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A note on lungs and clotting. Fibrin is an essential part of alveolar damage because whilst it impairs gas exchange it is also vita as a scaffold for tissue repair. Pneumocytes have considerable interaction with the clotting cascade, not least through immune cytokines.
Some of their interactions are complex, for example post translational modification of genes relating to plasminogen (the clot clearing pathway) revolving around cis-trans mRNA interactions. Overall in lung injury this leads to impaired fibrinolysis.
Compressive factors also induce genetic changes in epithelial cells - mechanosensitive genes are widespread and include varied plasminogen family members.
Coagulation links tissue invasion and immune response - some species secrete serum molecules that are both immunoglobulins and fibrinogen, both immune and clotting facades have phylogenetic similarities and require calcium to work, and mutually enhance each other.
NETS - dna/actin traps from neutrophils help block routes of escape for invading pathogens. Disrupted clotting can enhance systemic spread of disease. In mice, disrupting plasminogen activator inhibitor (a clot stabilising protein) increased lethality in pseudomonas
In this example, the early clotting response neatly supported host defences and bridged to innate immune responses that enabled pathogen clearance. The two are synergistic, and I suspect we don’t often consider the immunological effects of anti coagulation, or how to soften.
