The contribution of animal models to understanding the role of the immune system in human idiopathic pulmonary fibrosis

Pulmonary fibrosis occurs in a heterogeneous group of lung disorders and is characterised by an excessive deposition of extracellular matrix proteins within the pulmonary interstitium, leading to impaired gas transfer and a loss of lung function. In the past 10 years, there has been a dramatic increase in our understanding of the immune system and how it contributes to fibrogenic processes within the lung. This review will compare some of the models used to investigate the pathogenesis and treatment of pulmonary fibrosis, in particular those used to study immune cell pathogenicity in idiopathic pulmonary fibrosis, highlighting their advantages and disadvantages in dissecting human disease

Immunopathobiology of chronic lung disease

The lung epithelium is a cellular barrier that protects the lung from environmental exposure to pathogens and chemical insults that could otherwise compromise its physiological role in gas exchange during respiration..

Susceptibility of Branhamella catarrhalis to sulphamethoxazole and trimethoprim

Fifty strains of Branhamella catarrhalis were examined for susceptibility to sulphamethoxazole, trimethoprim and a combination of the two by determinating minimum inhibitory concentrations (MICs) and fractional inhibitory concentrations (FICs). All strains were susceptible to sulphamethoxazole and resistant to trimethoprim. On the basis of the MIC results it was predicted that greater synergy between sulphamethoxazole and trimethoprim would be observed with approximately equal proportions of each component. The lowest FIC values were obtained with a ratio of 1:1 and the greatest synergy was observed at this ratio with 39 strains (78%). Only seven strains were most synergistically inhibited at the ratio of 20:1 (sulphamethoxazole: trimethoprim) although this ratio was still synergic for most strains. Overall the 1:20 ratio was not synergic

Idiopathic pulmonary fibrosis and a role for autoimmunity

Idiopathic pulmonary fibrosis (IPF) is the most common of the idiopathic interstitial pneumonias. It is typically associated with extensive and progressive fibrosis, and is fatal and has limited treatment options. Characteristically IPF patients display large lymphocyte aggregates composed of CD3+ T cells and CD20+ B cells within the lung tissue that are located near sites of active fibrosis. In addition, IPF patients can have autoantibodies to a range of host antigens, suggesting a breakdown in immunological tolerance. In this review, we examine the role of T and B cells in IPF pathogenesis and discuss how loss of self-tolerance to lung-specific proteins could exacerbate disease progression in IPF. We discuss what these results mean in terms of future prospects for immunotherapy of IPF

Mesothelial cells regulate immune responses in health and disease: Role for immunotherapy in malignant mesothelioma

The mesothelium when first described was thought to function purely as a non-adhesive surface to facilitate intracoelomic movement of organs. However, the mesothelium is now recognized as a dynamic cellular membrane with many important functions that maintain serosal integrity and homeostasis. For example, mesothelial cells interact with and help regulate the body’s inflammatory and immune system following infection, injury, or malignancy. With recent advances in our understanding of checkpoint molecules and the advent of novel immunotherapy approaches, there has been an increase in the number of studies examining mesothelial and immune cell interaction, in particular the role of these interactions in malignant mesothelioma. This review will highlight some of the recent advances in our understanding of how mesothelial cells help regulate serosal immunity and how in a malignant environment, the immune system is hijacked to stimulate tumor growth. Ways to treat mesothelioma using immunotherapy approaches will also be discussed

Effect of exercise on acute postprandial glucose concentrations and interleukin-6 responses in sedentary and overweight males

This study examined the effect of two forms of exercise on glucose tolerance and concurrent changes in markers associated with the interleukin-6 (IL-6) pathways. Fifteen sedentary, overweight males (29.0±3.1 kg/m2) completed two separate, 3-day trials in randomised and counterbalanced order. An oral glucose tolerance test (OGTT; 75g) was performed at the same time on each successive day of the trial. Day two of each trial, consisted of a single 30-min workload-matched bout of either high-intensity interval exercise (HIIE; alternating 100% and 50% of V̇O2peak) or continuous moderate intensity exercise (CME; 60% V̇O2peak) completed 1h prior to the OGTT. Venous blood samples were collected pre-, immediately post-, 1h post- and 25h post-exercise for measurement of insulin, C-peptide, IL-6 and the soluble IL-6 receptors (sIL-6R; sgp130). Glucose area under the curve (AUC) were calculated from capillary blood samples collected throughout the OGTT. Exercise resulted in a modest (4.4%; p = 0.003) decrease in the glucose AUC when compared to the pre-exercise AUC; however, no differences were observed between exercise conditions (p = 0.65). IL-6 was elevated immediately and 1h post-exercise, whilst sgp130 and sIL-6R concentrations were reduced immediately post-exercise. In summary, exercise was effective in reducing glucose AUC which was attributed to improvements between 60 and 120 min of the OGTT, was in parallel with an increased ratio of IL-6 to sIL-6R, which accords with an increased activation via the ‘classical’ IL-6 signalling pathway. Our findings suggest acute HIIE did not improve glycaemic response when compared to CME. Trial Registration: ACTRN1261300108675

Strength Training for Long-Distance Triathletes

Concurrent training, commonly acknowledged as a training method where strength and endurance training are completed complementary to each other, is a strategy often implemented in endurance cyclists' and runners' programs to improve physiological determinants of success such as exercise economy. Although concurrent training methods and strategies have been examined to a large extent in endurance cyclists and runners, literature examining optimal concurrent training methods to improve physiological variables in long-distance triathletes is minimal, leaving optimal programming relatively unknown. This practical applications paper identifies and outlines current concepts and considerations regarding concurrent training for long-distance triathletes including mechanisms contributing to improved performance, muscle and movement patterns used, exercise selection, load, velocity of movement, scheduling, frequency, and duration of training. Common misconceptions related to concurrent training are also identified and practical considerations for the application of concurrent training for coaches, athletes, and other professionals to improve all 3 disciplines of triathlon are discussed