學士後西醫-普通生物及生化概論題庫下載題庫

Inhaled asbestos is usually handled by alveolar macrophages. 

The following cellular and molecular events then occur.

(1) Capture of silica/asbestos by macrophages and entrapment within lysosomes.

(2) Activation of NLRP3 inflammasome to cleave procaspase 1 to an active form.

(3) Cleavage of prointerleukin (IL)-1β to an active form for release to form fibrotic nodules.

(4) Production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the macrophages.

(5) Induction of cellular and tissue damage due to the production of ROS and RNS.

(6) Apoptosis of the alveolar macrophages....

Inhaled asbestos is usually handled by alveolar macrophages. 

The following cellular and molecular events then occur.

(1) Capture of silica/asbestos by macrophages and entrapment within lysosomes.

(2) Activation of NLRP3 inflammasome to cleave procaspase 1 to an active form.

(3) Cleavage of prointerleukin (IL)-1β to an active form for release to form fibrotic nodules.

(4) Production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the macrophages.

(5) Induction of cellular and tissue damage due to the production of ROS and RNS.

(6) Apoptosis of the alveolar macrophages.

(7) Production of various cytokines/chemokines such as IL-1β tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-1/2, monocyte-chemoattractant protein-1, and IL-8 to cause chronic inflammation and proliferation of collagenic fibers.

(8) Release of silica particles and asbestos fibers from alveolar macrophages and the repetition of similar cellular reactions described above by newly recognized nearby macrophages.

(9) Transfer of silica particles and (partially cleaved) asbestos fibers to regional lymph nodes.

(10) As these cellular and molecular reactions are continuously repeated, pulmonary fibrosis will appear gradually and progressively