Targeting active sites of inflammation using inherent properties of tissue-resident mast cells

Acta Biomater. 2023 Mar 15:159:21-37. doi: 10.1016/j.actbio.2023.01.024. Epub 2023 Jan 16.

Abstract

Mast cells play a pivotal role in initiating and directing host's immune response. They reside in tissues that primarily interface with the external environment. Activated mast cells respond to environmental cues throughout acute and chronic inflammation through releasing immune mediators via rapid degranulation, or long-term de novo expression. Mast cell activation results in the rapid release of a variety of unique enzymes and reactive oxygen species. Furthermore, the increased density of mast cell unique receptors like mas related G protein-coupled receptor X2 also characterizes the inflamed tissues. The presence of these molecules (either released mediators or surface receptors) are particular to the sites of active inflammation, and are a result of mast cell activation. Herein, the molecular design principles for capitalizing on these novel mast cell properties is discussed with the goal of manipulating localized inflammation. STATEMENT OF SIGNIFICANCE: Mast cells are immune regulating cells that play a crucial role in both innate and adaptive immune responses. The activation of mast cells causes the release of multiple unique profiles of biomolecules, which are specific to both tissue and disease. These unique characteristics are tightly regulated and afford a localized stimulus for targeting inflammatory diseases. Herein, these important mast cell attributes are discussed in the frame of highlighting strategies for the design of bioresponsive functional materials to target regions of inflammations.

Keywords: Biomaterials; Enzymes; MRGPRX2; Mast cells; ROS; Stimuli-responsive.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Catalytic Domain
  • Humans
  • Inflammation / metabolism
  • Mast Cells*
  • Receptors, G-Protein-Coupled / metabolism
  • Receptors, Neuropeptide* / metabolism

Substances

  • Receptors, Neuropeptide
  • Receptors, G-Protein-Coupled