Targeting Common Inflammatory Mediators in Experimental Severe Asthma and Acute Lung Injury.

Neutrophils, known to be mobilized and activated in high amounts through Il-17 stimulation, are a key factor for clinical manifestation and imbalance of redox systems favoring a dominant oxidative state in both severe asthma and acute lung injury (f). The aim of this study was to evaluate in mice, the effect of Secukinumab (SECU) in a model of ovalbumin-induced asthma exacerbated with LPS administration to induce ALI, compared to dexamethasone (DEXA), already known for its benefit in both asthma and ALI. Results on cytokine levels for specific Th1, Th2 and Th17 revealed an interplay of immune responses. For Th1 effector cytokines in BALF, DEXA treatment increased TNF-α levels, but TNF-α was not modified by SECU; DEXA and SECU significantly decreased IFN-γ and IL-6 levels. For typical Th2 cytokines, DEXA significantly increased Il-4, Il-5 and Il-13 levels, while SECU significantly inhibited Il-5 levels. Both SECU and DEXA significantly decreased Il-17 levels. Cytokine level changes in lung tissue homogenate were partly similar to BALF cytokines. Conclusion: in addition to DEXA, SECU possesses the ability to modulate inflammatory cytokine release and to decrease Th17 responses in ALI overlapped on exacerbated asthma in mice.

Amiodarone induced lung disease.

Amiodarone, a primarily class III antiarrhythmic drug is one of the most commonly used drug in atrial fibrillation. A possible rare side effect of amiodarone treatment is to develop a diffuse parenchymal lung disorder - amiodarone pulmonary toxicity (APT). There is no pathognomonic findings to diagnose APT. A 64-year-old patient with multiple comorbidities presented in our hospital with worsening a five-month history of grade 3 mMRC dyspnea, wheezing, frequent nonproductive cough, fatigue. She has a medical history of atrial fibrillation in treatment with amiodarone 400mg/day for 2 years. Her oxygen saturation was 90% on room air, chest radiography showed disseminated lung irregular opacities with a tendency to confluence in right and left lung and chest computed tomography scan showed asymmetric centrilobular nodules and asymmetrical areas of dense ground glass opacity with few consolidation. Amiodarone pulmonary toxicity was suspected, the drug was stopped and treatment with methylprednisolone started. Worsening and progression of the disease can still be noted despite stopping amiodarone because of the long persistence and elimination of the drug, with the tendency to concentrate in tissues, such as lung. In our patient case the evolution and prognosis were good even the case illustrates neglected effects of amiodarone, potential severe one.