The NLRP3 inflammasome is a critical component of the innate immune
system that mediates caspase-1 activation and the secretion of proinflammatory
cytokines IL-1β/IL-18 in response to microbial infection and cellular damage.
Nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain
3 (NLRP3), one of the members of the NLR family, consists of NLRP3, the adaptor
molecule, apoptosis-associated speck-like protein containing a caspase and recruitment
domain (ASC) and an inflammatory caspase-1 that causes excessive inflammasome
activation in respiratory diseases like asthma and could exacerbate the progression of
asthma by considerably contributing to ECM accumulation and airway remodeling.
NLRP3 is closely associated with airway inflammation and asthma exacerbations as
endotoxin (lipopolysaccharide, LPS) is one of its activators present in the environment.
Asthma is a complex immunological and inflammatory disease characterized by the
presence of airway inflammation, airway wall remodeling and bronchial
hyperresponsiveness (BHR). Symptomatic attacks of asthma can be caused by a myriad
of situations, including allergens, infections, and pollutants, which cause the rapid
aggravation of respiratory problems. The presence of LPS in the environment is
positively correlated with the incidence of asthma and allergic diseases. In this chapter,
we summarize our current understanding of the mechanisms of NLRP3 inflammasome
activation by multiple signaling events in asthmatic exacerbations and their regulation.
Keywords: Caspases and NLRP3 regulators, Fibrosis, Inflammation, Inflammasomes, Pyroptosis, ROS.
