Lung inflammatory signaling pathways

Lung inflammatory signaling pathways are integrated molecular networks, including the NF-κB, MAPK, and JAK/STAT cascades, that regulate the pulmonary immune response to stimuli such as pathogens and pollutants [2, 3, 10]. These pathways drive the production of pro-inflammatory mediators like IL-6, TNF-α, and various chemokines, which facilitate the recruitment of immune cells to the lung tissue [1, 11]. Dysregulation of these signaling events is a primary driver of chronic conditions like asthma and COPD, as well as acute respiratory distress syndrome (ARDS) [2, 10, 14]. Therapeutic strategies often involve the use of corticosteroids, JAK inhibitors, or monoclonal antibodies to modulate specific components of these pathways and reduce airway inflammation [1, 2, 15]. However, because these pathways are critical for normal host defense, their therapeutic modulation carries risks of immunosuppression and increased susceptibility to respiratory infections [1, 15].

Other names

Pulmonary inflammatory pathwaysAirway inflammatory signalingLung inflammation cascades

Therapeutic agents modulate these pathways by inhibiting specific kinases (e.g., JAK, MAPK), blocking cytokine receptors (e.g., IL-4R, IL-5R), or suppressing transcription factor activity (e.g., NF-κB) to reduce the production of pro-inflammatory mediators and prevent tissue damage [1, 2, 15].