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Review
. 2017 Jan:61:31-40.
doi: 10.1016/j.semcdb.2016.07.026. Epub 2016 Jul 29.

Humoral innate immunity at the crossroad between microbe and matrix recognition: The role of PTX3 in tissue damage

Andrea Doni  1 , Giovanna D'Amico  2 , Diego Morone  1 , Alberto Mantovani  3 , Cecilia Garlanda  1
Affiliations
Review

Humoral innate immunity at the crossroad between microbe and matrix recognition: The role of PTX3 in tissue damage

Andrea Doni et al. Semin Cell Dev Biol. 2017 Jan.

Abstract

Innate immunity is involved in regulating inflammatory and tissue repair responses to injury. In particular, humoral innate immunity plays functions related to wound clearance from tissue debris, and regulation of macrophage and stromal cell activities. PTX3, a component of humoral innate immunity, orchestrates tissue repair by interacting with plasminogen and fibrin. Fluid-phase molecules of innate immunity interact with elements of the extracellular matrix, and some of the latter display opsonic activity against certain bacterial species. Thus, recognition of extracellular matrix and microbial components is a recurrent theme in the humoral arm of the innate immune system.

Keywords: Inflammation; Innate immunity; Pattern recognition molecule; Pentraxin-3 (PTX3); Tissue repair.

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Figures

Fig. 1
Fig. 1
Schematic view of cellular and molecular mechanisms involved in inflammatory and proliferation phases of skin wound repair. Soluble mediators released by platelets, neutrophils, macrophages and MSCs, and ECM components are depicted here and described in the text. In early phases, reduced oxygen tension causes a shift in cell metabolism towards an anaerobic glycolytic pathway and pH lowering in the wound site. (TXA2, thromboxane 2; LPA, lysophosphatidic acid).
Fig. 2
Fig. 2
Role of PTX3 in skin wound repair. PTX3 regulates the thrombotic response to injury by interacting with FG and Plg. PTX3 produced by invading remodeling macrophages and MSCs interacts with fibrin and Plg (through its KR5 domain) and this tripartite interaction promotes pericellular fibrinolysis by remodeling cells. In wounded skin, PTX3-deficient cells display defective fibrinolysis and directional migration toward the wound bed and clot, and re-epithelialization is delayed. The acidic pH governs the interaction of PTX3 with fibrin and Plg. PTX3-deficiency is associated with increased thrombotic response, augmented fibrin deposition and persistence, decreased Plg deposition and defective pericellular fibrinolysis, hyperactivation of fibroblastic cells and augmented collagen deposition.
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