The Division of Cardiovascular Medicine, The Gill Heart Institute, Lexington, KY 40536-0509, United States.
Published: March 2011
AI Article Synopsis
Article Abstract
Platelets occupy a central role at the interface between thrombosis and inflammation. At sites of vascular damage, adherent platelets physically and functionally interact with circulating leukocytes. Activated platelets release soluble factors into circulation that may have local and systemic effects on blood and vascular cells. Platelets can also interact with a wide variety of microbial pathogens. Emerging evidence from animal models suggests that platelets may participate in a wide variety of processes involving tissue injury, immune responses and repair that underlie diverse diseases such as atherosclerosis, autoimmune disorders, inflammatory lung and bowel disorders, host-defense responses and sepsis. In this review, we summarize the general mechanisms by which platelets may contribute to immune function, and then discuss evidence for their role in host defense responses and sepsis from preclinical and clinical studies.
Background: Sepsis is the result of a dysregulated immune response to infection and is associated with acute organ dysfunction. The syndrome's complexity is contingent upon the underlying pathology and individual patient characteristics, including their immune response. The involvement of multiple organs and physiological functions adds complexity, with "organ cross-talk" emerging as a pivotal pathophysiological and clinical aspect.
University of Health Sciences, Ankara Oncology Training and Research Hospital, Department of Hematology & Apheresis Unit, Ankara, Turkey; Ankara Yildirim Beyazit University, School of Medicine, Department of Internal Medicine, Division of Hematology, Ankara, Turkey.
Objective: Graft-versus-host disease (GvHD) is a common and serious complication following allogeneic hematopoietic stem cell transplantation (allo-HSCT), significantly impacting transplant efficacy. In the treatment of GvHD, numerous therapeutic approaches have been explored, with mesenchymal stem cells (MSCs) emerging as a prominent immunomodulatory option. We aimed to evaluate efficacy and outcomes of using MSCs for steroid refractory acute GVHD (SR-aGvHD) management.
Sepsis is characterized by a concomitant early pro-inflammatory response by immune cells to an infection, and an opposing anti-inflammatory response that results in protracted immunosuppression. The primary pathological event in sepsis is widespread programmed cell death, or cellular self-sacrifice, of innate and adaptive immune cells, leading to profound immunological suppression. This severe immune dysfunction hampers effective primary pathogen clearance, thereby increasing the risk of secondary opportunistic infections, latent viral reactivation, multiple organ dysfunction, and elevated mortality.
Sepsis (sepsis) is a systemic inflammatory response triggered by infection, and its pathologic features include overproduction of peripheral inflammatory factors (e.g., IL-1β, IL-6, TNF-α), which ultimately leads to cytokine storm and multiple organ dysfunction syndrome (MODS).
Sepsis is a complicated clinical disease caused by a defective host response to infection, leading to elevated morbidity and fatality globally. Sepsis patients have a significant risk of life-threatening organ damage, including hearts, brains, lungs, kidneys, and livers. Nevertheless, the molecular pathways driving organ injury in sepsis are not well known.
