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Introduction: CX3CL1 (fractalkine), a membrane-bound chemokine that induces both the adhesion and migration of leukocytes, is involved in the recruitment of cells into tissues undergoing inflammatory responses. To explore the regulation of CX3CL1 in pulmonary inflammation and fibrosis, CX3CL1 expression of by lung fibroblast was examined. Methods: Normal human lung fibroblasts were obtained from Promocell were incubated in the presence or absence of various inflammatory stimuli. Culture supernatants were collected, and soluble CX3CL1 levels were determined with an enzyme-linked immunosorbent assay. Expression of CX3CL1 mRNA transcripts in lung fibroblast was examined using quantitative TaqMan real-time polymerase chain reaction. Results: Interleukine (IL)-1β or interferon (IFN)-γ alone induced negligible soluble CX3CL1 secretion by human lung fibroblasts after 24 h. However, the combination of IL-1β and IFN-γ induced dramatic increases in both soluble CX3CL1 protein and mRNA transcripts in dose- and time-dependent manners. The secretion and expression of lung fibroblast-derived CX3CL1 were markedly reduced by specific inhibitors of the STAT-1 transcription factor. Conclusions: These findings suggest that lung fibroblasts are an important cellular source of CX3CL1, and may play roles in pulmonary inflammation and fibrosis like interstitial pneumonia which merges to rheumatoid arthritis and other autoimmune diseases.