Dendritic cells inversely regulate airway inflammation in cigarette smoke-exposed mice.

The recruitment and activation of inflammatory cells into the respiratory system is considered a crucial feature in the pathophysiology of chronic obstructive pulmonary disease (COPD). Because dendritic cells (DCs) have a pivotal role in the onset and regulation of immune responses, we investigated the effect of modulating DC subsets on airway inflammation by acute cigarette smoke (CS) exposure. CS-exposed mice (5 days) were treated with fms-like tyrosine kinase 3 ligand (Flt3L) and 120g8 antibody to increase total DC numbers and deplete plasmacytoid DCs (pDCs), respectively. Flt3L treatment decreased the number of inflammatory cells in the bronchoalveolar lavage (BALF) of the smoke-exposed mice and increased these in lung tissue. DC modulation reduced IL-17 and increased IL-10 levels, which may be responsible for the suppression of the BALF cells. Furthermore, depletion of pDCs led to increased infiltration of alveolar macrophages while restricting the presence of CD103(+) DCs. This study suggests that DC subsets may differentially and compartment-dependent influence the inflammation induced by CS. pDC may play a role in preventing the pathogenesis of CS by inhibiting the alveolar macrophage migration to lung and increasing CD103(+) DCs at inflammatory sites to avoid extensive lung tissue damage.

Changes in athlete's redox state induced by habitual and unaccustomed exercise.

The purpose of this study was to assess the influence of sport-specific and nonspecific bouts of exercise on athletes' redox state. Blood samples were collected from 14 handball players immediately before and after graded exercise test on the cycle ergometer and handball training. Levels of superoxide anion radical (O(2) (-)), hydrogen peroxide (H(2)O(2)), nitrites (NO(2) (-)) as markers of nitric oxide, index of lipid peroxidation (TBARs), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activity were determined. Exercise intensity was assessed by a system for heart rate (HR) monitoring. Average athletes' HR was not significantly different between protocols, but protocols differed in total time and time and percentage of time that athletes spent in every HR zone. The laboratory exercise test induced a significant increase of H(2)O(2) and TBARs as well as the decrease of the SOD and CAT activity, while after specific handball training, levels of NO(2) (-) were increased and SOD activity decreased. It seems that unaccustomed short intensive physical activity may induce oxidative stress in trained athletes, while sport-specific activity of longer duration and proper warm-up period may not. Further research should show whether the change of protocol testing and the implementation of various supplementations and manual methods can affect the redox equilibrium.