Effect of Palmitic Acid on B2 Receptor Expression In Airway Smooth Muscle Cells

Introduction: People with asthma and obesity struggle to control asthma flares. B2 agonists are often the acute treatment of choice during these flares, so the decreased asthma control in this population may be due to a decrease in B2 receptor activity. We tested the hypothesis that B2 receptor expression will decrease in airway smooth muscle cells exposed to Palmitic Acid, a saturated fatty acid, compared to Oleic Acid and untreated cells. Methods: Airway smooth muscle cells were plated and treated with Palmitic Acid and Oleic Acid at 100uM and 200uM concentrations while other untreated cells served as controls. Cells were lysed at 24 and 48 hours and their RNA was harvested for expansion using PCR with B2 and GAPDH primers. RT-PCR was used to quantify RNA expression. GAPDH was used as an expression control to normalize B2 values for each condition and the resulting dCq values for each condition were compared. Results: The Palmitic Acid group did not show significant decrease in B2 expression compared to the control or Oleic Acid groups. This was consistent across all concentrations and time points. There was no significant change in receptor expression for any condition. Discussion: These results did not support our hypothesis that B2 expression would decrease in cells treated with Palmitic Acid. The expression of this receptor and its activity is not regulated as we hypothesized illustrating need to explore other factors that may contribute to the difference of the B2 receptor agonist response in obese people with asthma

Obesity and Obstructive Airways Disease: Clinical Correlates and Therapeutic Considerations

Obese patients are more likely to suffer from severe asthma symptoms and less likely to be able to control them. In obese patients, there is evidence that shows decreased efficacy of inhaled corticosteroids and beta-2 adrenergic agonists, the core treatment options for achieving and maintaining asthma control. This may be due to mechanical reasons like decreased ventilation and medication delivery, but there are many more pathologies of obesity that interact with pathways of both asthma pathology and asthma control. This review explores the epidemiological significance of obesity, many physiological changes in patients with obesity, the physiological interactions of asthma and obesity in patients with both issues, and the therapeutic impacts of these interactions with asthma to find appropriate areas where new research is needed. More research to understand the mechanism of decreased inhaled corticosteroid and beta-2 adrenergic agonist efficacy is necessary to improve treatment efficacy and decrease morbidity and mortality in this population of patients with asthma

The TeaComposition Initiative: Unleashing the power of international collaboration to understand litter decomposition

Collected harmonized data on global litter decomposition are of great relevance for scientists, policymakers, and for education of the next generation of researchers and environmental managers. Here we describe the TeaComposition initiative, a global and open research collaborative network to study organic matter decomposition in a standardized way allowing comparison of decomposition rate and carbon turnover across global and regional gradients of ecosystems, climate, soils etc. The TeaComposition initiative today involves 570 terrestrial and 300 aquatic ecosystems from nine biomes worldwide. Further, we describe how to get involved in the TeaComposition initiative by (a) implementing the standard protocol within your study site, (b) joining task forces in data analyses, syntheses and modelling efforts, (c) using collected data and samples for further analyses through joint projects, (d) using collected data for graduate seminars, and (e) strengthening synergies between biogeochemical research and a wide range of stakeholders. These collaborative efforts within/emerging from the TeaComposition initiative, thereby, will leverage our understanding on litter decomposition at the global scale and strengthen global collaborations essential for addressing grand scientific challenges in a rapidly changing world.This work was performed within the TeaComposition and TeaComposition H2O initiatives, carried by 290 institutions worldwide. We thank to UNILEVER for sponsoring the Lipton tea bags. The initiative is supported by the following grants: ILTER Initiative Grants, ClimMani Short-Term Scientific Missions Grants, INTERACT Remote Transnational Access and an Alfred Deakin Postdoctoral Research Fellowship. Nico Eisenhauer gratefully acknowledges the support of iDiv funded by the German Research Foundation (DFG– FZT 118, 202548816). ST-T was supported by the ARC DE210101029 and Deakin University’s ADPR Fellowship. Fernando T. Maestre acknowledges support from the European Research Council (ERC Grant agreement 647038 [BIODESERT]) and Generalitat Valenciana (CIDEGENT/2018/041)

Mucosa-associated microbiota drives pathogenic functions in IBD-derived intestinal iNKT cells

Inflammatory bowel disease (IBD) pathogenesis has been linked to the aberrant activation of the Gut-associated lymphoid tissues against components of the intestinal microbiota. Although the contribution of CD4+ T helper cells to inflammatory processes is being increasingly acknowledged, the functional engagement of human invariant natural killer T (iNKT) cells is still poorly defined. Here, we evaluated the functional characteristics of intestinal iNKT cells during IBD pathogenesis and to exploit the role of mucosa-associated microbiota recognition in triggering iNKT cells' pro-inflammatory responses in vivo. Lamina propria iNKT cells, isolated from surgical specimens of active ulcerative colitis and Crohn's disease patients and non-IBD donors, were phenotypically and functionally analyzed ex vivo, and stable cell lines and clones were generated for in vitro functional assays. iNKT cells expressing a pro-inflammatory cytokine profile were enriched in the lamina propria of IBD patients, and their exposure to the mucosa-associated microbiota drives pro-inflammatory activation, inducing direct pathogenic activities against the epithelial barrier integrity. These observations suggest that iNKT cell pro-inflammatory functions may contribute to the fuelling of intestinal inflammation in IBD patients

The effect of oxprenolol and indomethacin on renin and aldosterone of normal subjects during low sodium diet.

To study the mechanisms underlying renin and aldosterone increase during low sodium diet, eight normal subjects were studied during normal sodium diet (5 g of NaCl per day) for 5 days, after 4 days of low sodium diet, and, on continuing low sodium diet, after randomized treatment with oxprenolol (100 mg), indomethacin (200 mg) and oxprenolol + indomethacin (100 + 200 mg) each given for 24 h with a 48 h interval between each treatment. Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Both oxprenolol and indomethacin significantly reduced PRA to values similar to those during normal sodium intake, while the combination of the two drugs showed a net additive effect on PRA. PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin. Aldosterone excretion showed a trend similar to that of PRA, being related to PRA on normal and low sodium diet, and to a lesser extent after drug treatment. These studies suggest that both the sympathetic nervous system and prostaglandins may play a permissive role in the regulation of renin and aldosterone of normal subjects on low sodium diet