About this Research Topic
In addition to playing a prominent role in hemostasis and thrombosis, the clotting protein fibrin(ogen) lies at the interface of pathogen virulence and host defence mechanisms. Infection by either bacterial or viral pathogens instigates a potent host systemic inflammatory response. This acute phase response significantly increases circulating levels and the activity of a number of haemostatic proteins as several coagulation components, including fibrinogen, are known acute-phase proteins.
Fibrinogen-mediated host defence is considered to involve two general mechanisms. The first is the physical entrapment or encapsulation of microbes by soluble fibrinogen and fibrin, limiting growth and dissemination of predominantly bacterial pathogens. Secondly, fibrin supports the recruitment and local activation of host immune cells such as leucocytes and in so doing plays a critical role in activation of immune cell effector functions through binding both integrin (e.g. αMβ2) and non-integrin receptors. Indeed, such mechanisms may influence both bacterial or viral pathogenesis within infected hosts. Through pathogenic countermeasures, fibrin(ogen) is also the target of virulence factors expressed by invading pathogens. Thus, on balance, whether fibrin(ogen) is ultimately beneficial to the host or the pathogen, is dictated by the microbe, site of infection, and competency of the host immune system.
Most of the above evidence, however stems from in vitro and/or animal models. Much less is known regarding human patients with microbial infections. In this research topic, we welcome authors to submit Original Research, Review and Perspective articles related to the role of fibrinogen and fibrin clot properties in inflammation and infection. Studies using human, animal or cell models are welcomed. We anticipate that this special issue will help to further define the role of fibrin(ogen) in inflammation and infection and to provide mechanistic insight regarding its role in the intersection between host defense and pathogen virulence.
We particularly welcome articles on the following areas, but not limited to:
1) The role of fibrinogen and in fibrin clot properties (formation, structure, composition and lysis) in inflammation and infection;
2) Mechanisms focussing on binding and interaction of fibrin(ogen) to microbial virulence factors;
3) Fibrin(ogen)-dependent mechanisms of host immune cell activation, induction of inflammatory components, or other host defence functions.
4) Barrier function of fibrin.
Fibrinogen-mediated host defence is considered to involve two general mechanisms. The first is the physical entrapment or encapsulation of microbes by soluble fibrinogen and fibrin, limiting growth and dissemination of predominantly bacterial pathogens. Secondly, fibrin supports the recruitment and local activation of host immune cells such as leucocytes and in so doing plays a critical role in activation of immune cell effector functions through binding both integrin (e.g. αMβ2) and non-integrin receptors. Indeed, such mechanisms may influence both bacterial or viral pathogenesis within infected hosts. Through pathogenic countermeasures, fibrin(ogen) is also the target of virulence factors expressed by invading pathogens. Thus, on balance, whether fibrin(ogen) is ultimately beneficial to the host or the pathogen, is dictated by the microbe, site of infection, and competency of the host immune system.
Most of the above evidence, however stems from in vitro and/or animal models. Much less is known regarding human patients with microbial infections. In this research topic, we welcome authors to submit Original Research, Review and Perspective articles related to the role of fibrinogen and fibrin clot properties in inflammation and infection. Studies using human, animal or cell models are welcomed. We anticipate that this special issue will help to further define the role of fibrin(ogen) in inflammation and infection and to provide mechanistic insight regarding its role in the intersection between host defense and pathogen virulence.
We particularly welcome articles on the following areas, but not limited to:
1) The role of fibrinogen and in fibrin clot properties (formation, structure, composition and lysis) in inflammation and infection;
2) Mechanisms focussing on binding and interaction of fibrin(ogen) to microbial virulence factors;
3) Fibrin(ogen)-dependent mechanisms of host immune cell activation, induction of inflammatory components, or other host defence functions.
4) Barrier function of fibrin.
Keywords: fibrinogen, fibrin, inflammation, infection, pathogen virulence, host defence
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
