Tryptase and Exogenous Trypsin: Mechanisms and Ophthalmic Applications

Abstract

Ocular injuries caused by inflammation, surgery or accidents are subject to a physiological healing process that ultimately restores the structure and function of the damaged tissue. Tryptase and trypsin are essential component of this process and they play a role in promoting and reducing the inflammatory response of tissues, respectively. Following injury, tryptase is endogenously produced by mast cells and can exacerbate the inflammatory response both by stimulating neutrophil secretion, and through its agonist action on proteinase-activated receptor 2 (PAR2). In contrast, exogenously introduced trypsin promotes wound healing by attenuating inflammatory responses, reducing oedema and protecting against infection. Thus, trypsin may help resolve ocular inflammatory symptoms and promote faster recovery from acute tissue injury associated with ophthalmic diseases. This article describes the roles of tryptase and exogenous trypsin in affected tissues after onset of ocular injury, and the clinical applications of trypsin injection.

Choroidal Mast Cells and Pathophysiology of Age-Related Macular Degeneration

“…Ma et al argued for the urgency of more nuanced studies centered on the specific dynamics and mechanistic roles of mast cells in the outer retina, emphasizing the necessity to understand their intricate interactions with other ocular cells and molecular entities [ 45 ]. A deep dive into their genetic, molecular, and cellular pathways, along with their interactions with other cellular components, can shed light on the comprehensive etiology of retinal degenerative processes.…”

“…PAR-2 activation triggers a signaling cascade involving the phosphorylation of the MAPKs including ERKs1/2 and JNK, leading to the activation of the transcription factor AP-1. AP-1 induces the expression of the death receptor FasL, which binds to its receptor Fas on the same cell, triggering apoptosis [ 25 , 45 ]. Importantly, this process seems to be exacerbated by oxidative stress, a condition known to contribute to the pathogenesis of dry AMD.…”