BIOLOGICAL ROLE, MECHANISM OF ACTION AND IMPORTANCE OF INTERLEUKIN 1 AND TNF ALPHA IN ASTHMA PATHOGENESIS

Abstract

In asthmatic patients, the inflammatory responses within the airways are initiated and sustained by 
different inflammatory mediators or cytokines in which two vital cytokines which are responsible 
for the pathogenesis of asthma are TNF-α (Tumor Necrosis Factor) and IL (interleukin)-1. The IL1 aids to the development and progression of asthma by activating dendritic cells responsible for 
presenting antigens to T cells, and induction of Th2 cells, which produce key cytokines (IL-4, 5, 
and 13) included in asthma pathogenesis. TNF-α action leads to the development of inflammation 
by triggering the function of airway epithelium which activates the adhesion molecules and 
chemokines, which in turn attract and activate immune cells. Furthermore, TNF-α is additionally 
capable for inducing smooth muscle airway hyperresponsiveness (AHR) by activating ion 
channels, leading to bronchoconstriction. Importantly, TNF-α is responsible for inducing smooth 
muscle contractility and airway hyperresponsiveness (AHR), which occurs through ROS (Reactive 
Oxygen Species) incitement within cells there by activating distinctive signaling pathways, 
including the RhoA/ROCK pathway, which contributes to airway contraction. Therefore, focusing 
on the IL-1 and TNF-α pathway has ended up a potential restorative approach for the management 
of asthma and their wide-ranging effects making them viable interventions requiring for the 
prospective assessment