Circulating fibrocytes, identified as CD45⁺ collagen I⁺ CXCR4⁺ cells, migrate to the lungs in response to CXCL12 and contribute to pulmonary fibrosis. This study demonstrates that human and murine fibrocytes traffic to the lungs in a bleomycin-induced pulmonary fibrosis model, with maximal recruitment correlating with increased collagen deposition. Neutralizing anti-CXCL12 antibodies inhibited fibrocyte recruitment and reduced fibrosis, indicating that CXCL12/CXCR4 signaling is critical for fibrocyte recruitment. Fibrocytes express markers such as CD45, Col I, and CXCR4, and their migration is directed by CXCL12 gradients. In vivo, fibrocytes are recruited to fibrotic lungs, and their numbers correlate with collagen deposition. CXCR4 is the predominant chemokine receptor for fibrocyte recruitment, while CCR7 also plays a role. Neutralizing anti-CXCL12 antibodies reduced fibrocyte infiltration and attenuated fibrosis, suggesting that CXCL12/CXCR4 signaling is a key pathway in fibrocyte recruitment. Fibrocytes may differentiate into myofibroblasts, which are involved in collagen deposition. The study provides the first evidence that circulating fibrocytes contribute to the pathogenesis of pulmonary fibrosis.Circulating fibrocytes, identified as CD45⁺ collagen I⁺ CXCR4⁺ cells, migrate to the lungs in response to CXCL12 and contribute to pulmonary fibrosis. This study demonstrates that human and murine fibrocytes traffic to the lungs in a bleomycin-induced pulmonary fibrosis model, with maximal recruitment correlating with increased collagen deposition. Neutralizing anti-CXCL12 antibodies inhibited fibrocyte recruitment and reduced fibrosis, indicating that CXCL12/CXCR4 signaling is critical for fibrocyte recruitment. Fibrocytes express markers such as CD45, Col I, and CXCR4, and their migration is directed by CXCL12 gradients. In vivo, fibrocytes are recruited to fibrotic lungs, and their numbers correlate with collagen deposition. CXCR4 is the predominant chemokine receptor for fibrocyte recruitment, while CCR7 also plays a role. Neutralizing anti-CXCL12 antibodies reduced fibrocyte infiltration and attenuated fibrosis, suggesting that CXCL12/CXCR4 signaling is a key pathway in fibrocyte recruitment. Fibrocytes may differentiate into myofibroblasts, which are involved in collagen deposition. The study provides the first evidence that circulating fibrocytes contribute to the pathogenesis of pulmonary fibrosis.