![]() ![]() Among various inflammasome complexes, the NLRP3 inflammasome has been under intensive investigation and linked with various human autoinflammatory and autoimmune diseases. discovered the inflammasome, a new platform for protein-containing PRRs. TLRs and CLRs control the extracellular environment and endosomal compartments, while RLRs and NLRs recognize microbial patterns or danger signals within the cellular cytoplasm. PRRs are classified into four significant subfamilies: toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD), leucine-rich repeat (LRR)-containing receptors (NLRs), retinoic acid-inducible gene-1 (RIG-1)-like receptors (RLRs), and C-type lectin receptors (CLRs). Upon infection with a respiratory virus, innate immune response signaling cascades start with the recognition of specific viral components, or pathogen-associated molecular patterns (PAMPs) and endogenous danger molecules that are generated and exposed from damaged or dying cells, damage-associated molecular patterns (DAMPs), by germline-encoded receptors called pattern recognition receptors (PRRs). Inflammation induced by viral infections and co-expression of virus-related proteins were firmly associated with IPF. Along with previous studies, innate and adaptive immune and inflammatory cells produced heterogeneous contributions in remodeling and fibrosis processes. Innate and adaptive inflammation appears to be a prominent feature, markedly increased in the IPF group with rapid disease progression. Intrinsic factors, occupation, environmental influences, including exposure to microbes, particles, irritants, pollutants, allergens, and toxic molecules, genetic and epigenetic risk factors may lead to chronic inflammation that in turn leass to the development of IPF. Inflammation also has contributions to IPF initiation and progression. Although IPF has been redefined due to repeated micro-injury of the alveolar epithelium and aberrant epithelial-mesenchymal transition (EMT) crosstalk in a genetically susceptible aging individual, chronic inflammation still plays an important role. IPF is characterized by progressive extracellular matrix (ECM)-producing fibroblasts, fibroblast-myofibroblast transition, and extensive deposition of ECM by transforming growth factor-β1 (TGF-β1)-induced myofibroblasts. ĭespite less knowledge about the defined etiology and precise mechanisms, considerable advances in understanding IPF pathogenesis have been achieved in recent years. Based on a recent study, IPF incidence and prevalence are variable worldwide, about to be in the range of 0.09–1.30 and 0.33–4.51 per 10,000 persons, respectively therefore, in all but South Korea, IPF would be classified as a rare disease according to national guidelines. IPF is as a critical public health problem with an estimated conservative incidence range of 3–9 cases per 100,000 per year for Europe and North America, and lower in East Asia and South America (less than 4 cases per 100,000). IPF is a severe, permanent, and chronic respiratory disease that causes lung parenchyma scars and stiffness, making it gradually worse over time and more complicated to breathe. Overall, the crosstalk of the NLRP3 inflammasome and viruses can activate immune responses and inflammasome-associated molecules in the development, progression, and exacerbation of IPF. During viral infection, activation of the NLRP3 inflammasome by integrating multiple cellular and molecular signaling implicates robust inflammation, fibroblast proliferation, activation of myofibroblast, matrix deposition, and aberrant epithelial-mesenchymal function. The exact triggers that initiate the fibrotic response in IPF remain enigmatic, but there is now increasing evidence supporting the role of chronic exposure of viral infection. ![]() Environmental influences, intrinsic factors, genetic and epigenetic risk factors that lead to chronic inflammation might be implicated in the development of IPF. Idiopathic pulmonary fibrosis (IPF), one of the most common fibrosing interstitial lung diseases (ILD), is a chronic-age-related respiratory disease that rises from repeated micro-injury of the alveolar epithelium. ![]()
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