Neutrophils Function in Tissue Destruction

TNF receptor activation of these kinases stimulates NFkB, a transcription factor that induces the expression of proteins responsible for inflammation and demineralization (Sect. 10.2.2), not growth. Expressed NFkB gene products cause the IL-1 and TNF-a activities listed in Fig. 13.5. 

In gingivitis, IL-1 production by PAMP activation of external and cytosolic PRRs is maximal within the junctional epithelium. As little as 0.1 ng/mL of IL-1 will bind to and activate IL-1 receptors in capillary endothelium where they (a) Open intercellular junctions allowing plasma to exude (b) Promote secretion of plasminogen activator to prevent the plasma fluid exudate from clotting in the stroma (Sect. 11.4.2) (c) Induce intercellular adhesion molecule-1 (ICAM-1) to arrest and transfer neutrophils from blood to the exudate and D) Induce TNF-a to enhance ICAM-1 and VEGF production. 

During passage through the capillary wall, the neutrophil tertiary granules release neutral gelatinase (MMP-9) with which the neutrophils cut through type IV collagen in the 

Gingivitis is Reversible Antiinflammatory Cytokines Mediate Repair 

Interestingly, the secretion of FGF family members that mediate tissue repair resembles IL-1 secretion, that is, not involving the Golgi. The FGF family proteins also bind to their receptors by P-barrel structures that interact with a glycan (in this case known to be heparin) during activation. Hyaluronan and heparin are glycosaminoglycans (Sect. 6.3.1). 

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