Abstract
Pathogens have developed particular strategies to infect and invade their hosts. Amongst these strategies’ figures the modulation of several components of the innate immune system participating in early host defenses, such as the coagulation and complement cascades, as well as the fibrinolytic system. The components of the coagulation cascade and the fibrinolytic system have been proposed to be interfered during host invasion and tissue migration of bacteria, fungi, protozoa, and more recently, helminths. One of the components that has been proposed to facilitate pathogen migration is plasminogen (Plg), a protein found in the host’s plasma, which is activated into plasmin (Plm), a serine protease that degrades fibrin networks and promotes degradation of extracellular matrix (ECM), aiding maintenance of homeostasis. However, pathogens possess Plg-binding proteins that can activate it, therefore taking advantage of the fibrin degradation to facilitate establishment in their hosts. Emergence of Plg-binding proteins appears to have occurred in diverse infectious agents along evolutionary history of host–pathogen relationships. The goal of the present review is to list, summarize, and analyze different examples of Plg-binding proteins used by infectious agents to invade and establish in their hosts. Emphasis was placed on mechanisms used by helminth parasites, particularly taeniid cestodes, where enolase has been identified as a major Plg-binding and activating protein. A new picture is starting to arise about how this glycolytic enzyme could acquire an entirely new role as modulator of the innate immune system in the context of the host–parasite relationship.
Highlights
Infectious agents migrate to their predilection sites in the host tissues, sometimes requiring to trespass physical barriers of the host such as epithelia, extracellular matrices (ECM), basement membranes, or circumvent several effector systems along their journey through the bloodstream [1,2,3]
PLG bound to Lsa23 could be converted into Plm, which in turn degrades C3b and C4b [70]. These results suggest that Lsa23 might be involved in complement evasion processes by acting on three different mechanisms and could assist Leptospira to overcome lysis promoted by the membrane attack complex (MAC)
As Plm has been involved in the degradation of fibrin clots and ECM, we proposed that binding and activation of Plg might help the parasite to colonize host tissues
Summary
Infectious agents migrate to their predilection sites in the host tissues, sometimes requiring to trespass physical barriers of the host such as epithelia, extracellular matrices (ECM), basement membranes, or circumvent several effector systems along their journey through the bloodstream [1,2,3]. They evade innate and adaptive host’s immune responses, involving the participation of multiple proteins, including proteolytic enzymes, receptors, immunomodulatory molecules, amongst many other factors that facilitate their dissemination and establishment in host’s tissues [4,5,6,7,8].
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