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Respiratory system (COPD (Causes (smoking (leads to release of DAMPs…

- - - - leads to release of DAMPs
        
        inflammatory response
  - - - scars on walls of bronchioles
        
        Caused the mucous membrane to thicken
        
        narrowed airway
        
        hard to breath
      - increased number of alveolar macrophages, neutrophils, T-lymphocytes and innate lymphoid cells
        
        Secrete pro-inflammatory mediators like cytokines, chemokines and growth factors.
  - - - lose structure
        
        not efficient anymore in gas exchange
    - - pulmonary emphysems
  - - - inflammaging
- - - - Decreased lung volume
  - - - reduced pO2
- - - - HDAC reverses the histone acetylation
        and thereby represses genes
        
        An increased acetylation of histones in the promoter region of pro-inflammatory genes resulting in increased production of cytokines and chemokines.
        
        Chronic inflammation
      - Deficiencies in SIRT1
        
        Associated with COPD onset and oxidative stress
  - - - In alveoli poor clearance of damaged proteins
        
        apoptosis and chronic inflammation
- - - - Glutathione S-transferase (GST)
        
        polymorphism causes gene associated with airflow limitations
        
        lower FEV
    - - α₁ antitrypsin deficiency
        
        shortness of breath
        
        can lead to COPD
        
        produced in liver
        
        function is to protect from neutrophil elastase, an enzyme that can disrupt connective tissue
    - - TGF-ß1
        
        important factor involvend in inflammation
        
        can regulate the induction of inflammatory factors involved in the development and progression of COPD