-4]. In addition, the ocular administration of the COX-1-inhibiting NSAID ketorolac has been linked to AEA[4]. Individuals with AEA usually have moderate to severe persistent asthma and often require treatment with high-dose inhaled corticosteroids and even systemic corticosteroids in some instances[2,5]. Although the exact mechanism causing the AEA has yet to be fully elucidated, there is considerable evidence that an alteration in the metabolism of arachidonic acid is responsible [5-8].Another clinical entity, chronic idiopathic urticaria with aspirin sensitivity, although perhaps similar at a biochemical level to AEA, is clinically different as this reaction is confined to the skin and subcutaneous tissues[9]. This review focuses on AEA.The medicinal properties of the group of alkali metal salts and esters known as salicylates have been known since ancient times. Records dating back to the time of Hippocrates (460 BC) describe powders derived from the bark of the white willow tree (Salix alba) used for pain relief; the name salicylic acid is derived from Salix, the Latin name for this tree [10-13]. In 1853, the French chemist Gerhardt neutralized salicylic acid by buffering it with sodium salicylate and acetylchloride, creating acetylsalicylic acid or aspirin. The discovery of aspirin by Gerhardt was abandoned until Felix Hoffman, a German chemist, rediscovered it in 1887 and learned of its unique pro
Respiratory syncytial virus infection: from biology to therapy A Perspective
Shyam S Mohapatra, Richard F Lockey
World Allergy Organization Journal , 2008, DOI: 10.1097/wox.0b013e31816549a2
Abstract:
Interleukin-13 Signaling and Its Role in Asthma
Efren L Rael, Richard F Lockey
World Allergy Organization Journal , 2011, DOI: 10.1097/wox.0b013e31821188e0
Abstract:
Oxymetazoline hydrochloride combined with mometasone nasal spray for persistent nasal congestion (pilot study)
Efren L Rael, John Ramey, Richard F Lockey
World Allergy Organization Journal , 2011, DOI: 10.1097/wox.0b013e31820f8fae
Abstract:
Respiratory syncytial virus infection in Fischer 344 rats is attenuated by short interfering RNA against the RSV-NS1 gene
Kong Xiaoyuan,Zhang Weidong,Lockey Richard F,Auais Alexander
Genetic Vaccines and Therapy , 2007, DOI: 10.1186/1479-0556-5-4
Abstract: Background Respiratory syncytial virus (RSV) causes severe bronchiolitis and is a risk factor for asthma. Since there is no commercially available vaccine against RSV, a short interfering RNA against the RSV-NS1gene (siNS1) was developed and its potential for decreasing RSV infection and infection-associated inflammation in rats was tested. Methods Plasmids encoding siNS1 or an unrelated siRNA were complexed with a chitosan nanoparticle delivery agent and administered intranasally. Control animals received a plasmid for a non-specific siRNA. After expression of the plasmid in lung cells for 24 hours, the rats were intranasally infected with RSV. Results Prophylaxis with siNS1 significantly reduced lung RSV titers and airway hyperreactivity to methacholine challenge compared to the control group. Lung sections from siNS1-treated rats showed a sizable reduction in goblet cell hyperplasia and in lung infiltration by inflammatory cells, both characteristics of asthma. Also, bronchoalveolar lavage samples from siNS1-treated animals had fewer eosinophils. Treatment of rats with siNS1 prior to RSV exposure was effective in reducing virus titers in the lung and in preventing the inflammation and airway hyperresponsiveness associated with the infection that has been linked to development of asthma. Conclusion The use of siNS1 prophylaxis may be an effective method for preventing RSV bronchiolitis and potentially reducing the later development of asthma associated with severe respiratory infections.
