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Article in Press

September 2015  

Volume 2 Issue 3

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Research Article

Targeting the PAF:PAF Receptor Interaction to Manage PMN Recruitment to the Lung of Smokers

John O. Marentette, Janhavi Sharma and Jane McHowat*

Cigarette smoking is associated with a high degree of mortality and morbidity and is associated with damage to almost every organ in the body, particularly the lungs. Smokers are at increased risk for pulmonary diseases such as chronic obstructive pulmonary disease (COPD) which involves a robust migration of leukocytes. We have demonstrated previously that adherence of polymorphonuclear leukocytes (PMN) to lung endothelial cells exposed to cigarette smoke extract (CSE) is mediated via inhibition of platelet-activating factor acetylhydrolase (PAF-AH) activity, leading to PAF accumulation.

                                                                                                                                                                                                                              Full textDownload PDF

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Mini Review

Characterization of Secondary Autoimmune Etiologies Related to Rheumatic Fever

Mesquita, J.O.#, Machado, A.R.# Del Sarto, R.P., Martins, A.M.A*

The rheumatic fever (RF) is a systemic inflammatory autoimmune disease, which occurs after a pharyngeal infection by Streptococcus pyogenes. The disease can cause arthritis, erythema marginatum, subcutaneous nodules, carditis and Sydenham’s chorea. The signs and symptoms of the disease are caused by the immune response against Streptococcus sp., however, only individuals with a genetic predisposition may be affected by this disease. It was noted in some cases, where the person with RF also have positive diagnostic of other autoimmune diseases such as systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), and Hashimoto’s thyroiditis (HT)

                                                                                                                                                                                                                              Full textDownload PDF

 

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Research Article

Requirement for JNK1 in OVA-induced Airway Hyperresponsiveness in vivo

Junya Onuki, Eiko Takada, Masae Furuhata, Katsuko Sudo, Kuniaki Shimo and Junichiro Mizuguchi*

Bronchial asthma is a chronic inflammatory disease characterized by airway hyperreactivity (AHR) and inflammatory cell infiltration of the airway. c-Jun N-terminal kinase 1 (JNK1), a member of the mitogen-activated protein kinases, is activated by a variety of stimuli including environmental stress and cytokine(s) and plays a crucial role in the induction of inflammation. To assess the role of JNK1 in the induction of bronchial asthma, we examined the production of AHR, inflammatory reaction, and cytokine production using an ovalbumin (OVA)-induced airway inflammation model.

                                                                                                                                                                                                                              Full textDownload PDF

 

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