摘要Background The condition of concomitant upper lobe emphysema and lower lobe fibrosis as identified by computer tomography is known as combined pulmonary fibrosis and emphysema (CPFE).CPFE has distinct clinical characteristics compared with emphysema alone (EA) and idiopathic pulmonary fibrosis (IPF) without emphysema.However,the pulmonary inflammation characteristics of CPFE are not well known,and the differences between CPFE and the other two diseases with regards to pulmonary inflammation need to be explored.The pulmonary inflammatory characteristics were investigated in CPFE patients and compared with EA and IPF.Methods Fraction exhaled nitric oxide (Fe,NO) and differential cell counts,the concentrations of monokine induced by interferon gamma (MIG/CXCL9),interferon-inducible protein 10 (IP-10/CXCL10),and interferon-inducible T cell alpha chemoattractant (I-TAC/CXCL11) were measured in induced sputum obtained from subjects with CPFE (n=22),EA (n=22),IPF (n=14),and healthy volunteers (HV,n=12).In addition,immunohistochemistry was used to quantify the expression of nitric oxide synthases in alveolar macrophages in 23 lung tissues from patients and control subjects.Results The CPFE group had higher alveolar NO than subjects in the EA and HV groups (P=0.009,P=0.001,respectively) but not than the IPF group (P ＞0.05).Numbers of sputum eosinophils were significantly elevated in CPFE and IPF groups compared with the HV group (P=0.001,P=-0.008).In contrast,eosinophil counts in EA group did not differ from those in the HV group.Compared with the EA and HV groups,the CPFE group had a lower concentration of Ⅰ-TAC/CXCL11 in sputum supernatants (P=-0.003,P=0.004).Immunoreactivity for inducible nitric oxide synthase (iNOS)was higher in the CPFE group than in the EA group (P=-0.018,P=0.006,respectively).Conclusions The pulmonary inflammation of CPFE group is more similar to IPF group,while the distal airway inflammation is more significant in CPFE and IPF groups than in EA group.Lung eosinophil cell infiltration and high NOS expression in alveolar macrophage might participate in this pathogenesis.