Childhood asthma and anthropogenic CO2 emissions

Amrita DosanjhPediatric Pulmonologist, San Diego, California, USATrends in the incidence of childhood asthma worldwide have paralleled the sharp increase in carbon dioxide (CO2) emissions, over at least the last two decades. The prevalence of asthma in the United States has quadrupled over the last 20 years in part due to climate-related factors. In a report released by Harvard Medical School and the Center for Health and the Global Environment, it was noted that there was an increase in asthma incidence of 160% from 1980–1994 among preschool children. &nbsp

The Inhibition of Superoxide Production by the Soluble Phase of CF Sputum

Abstract: Background: Cystic fibrosis (CF) lung disease is characterized by an infiltration of activated neutrophils. Oxidative radical formation and neutrophil proteases may interact with the components of CF airway secretions. This study examined the soluble factors in CF airway secretions (sol) and determined their effect on the production of superoxide radicals. Methods: Neutrophils were isolated from three normal subjects. Each preparation of neutrophils can be used in several experiments on the same day of preparation. Using a standardized cytochrome c reduction method, the effect of pooled CF sol isolated from nine CF patients, on neutrophil superoxide production was studied. Results: CF sol phase significantly attenuates the production of superoxide by phorbol stimulated control neutrophils in a time and concentration dependent manner. When CF sol is boiled, the inhibitory effect on superoxide was reversed. CF soluble heat labile factors clearly attenuated superoxide production, independent of elastase concentration. We conclude that the presence of heat labile soluble factors in CF sputum, serve to attenuate superoxide production by human neutrophil

Complex pathways leading to future paediatric asthma exacerbations

Childhood asthma studies to identify additional risk factors, triggers and biomarkers may reveal novel pathways leading to exacerbation https://bit.ly/3BOhSW

Pirfenidone: Anti-fibrotic agent with a potential therapeutic role in the management of transplantation patients

Chronic allograft dysfunction is a leading cause of allograft failure, morbidity and mortality following solid organ transplantation. The pathogenesis of chronic allograft failure has a final common pathway leading to organ fibrosis. Pirfenidone is an effective and novel anti-fibrotic agent with anti-inflammatory properties. Clinical use of the agent has been tested in a number of non-transplant recipients and has a favorable safety profile based on available clinical data. Building on these observations and findings, and considering the role of fibrosis in chronic allograft rejection, Pirfenidone (PFD) was initially investigated as adjunctive therapy in a rat heterotopic tracheal transplantation model. This led to several studies which confirmed that PFD may well be worth considering for further investigation. This paper reviews the possibility of using PFD in clinical transplantation management

Endothelin-1 Induces Expression of Connective Tissue Growth Factor in Bronchial Epithelial Cells

Endothelin-1 (ET-1) is a potent vaso and bronchoconstrictor. We have previously shown that in the presence of ET-1 bronchial epithelial cells migrate more slowly. Connective tissue growth factor (CTGF) is a cysteine rich secreted protein and regulates fibrosis. In addition, we have previously shown that CTGF is expressed in airway epithelial cells under the conditions of stress starvation. The aim of this study was to describe the effect of ET-1 on CTGF expression, using a lung epithelial-fibroblast co-culture system. Bronchial epithelial cells (BEC) were grown and stimulated with ET-1, 100ng/ml of media, for 24 hours. At 0, 4 and 24 hours, total RNA was isolated. Reverse transcription PCR was performed and CTGF transcripts were semi-quantified. In addition, BEC were grown in co-culture, in the presence of human lung fibroblasts (FB). The same experiment was conducted for FB grown in the presence or absence of ET-1. Control cells were grown only in the basal media. At both time points, following exposure to ET-1, BEC expressed more CTGF as compared to control. Cells in co-culture with FB, expressed no CTGF at 4 hours, and detectable CTGF at 24 hours. CTGF was detected at all time points for FB in both control and stimulated cells. ET-1 induces expression of CTGF in BEC as compared to control. ET-1 may be an important regulator of CTGF expression in the airway. Lung fibroblasts may secrete epithelial cell regulatory factors, controlling the expression of CTGF in the presence of ET-1