Acute and chronic inflammation impact on human productivity and well-being. While blood cells participate in both hemostatic and immune functions, it is primarily the leukocytic cellular compartment in conjunction with vascular endothelial and smooth muscle cells, which is credited with promoting inflammatory responses, and platelets together with clotting factors are historically credited with execution of the hemostatic response to vascular injury. It is becomingly increasingly evident, however, that divisionary boundaries between hematology and inflammation are fluid, and that blood cells exhibit multidisciplinary roles. While the drive to understand these behaviors has been largely focused at the cellular level, the cross-over functions are driven by specific molecular bridges that transcend their known cellular origins and functions. They may traffic in intercellular or interstitial space, primarily blood, or act as intracellular switches that can redirect cell function upon appropriate stimulation. As an example, platelets contain storage granules with hundreds of cytokines, chemokines and factors that when released, can modulate activation and proliferation of other cells. These released inflammatory proteins may also feed back to support platelet aggregation, as illustrated by IL-ß and CD40L. Thus, not surprisingly, the inflammatory response to infection by immune cells is often accompanied by dysregulation of the clotting and fibrinolytic pathways, and may be driven by specific molecular bridges.
In this topic, we would like to include review and original research papers that would update and expand the current known molecular mediators that bring together the fields of hematology and inflammation. What are the mechanisms employed by molecular bridges? Communication is known to occur by way of surface receptor-mediated heterocellular contact, release of soluble factors that modulate hematological or inflammatory function, feedback activation loops, microparticle-mediated transport of actionable molecules that regulate hemostasis, or inflammation. Are there other previously undocumented pathways? Can we use inflammatory disease models, for example of arthritis or systemic lupus erythematous (SLE), to explore the link between hematology and inflammation at a molecular level? How do clotting abnormalities impact on inflammation? Are there novel functional assays, high-throughput or otherwise, that would help advance the identification of such, or provide bases for destroying the bridges to reinstate a balance between physiologic hematologic, vascular, and anti-inflammatory states?
This is a fairly wide field that is just beginning to be studied, particularly with an emphasis at the molecular level, rather than primarily at the cellular level. It is our hope that these efforts will be of interest to both the hematologic and inflammatory communities.
Acute and chronic inflammation impact on human productivity and well-being. While blood cells participate in both hemostatic and immune functions, it is primarily the leukocytic cellular compartment in conjunction with vascular endothelial and smooth muscle cells, which is credited with promoting inflammatory responses, and platelets together with clotting factors are historically credited with execution of the hemostatic response to vascular injury. It is becomingly increasingly evident, however, that divisionary boundaries between hematology and inflammation are fluid, and that blood cells exhibit multidisciplinary roles. While the drive to understand these behaviors has been largely focused at the cellular level, the cross-over functions are driven by specific molecular bridges that transcend their known cellular origins and functions. They may traffic in intercellular or interstitial space, primarily blood, or act as intracellular switches that can redirect cell function upon appropriate stimulation. As an example, platelets contain storage granules with hundreds of cytokines, chemokines and factors that when released, can modulate activation and proliferation of other cells. These released inflammatory proteins may also feed back to support platelet aggregation, as illustrated by IL-ß and CD40L. Thus, not surprisingly, the inflammatory response to infection by immune cells is often accompanied by dysregulation of the clotting and fibrinolytic pathways, and may be driven by specific molecular bridges.
In this topic, we would like to include review and original research papers that would update and expand the current known molecular mediators that bring together the fields of hematology and inflammation. What are the mechanisms employed by molecular bridges? Communication is known to occur by way of surface receptor-mediated heterocellular contact, release of soluble factors that modulate hematological or inflammatory function, feedback activation loops, microparticle-mediated transport of actionable molecules that regulate hemostasis, or inflammation. Are there other previously undocumented pathways? Can we use inflammatory disease models, for example of arthritis or systemic lupus erythematous (SLE), to explore the link between hematology and inflammation at a molecular level? How do clotting abnormalities impact on inflammation? Are there novel functional assays, high-throughput or otherwise, that would help advance the identification of such, or provide bases for destroying the bridges to reinstate a balance between physiologic hematologic, vascular, and anti-inflammatory states?
This is a fairly wide field that is just beginning to be studied, particularly with an emphasis at the molecular level, rather than primarily at the cellular level. It is our hope that these efforts will be of interest to both the hematologic and inflammatory communities.
