What is meant by host defense mechanism

The respiratory tract has upper airway filters. If invading organisms reach the tracheobronchial tree, the mucociliary epithelium transports them away from the lung. Coughing also helps remove organisms. If the organisms reach the alveoli, alveolar macrophages and tissue histiocytes engulf them. However, these defenses can be overcome by large numbers of organisms, by compromised effectiveness resulting from air pollutants (eg, cigarette smoke), interference with protective mechanisms (eg, endotracheal intubation, tracheostomy), or by inborn defects (eg, cystic fibrosis Cystic Fibrosis Cystic fibrosis is an inherited disease of the exocrine glands affecting primarily the gastrointestinal and respiratory systems. It leads to chronic lung disease, exocrine pancreatic insufficiency… read more ).

The coordinated activation of inflammatory and hemostatic responses following infection or tissue injury is a phylogenetically conserved defense mechanism that can be traced back to early invertebrates. 1 In these primitive organisms, a single cell (the hemocyte) can perform basic inflammatory, immune, and hemostatic functions. 1 However, most higher-order mammals have evolved a complex multicellular system encompassing platelets and a variety of leukocyte subsets, including neutrophils, monocytes, and a series of antigen-presenting cells. Similarly, some of the major humoral components of innate immunity have evolved from a rudimentary complement system into a sophisticated series of highly integrated protease cascades, including the complement, coagulation, fibrinolysis, and contact-kinin systems. Despite this close evolutionary development, thrombosis and inflammation have traditionally been viewed as distinct complementary processes. Thrombosis can be best defined as an exaggerated hemostatic response, leading to the formation of an occlusive blood clot obstructing blood flow through the circulatory system. By comparison, inflammation is the term applied to the complex protective immune response to harmful stimuli, such as pathogens, damaged cells, or irritants. However, with the recognition that inflammation stimulates thrombosis, and in turn, thrombosis promotes inflammation, the functional interdependence of these processes has becoming increasingly well defined ( Figure 1A ).

Thromboinflammation: an important pathogenic process linked to a diverse range of human diseases. (A) A broad spectrum of human disorders is associated with thromboinflammatory complications, many of which have microvascular dysfunction. It is likely that the level of α-thrombin generation is a key determinant of the extent of the thromboinflammatory response. For example, diseases such as sepsis, ischemia reperfusion (IR) injury (the focus of this review), and organ transplant rejection are associated with widespread activation of coagulation throughout the microcirculation, which is accompanied by an intense thrombotic and inflammatory response. At the extremes of this spectrum, the microvascular thrombotic disorder thrombotic thrombocytopenia purpura (TTP) exhibits limited α-thrombin generation and is associated with a limited inflammatory response in the early phase of the disease. At the other end of the spectrum, autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus (SLE), are primarily considered inflammatory disorders, with a limited role for α-thrombin. Nonetheless, other hemostatic components appear to contribute to the pathogenesis of these diseases. (B) Tissue or organ injury by diverse pathogenic mechanisms is commonly associated with microvascular thromboinflammatory responses. Microvascular obstruction can be mediated by all cellular elements in blood, including platelets, neutrophils, and red blood cells (RBCs), with stable occlusion typically linked to the activation of coagulation and fibrin generation. Regardless of the primary insult to tissues or organs (infection, ischemia, or trauma), the ultimate outcome of these disorders is heavily influenced by the extent of the microvascular thrombotic and inflammatory responses. EC, endothelial cell; HUS, hemolytic-uremic syndrome; NO, nitric oxide; TRALI, transfusion-related acute lung injury.

A growing body of evidence indicates that some autoimmune disorders, such as rheumatoid arthritis and systemic lupus erythematosus, are regulated by components of the hemostatic system.2 Thrombotic disorders, such as paroxysmal nocturnal hemoglobinuria or atypical hemolytic uremic syndrome, are triggered by humoral components of innate immunity (complement), and many microvascular inflammatory disorders promote platelet activation and coagulation. This is most clearly demonstrated in the acute exaggerated thromboinflammatory responses that accompany sepsis, ischemia-reperfusion (IR) injury, and major trauma. In these latter disorders, the ultimate extent of organ injury is dependent on the primary insult (bacterial invasion, organ ischemia, or traumatic injury), as well as on the extent of the ensuing microvascular thromboinflammatory response (Figure 1B). When severe, thromboinflammation can extend systemically and damage remote organs, particularly the lung (acute lung injury or acute respiratory distress syndrome) and kidneys (acute kidney injury). This is a major issue in critically ill patients and can lead to the development of multiorgan dysfunction syndrome and death. Thus, defining the molecular mechanisms regulating thromboinflammation in specific disease states is of major clinical importance. The primary focus of this review will be on the role of coagulation in promoting acute microvascular thrombosis and inflammation during sepsis and IR injury. These disorders have been most intensively investigated in the context of thromboinflammation, and much has been learned from sepsis and IR injury about the potential benefits and limitations of targeting coagulation processes in the clinic. For more detailed information on the interaction between coagulation and other components of the hemostatic and innate immune system, several excellent review articles have been published.3-7

host

[

hōst

]

1. an animal or plant that harbors and provides sustenance for another organism (the parasite).

2. the recipient of an organ or other tissue derived from another organism (the donor).

accidental host one that accidentally harbors an organism that is not ordinarily parasitic in the particular species.

definitive host (final host) a host in which a parasite attains sexual maturity.

intermediate host a host in which a parasite passes one or more of its asexual stages; usually designated first and second, if there is more than one.

paratenic host a potential or substitute intermediate host that serves until the appropriate definitive host is reached, and in which no development of the parasite occurs; it may or may not be necessary to the completion of the parasite’s life cycle.

host of predilection the host preferred by a parasite.

primary host definitive host.

reservoir host an animal (or species) that is infected by a parasite, and which serves as a source of infection for humans or another species.

secondary host intermediate host.

transfer host one that is used until the appropriate definitive host is reached, but is not necessary to completion of the life cycle of the parasite.