Inflammation is a normal part of the human immune response, whereby leukocytes (white blood cells), including neutrophils (white blood cells that specialize in causing inflammation), gather, and chemokines (proteins released from certain cells, which activate or elicit a response from other cells) accumulate at any location in the body where bacterial or viral infections occur. Inflammation interferes with the activity of bacteria and viruses, and serves to clear them from the body. In<unk> , bacteria such as Haemophilus influenzae and Pseudomonas aeruginosa can cause the proliferation of inflammatory cells into the bronchiolar tissues. However, when neither bacteria are present with<unk> , the inflammation continues for an as yet unknown reason. In either circumstance, inflammation in<unk>  can be so severe that nodules containing inflammatory cells form in the walls of the bronchioles. The presence of inflammation and infection in the airways also results in the production of excess mucus, which must be coughed up as sputum. The combination of inflammation, nodule development, infection, mucus, and frequent cough contributes to the breathing difficulties in<unk> . The fact that inflammation in<unk>  persists with or without the presence of P. aeruginosa and H. influenzae provides a means to determine several mechanisms of<unk>  pathogenesis. Leukotrienes are eicosanoids, signaling molecules made from essential fatty acids, which play a role in many lung diseases by causing the proliferation of inflammatory cells and excess mucus production in the airways. In<unk>  and other lung diseases, the predominant mediator of neutrophil-related inflammation is leukotriene B4, which specializes in neutrophil proliferation via chemotaxis (the movement of some types of cells toward or away from certain molecules). Inflammation in<unk>  is also caused by the chemokine MIP-1alpha and its involvement with CD8+ T cells. Beta defensins, a family of antimicrobial peptides found in the respiratory tract, are responsible for further inflammation in<unk>  when a pathogen such as P. aeruginosa is present. If present with<unk> , the human T-lymphotropic virus, type I, a retrovirus, modifies<unk>  pathogenesis by infecting T helper cells and altering their effectiveness in recognizing the presence of known or unknown pathogens involved with<unk> .
Diffuse panbronchiolitis
Emphysema
Acute eosinophilic pneumonia
Plastic bronchitis
Cryptogenic organizing pneumonia
Eosinophilic bronchitis
Hypersensitivity pneumonitis
Mineral dust airway disease