Respuesta :
A thrombin inhibitor that is connected with cells and the extracellular matrix is the serine proteinase inhibitor, clade E, member 2 (SERPINE2).
Although the protease inhibitor SERPINE2 is a putative susceptibility gene for chronic obstructive pulmonary disease, it is unclear what physiological function it serves in lung development and homeostasis.
- At or before the time of lung maturity, we noticed spontaneous monocytic-cell infiltration in the lungs of Serpine2-deficient (SE2(-/-)) mice, which led to lesions that resembled bronchus-associated lymphoid tissue (BALT).
- The increased expression of chemokines, cytokines, and adhesion molecules—which are necessary for BALT formation, organization, and maintenance—led to the beginning of lymphocyte buildup in the lungs of SE2(-/-) animals.
- Additionally, a considerable rise in the activation of thrombin, a known target of SE2, and excessive stimulation of NF-B, a key regulator of chemokine production and inflammation, were linked to the development of BALT-like lesions in the lungs of SE2(-/-) mice.
- Last but not least, systemic administration of thrombin accelerated lung chemokine expression in vivo.
- These findings reveal a novel mechanism by which lung lymphocyte accumulation results from a loss of serine protease inhibition.
- Lack of serpine2 causes bronchus-associated lymphoid tissue to develop and lung lymphocyte buildup.
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