Thiolated chitosan nanoparticles enhance anti-inflammatory effects of intranasally delivered theophylline
Dong-Won Lee, Shawna A Shirley, Richard F Lockey, Shyam S Mohapatra
Respiratory Research , 2006, DOI: 10.1186/1465-9921-7-112
Abstract: We sought to develop an improved drug-delivery matrix for theophylline based on thiolated chitosan, and to investigate whether thiolated chitosan nanoparticles (TCNs) can enhance theophylline's capacity to alleviate allergic asthma.A mouse model of allergic asthma was used to test the effects of theophylline in vivo. BALB/c mice were sensitized to ovalbumin (OVA) and OVA-challenged to produce an inflammatory allergic condition. They were then treated intranasally with theophylline alone, chitosan nanoparticles alone or theophylline adsorbed to TCNs. The effects of theophylline on cellular infiltration in bronchoalveolar lavage (BAL) fluid, histopathology of lung sections, and apoptosis of lung cells were investigated to determine the effectiveness of TCNs as a drug-delivery vehicle for theophylline.Theophylline alone exerts a moderate anti-inflammatory effect, as evidenced by the decrease in eosinophils in BAL fluid, the reduction of bronchial damage, inhibition of mucus hypersecretion and increased apoptosis of lung cells. The effects of theophylline were significantly enhanced when the drug was delivered by TCNs.Intranasal delivery of theophylline complexed with TCNs augmented the anti-inflammatory effects of the drug compared to theophylline administered alone in a mouse model of allergic asthma. The beneficial effects of theophylline in treating asthma may be enhanced through the use of this novel drug delivery system.Asthma is a chronic inflammatory disease of the airway characterized by the infiltration of eosinophils, epithelial hyperplasia leading to hypersecretion of mucus and the presence of airway hyperresponsiveness (AHR) to a variety of stimuli [1,2]. Theophylline had been used worldwide for the treatment of asthma for several decades, but its use has recently declined owing to the increased use of inhaled glucocorticoids. Theophylline's side effects, such as nausea, headache and cardiac arrhythmias, at the dose necessary to achieve bronchodilation (pla
Mechanism of cigarette smoke condensate-induced acute inflammatory response in human bronchial epithelial cells
Gary R Hellermann, Szilvia B Nagy, Xiaoyuan Kong, Richard F Lockey, Shyam S Mohapatra
Respiratory Research , 2002, DOI: 10.1186/rr172
Abstract: The human alveolar epithelial cell line A549 and normal human bronchial epithelial cells (NHBEs) were exposed to 0.4 μg/ml CSC, a concentration that resulted in >90% cell survival and <5% apoptosis. Changes in gene expression and signaling responses were determined by RT-PCR, western blotting and immunocytofluorescence.NHBEs exposed to CSC showed increased expression of the inflammatory mediators sICAM-1, IL-1β, IL-8 and GM-CSF, as determined by RT-PCR. CSC-induced IL-1β expression was reduced by PD98059, a blocker of mitogen-actived protein kinase (MAPK) kinase (MEK), and by PDTC, a NFκB inhibitor. Analysis of intracellular signaling pathways, using antibodies specific for phosphorylated MAPKs (extracellular signal-regulated kinase [ERK]-1/2), demonstrated an increased level of phosphorylated ERK1/2 with increasing CSC concentration. Nuclear localization of phosphorylated ERK1/2 was seen within 30 min of CSC exposure and was inhibited by PD98059. Increased phosphorylation and nuclear translocation of IκB was also seen after CSC exposure. A549 cells transfected with a luciferase reporter plasmid containing a NFκB-inducible promoter sequence and exposed to CSC (0.4 μg/ml) or TNF-α (50 ng/ml) had an increased reporter activity of approximately 2-fold for CSC and 3.5-fold for TNF-α relative to untreated controls.The acute phase response of NHBEs to cigarette smoke involves activation of both MAPK and NFκB.The association of inhaled particulate pollution and cigarette smoking with pulmonary disease, such as chronic obstructive pulmonary disease, is well documented [1], but the specific early responses of lung epithelial cells to toxic substances in particulates — that predispose the cells to disease — have not been elucidated. Cigarette smoke has also been considered a major player in the pathogenesis of asthma and as a trigger for acute symptoms [2]. Exposure to cigarette smoke activates an inflammatory cascade in the airway epithelium resulting in the production of a
A Case of Common Variable Immunodeficiency (CVID) and Antineutrophilic Cytoplasmic Antibody (ANCA)-Associated Vasculitis
Adeeb A. Bulkhi,Jennifer E. Fergeson,Mark C. Glaum,Richard F. Lockey
- , 2017, DOI: 10.1016/j.jaci.2016.12.016
Abstract: CVID is a primary humoral immunodeficiency characterized by recurrent sinopulmonary infections, hypogammaglobulinemia and poor polysaccharide antibody responses. More severe forms of CVID are associated with autoimmunity, granulomatous disease, and malignancy. An ANCA-associated vasculitis with CVID is presented.
Matrix Metalloproteinase 7: Role in Epithelial Integrity and Ciliogenesis in Pulmonary Fibrosis in a Mouse Model
Conor C. Lynch,Emma Westermann-Clark,Jutaro Fukumoto,Narasaiah Kolliputi,Ramani Soundararajan,Richard F. Lockey
- , 2017, DOI: 10.1016/j.jaci.2016.12.295
Abstract: Matrix metalloproteinase 7 (MMP7) is a potential preclinical serum biomarker for idiopathic pulmonary fibrosis (IPF). The role of MMP7 in IPF is examined using the novel Atp8b1 mutant mouse, which spontaneously develops lung/liver fibrosis with age. MMP7 restrains ciliogenesis and impacts epithelial integrity via E-cadherin cleavage.
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