Hypothesis and key scientific questions Based on analysis above, the investigators propose the following hypothesis: certain level of immunological imbalance exists in those relatively stable IPF patients, making them susceptible to infection by various pathogens. Once infected, especially by viruses (e.g. common cold related viruses), AE-IPF can be quickly triggered, leading to ARDS-like reaction. To validate this hypothesis, four key scientific questions need to be answered by studies with scrupulous design: 1) what are the characteristic changes of immunological function in IPF/AE-IPF patients so as to make the patients more susceptible to common cold viruses? 2) What kind of pathogens, especially those common cold viruses, are the key triggering factors during the development of AE-IPF? 3) What kind of inflammatory cascade reaction occurs in AE-IPF leading to ARDS-like prompt development of pulmonary inflammation? Key research direction and scientific rationale In order to address the key scientific questions above, the investigators will conduct comprehensive studies based on detailed screen and analysis of large amount of clinical cases, integrated research methods in such areas as immunology, molecular, cytology and animal model, as well as high throughput data collection and big data analysis: 1) Extensive screening and identification of those pathogens closely related with AE-IPF; 2) Comprehensive analysis of the change of immunology function, focusing on the pathological-physiological alteration in virus induced immunologic imbalance in IPF, as well as the characteristic changes in relevant cytological signal transduction, so as to identify important AE-IPF bio-markers and explain the pathological molecular mechanism and network of ARDS-like inflammatory cascade reaction, which will be significant efforts in terms of prevention of AE-IPF, reduction of mortality, improvement of quality of life, delaying of disease progression and increase of survival.