BookMieczyslaw Pokorski, editor.
Summary: The mechanistic basis of chronic inflammation remains unclear. The research sheds new light on the immune cells expressing the activation markers HLA-DR and regulatory T cells (Tregs) and the cells expressing Siglec receptors as being key players in the immune system responsiveness to antigens and thus in lung tissue damage of chronic inflammation. The results help understand the mechanisms of action of common drugs used in COPD, such as formoterol, tiotropium, or corticosteroids, and point to novel drug targets. The chapters also deal with brain damaging effects, by far unrecognized, of inhaled corticosteroid therapy, a time-proven management of chronic inflammatory airway conditions; asthma being a case in point. Novel methods, likely less producing side effects, of macrolide antibiotics administration by inhalation are discussed, emphasizing not only bacteriostatic but also anti-inflammatory action.
Contents:
Inhaled Corticosteroids Increase Siglec-5/14 Expression in Sputum Cells of COPD Patients
Tregs and HLA-DR Expression in Sputum Cells of COPD Patients Treated with Tiotropium and Formoterol
Inhalation of Macrolides: A Novel Approach to Treatment of Pulmonary Infections
Influence of Denture Plaque Biofilm on Oral Mucosal Membrane in Patients with Chronic Obstructive Pulmonary Disease
Biophysical Activity of Animal-Derived Exogenous Surfactants Mixed with Rifampicin
Organic Changes in the Central Nervous System in Children on Chronic Inhaled Corticosteroid Therapy
Stem Cell Experiments Moves into Clinic: New Hope for Children with Bronchopulmonary Dysplasia
Soluble Ligand CD40 and Uric Acid as Markers of Atheromatosis in Patients with Obstructive Sleep Apnea
Carotid Artery Intima-Media Thickness in Hypertensive Patients with Obstructive Sleep Apnea.
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