Benefits of a 7-week outpatient pulmonary rehabilitation program in COPD patients.

BACKGROUND: Respiratory rehabilitation programs (RR) are essential tools in the management of COPD. AIM: We present the results of a 7-week outpatient rehabilitation program in terms of dyspnea, exercise tolerance and quality of life. MATERIAL AND METHOD: The following parameters were evaluated before and after RR: dyspnea (mMRC scale), pulmonary function (FEVI, RV- residual volume), exercise tolerance (6MWT- 6 minutes walk test, CPET - cardiopulmonary exercise test), quality of life (SGROQ questionnaire). The RR program was outpatient, hospital based (7 weeks, 3 sessions/ week) and included: exercise training, therapeutic education, and psychological support. RESULTS: 25 patients, COPD stage II-IV GOLD (mean FEVI 44.5 +/-13% predicted), mean age 60.4 +/-12 years, 7 females, average BMI 27.14+/-4 kg/m2, average RV residual volume 221.55+/-86% predicted. Mean 6MWTdistance: 407.48 +/- 84 m and mean maximum power (Pmax) obtained on CPET: 75.67+/-30 Watts. All patients were symptomatic with significant dyspnea (3.06+/-0.7 on mMRC scale) and showed a significant impairment of quality of life: SGRO score 46.23+/- 14. At the end of RR program: dyspnea decreased with 0.67points on mMRC scale (p = 0.000), 6MWT distance increased with 58.5 m (p = 0.0071), Pmax obtained during CPET increased with 11.2 W, without reaching statistical significance (p> 0.05). SGRO score decreased by 5.59 points (p = 0.02). There were no significant improvements in FEV1 and RV values (p> 0.05). CONCLUSION: In our COPD patients, the 7 week outpatient rehabilitation program was effective, leading to improvement ofsymptoms, exercise tolerance and quality of life.

Plasticity of regulatory T cells under cytokine pressure.

CD4+ T helper (Th) cells have been divided into different subsets as defined by their cytokine products and functions after their activation. CD4+ T cell subsets are continuously discovered and until now Th1, Th2, Th9, Th17, and regulatory T (Treg) cells have been almost unanimously recognized but yet not completely characterized. The selective production of cytokines by each of the subsets is probably the master key of the mechanisms of immune regulation. The cytokine milieu is extremely important on deciding the fate of T cells. Generally, more than one cytokine is needed for differentiating to a particular lineage and just recently it was shown that this status quo of commitment could be challenged. It is well known that cytokines bind to Type I/II cytokine receptors signaling via Janus kinases (JAKs) followed by activation of Signal Transducer and Activator of Transcription (STAT). STAT molecules work together with other transcription factors (Foxp3, RORgammat and RORalpha, T-bet, GATA3, Runx 1, NFAT, etc.) also controlled by cytokines, in modulating the Th phenotype and functions. In this review, we analyze the plasticity of Treg population focusing on the most recent discoveries on how microenvironmental cytokines refine/modify Treg phenotype and function, thus changing their fate.