Targeting CXCR2 signaling in inflammatory lung diseases: neutrophil-driven inflammation and emerging therapies

Inflammatory lung diseases (ILDs) such as asthma, acute respiratory distress syndrome, bronchiectasis, chronic obstructive pulmonary disease, COVID-19, cystic fibrosis, and lung cancer impose a substantial worldwide healthcare impact. The pathophysiology of these disorders is primarily influenced by the involvement of neutrophils, which are crucial triggers in the natural immune reaction. Neutrophils participate in pulmonary inflammation and tissue destruction. When neutrophils are activated and recruited, they migrate to inflammatory lung tissues via the chemokine receptor CXCR2. This study explores how neutrophils, directed by CXCR2 signaling, participate in the inflammatory environment in the lung, inducing tissue injury and the development of illness. We investigate both the functional and structural features of CXCR2, emphasizing its relationship with ligands such as IL-8 (CXCL8) and GRO-alpha (CXCL1) and its involvement in ILDs. The article also explores novel treatment approaches that focus on CXCR2, such as the use of small molecule antagonists. These compounds can regulate neutrophil behavior and reduce signs of the illness. The study provides a detailed analysis of current clinical studies and the results of inhibiting CXCR2, specifically looking at the effectiveness and safety of these new medicines. This study seeks to deliver a thorough analysis of the important function of neutrophils and CXCR2 in ILDs, as well as the possibility of CXCR2-targeted therapeutics to enhance clinical outcomes.