Mediating pathways shared by all three pulmonary disorders favor innate immune and inflammation-related processes, including toll-like receptor (TLR) signaling, PDGF- and angiotensin-regulated airway remodeling, the JAK-STAT signaling pathway, and interferon gamma.
Interferon gamma (IFNγ) plays an important role in the development of chronic lung diseases via the production of inflammatory mediators, although the exact mechanism remains unclear.
Urine interferon gamma inducible protein 10 (IP-10) is a potential biomarker of treatment response in chronic hepatitis C virus infection and lung diseases, including tuberculosis.
We have previously shown that children with chronic suppurative lung disease have a reduced capacity to produce IFN-γ in response to NTHi compared with healthy control children.
The IFN-gamma +874 and IFN-gammaR1 -611 and -56 polymorphisms do not appear to be responsible for host susceptibility to NTM lung disease, at least in the Korean population.