Harvey Macrophages in Patients with COPD and in a Mouse Model Targeting Nrf 2 Signaling Improves Bacterial Clearance by Alveolar

Nrf2 or its targets can protect the lungs of COPD patients from serial assaults. that cause oxidative stress. These findings suggest that by boosting macrophage function, therapies that regulate macrophages required direct transcriptional activation of the gene that encodes MARCO, a scavenger of molecules mice but not in Nrf2-deficient mice. Molecular analyses of Nrf-regulated genes revealed that the restorative effects on chemical, which cooled inflammation and enhanced macrophage-driven bacterial clearance in the lungs of wild-type . The authors then treated mice that had been sucking in smoke for 6 months with the same P. aeruginosa and H. influenzae phytochemical, sulforaphane, and showed that the macrophages were able to recognize and internalize . treated these cells with an Nrf2-stimulating et al to internalize and obliterate bacteria. To this end, Harvey ability antioxidants in lung macrophages from COPD patients would reduce oxidative stress and thus restore the cells' genes that encode antioxidant proteins. The authors hypothesized that enhancing the synthesis of Nrf2-inducing oxidative stress, Nrf2 moves into the cell's nucleus, binds to antioxidant response elements in DNA, and activates related factor 2) in protection from emphysema and in the severity of COPD. In response to − (nuclear erythroid oxidative stress. Studies in mice subjected to secondhand smoke reveal a role for the transcription factor Nrf2 these bacterially induced exacerbations. It has been suggested that macrophage defects in COPD result from ; these conditions aggravate COPD symptoms, and there are no therapies that prevent Pseudomonas aeruginosa and Haemophilus influenzae bacteria, which promotes inflammation, and frequent bacterial infections often caused by (phagocytosing) bacteria for eventual destruction. This aberration gives rise to both the persistent presence of Although the mechanism is unclear, lung macrophages from patients with COPD are defective in taking up macrophages to sequester and inactivate the bacteria that often causes exacerbations of COPD. model of COPD, a phytochemical found in broccoli can activate this pathway and improve the ability of lung defense against oxidative stress, which may impair lung macrophage function. In both COPD patients and a mouse triggered change in a signaling pathway that regulates − Harvey and colleagues have fingered a cigarette smoke Now, mechanistic details of how irritants in the air disable the lung's defenses can help uncover possible drug targets. an inflammation of the airway passages (bronchi). Understanding the −− and bronchitis −− destruction of lung tissue which is associated with progressive −− breath, wheezing, chronic cough, and tightness in the chest: emphysema obstructive pulmonary disease). This common disease is characterized by two conditions that cause shortness of cigarette smoke or pollution can interfere with this self-cleaning system and cause the lung ailment COPD (chronic innate immune defense system driven by macrophages that subdue infectious invaders. But constant exposure to and microbes. A well-functioning lung cleanses itself with broom-like cilia that sweep out debris and with a robust With every breath we take, the outside air assaults the lungs. Along with life-sustaining oxygen come dust, dirt, Cleansing Breath