Prolonged exposure to cold air may induce a chronic asthma-like condition in healthy subjects as has been demonstrated in cross-country skiers. In the present controlled study, our aim was to elucidate further the link between cold air exposure and airway inflammation by assessing the cellular influx and mediator levels within the airways following acute exposure to cold air. Bronchoalveolar (BAL) and nasal lavages were performed after exposure to cold air (-23 degrees C) and normal indoor air (+22 degrees C) during a light, intermittent work for 2 h in a cross-over design in eight healthy, nonsmoking, subjects. Analyses of inflammatory cell number, cell activation markers, pro-inflammatory cytokines, albumin and interleukin (IL)-8 in lavage fluids were performed. The number of granulocytes and of alveolar macrophages in BAL fluid was significantly higher after cold air exposure (p<0.05). No increase in BAL fluid lymphocytes and no signs of lymphocyte activation in BAL fluid were found. The concentration of IL-8 was unchanged. There were no signs of granulocyte activation (myeloperoxidase, eosinphilic cationic protein) in BAL fluid. Cold air did not influence the number of inflammatory cells or the concentration of albumin and IL-8 in nasal lavage fluid. In conclusion, exposure to cold air induces an increased number of granulocytes and macrophages in the lower airways in healthy subjects without influencing other inflammatory indices such as cellular activation, plasma leakage and pro-inflammatory cytokines. These findings support the hypothesis that cold air could be of pathogenetic importance in the asthma-like condition previously found in cross-country skiers.

SummaryIn pulmonary sarcoidosis, the typical T helper 1-mediated immune response in the lungs has been proposed to be co-ordinated by regulatory T cells; however, their exact role needs to be clarified. We used real-time polymerase chain reaction to study genes involved in regulatory T cell functions in CD4 + AV2S3 -T cells. The main conclusion of our study is that there is a reduced expression of regulatory T cell associated genes in BALF CD4 + T cells in sarcoidosis. In addition, our data suggest an effector function of AV2S3 + lung-accumulated T cells in sarcoidosis.

Atopic and non-atopic subjects shared some immune changes in response to stress, such as a dramatic decline in cytokines and an increase in the number of regulatory T cells in peripheral blood. However, other stress-induced immune changes were unique to atopic individuals, such as a skewed Th1/Th2 ratio and reduced NK cell numbers, indicating that some pathogenic mechanisms in atopics may be more strongly affected by stress than others.

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The aim of the present investigation was to measure the back-leak of pelvic urine to the blood circulation. In normopenic hydronephrotic, dehydrated hydronephrotic and dehydrated control kidneys the back-leak was estimated from a servocontrolled machine which regulated infused saline to keep a present pelvic pressure constant. The disappearance of fluid from the renal pelvis could be measured at different pressure levels, and a pressure-dependent outflow of fluid was found. From these measurements a back-leak conductance could be calculated which proved to be independent of pressure. In the lower pressure range (15-20 mmHg) there was a significantly lower conductance in the dehydrated controls compared with the dyhydrated hydronephrotic kidneys, while in the higher pressure range (25-30 mmHg) no difference was found. From electron microscopical studies the pyelorenal back-leak of fluid in both hydronephrotic and control animals seemed to be most pronounced in the fornix region, as documented by a heavy presence of horseradish peroxidase in the intracellular spaces there. Other experiments with radioactively labelled inulin, which was injected into the pelvic cavity, indicated that most of the back-leak occurred via the renal blood vessels and not through the lymphatic system. The importance of this back-leak was evident from the measurements of the total kidney glomerular filtration rate (GFR) at a slightly increased pelvic pressure, where some of the urine with radioactive tracer flows back to circulation. The back-leak of pelvic urine could also affect the concentration mechanism by removing diluted urine which had flowed over the renal papilla, and through water and urea diffusion increased papillary interstitial osmolarity.