Pharmacological inhibition of the CCL2-CCR2 axis fails to reduce inflammation in a rat model of acute lung injury.

ABSTRACT: New therapeutic approaches are needed to regulate inflammation and control monocyte recruitment in acute respiratory distress syndrome (ARDS). Excessive monocyte influx into the alveolar space can exacerbate lung damage, worsening patient outcomes. Delaying or reducing monocyte recruitment into the alveoli space after the injury has been proposed as a strategy to balance the inflammatory response and mitigate lung damage. In the present study, we assessed the possible role of the CCL2-CCR2 axis as a therapy for controlling acute lung injury after the initial neutrophil-driven influx. We administered a CCL2-antibody (CCL2-Ab) or a CCR2-antagonist (CCR2-Ant) locally into the lung following lung injury induced by HCl/LPS instillation. Our results show that after 24 h, both treatments transien

SUBMITTER: Camprubi-Rimblas M 

PROVIDER: S-EPMC12381131 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature