The use of asthma therapies as novel agent to reduce inflammation in vitro macrophage model

Abstract

Asthma is a chronic reversible airway obstruction. Etiology of asthma is multifactorial with various pathophysiological mechanisms according to the type of asthma. The most common pathophysiology of asthma is inflammation and airway remodeling. A macrophage plays an important role in the inflammatory cascade of asthma. That’s why our focus here is to investigate the anti-inflammatory activity of some drugs that are currently used in management of asthma, like fenoterol, salbutamol, salmeterol, ipratropium and tiotropium, on the cell line of the macrophage. We challenged THP-1 cell line with Lipopolysaccharide (LPS) to mimic the inflammatory reaction of the airways. Our methods involve an in-vitro experimental model where THP-1 cells were incubated with LPS for 24 hours in the presence or absence of the aforementioned drugs. This was followed by measuring IL-6, IL-1β and TNF- in the supernatants of cells. Each drug was investigated as 10-6 , 10-7 and 10-8 M concentrations. Budesonide was used a reference compound. Results indicated that all LPS induced IL-1β release was significantly attenuated by all used concentrations of budesonide, all used concentrations of fenoterol and only 10-6 M concentration of salbutamol or ipratropium. Moreover, all used concentrations of budesonide, fenoterol, salmeterol, salbutamol and tiotropium, in addition to the 10-6 M of ipratropium, significantly attenuated LPS-induced IL-6 release from THP-1 cells. Furthermore, all investigated concentrations of budesonide, fenoterol and ipratropium, in addition to 10-6 M salmeterol, attenuated LPS-induced TNF- release from THP-1 cells. Thus, it can be concluded that some of the used bronchodilators used in asthma and COPD have anti-inflammatory effects on macrophages. More trials are required to find the favorable combination with corticosteroid for the most effective and safest management of asthma.