An adult human body contains about 5 liters of blood. The liquid component of blood is plasma, and contains (besides water) proteins, nutrients, hormones, electrolytes and metabolic waste products. Its yellow color is due to the presence of bilirrubin (a waste product of haem degradation). Plasma proteins are synthesized by the liver and play a large variety of roles: transport of small molecules, mantaining osmotic pressure and clotting. Blood cells may be:
All blood cells arise in the bone marrow from adult stem cells which differentiate under the control of a large array of hematopoietic factors.
When veins rupture, blood loss is relatively slow (due to low blood pressure) and can often be controlled by raising the affected region above the level of the heart. If the hemorrhage occurs towards the surrounding tissue, blood accumulation (hematome) may itself be enough to rise the pressure of the interstitial fluid to the level of the venal pressure, thus stoping blood loss.
Hemorrhages due to the rupture of medium or large arteria canot ussually be controlled by the organism. However, the physiological clotting mechanism are quite effective in dealing with lesions to small vessels, which are the most common in daily life.
The most immediate body response to a vascular lesion is the constriction of the affected blood vessel, leading to a decrease of blood flow through the injured area. Such constriction presses the endothelial surfaces of the vessel towards each other, thus inducing a contact that blocks it. However, this mechanism is only able to block permanently the rupture in the thinnest capillaries, and termination of bleeding usually depends on two further mechanisms, which require platelet intervention:
Tissue damage caused by pathogens causes the release of chemical messengers that stimulate vasodilation around the affected area, as well as an increase in protein permeability of the blood vessels' epithelium. This permeability increase leads to protein (and plasma) diffusion into the affected area (edema). As the inflammatory response progresses, circulating neutrophiles (atracted by chemotactic molecules like leukotrienes) adhere to endothelial cells in the concerned region. Adhesion prevents neutrophiles from being washed away by the blodstream, and allows their local accumulation. Neutrophils then "squeeze" through the interstitialspaces beteen endothelial cells and migrate into the interstitial fluid - diapedesis.
Monocytes also migrate towards the interstitial fluid, and then mature into macrophages. Contact between the fagocytic cell (neutrophile or macrophage) and the lipids and carbohydrates present on the bacterail pathogen cell wall then trigger fagocytosis. The fagocyte surrounds the foreign cell, and upon endocytosis attacks it with the hydolitic enzymes form its lysossomes. Further enzymes release powerful and highly toxic oxidizing substances (NO, hydrogen peroxide, hypochlorite).
A set of plasma proteins (called complement) (which, like coagulation factors, activate each other through a cascade) is also able to ellicit extracellular destruction of pathogens. Complement is activated in response to infection and leads to the formation of a membrane attack complex (MAC). The MAC is able to fuse with the membrane of the pathogen, thereby forming a water-filled channel that disrupts the pathogens osmotic balance and lysing it. Some components of the complement system are also opsonins, i.e., they are able to facilitate the phagocytosis of the pathogen.
The mechanisms described above are non-specific. Specific immunity (which is responsible, e.g. for immunization) depends on the action of molecules (immunoglobulins) that can recognize specific molecular markers (the antigens) present on the foreign cell. Immunoglobulins are produced by lymphocytes and contain conserved regions, as well as variable (and hypervariable) sequences which are responsible for selective binding to the antigens. Immunoglobulin synthesis entails random rearrangement of specific regions in each lymphocyte's immunoglobulin genes, and each lyphocyte therefore produces only own immunoglobulin, which is different from those of other lymphocytes. When a lymphocyte recognizes an antigen, it becomes activated, and undergoes accelerated division. Each daughter cell will be specific for the same antigen recognized by its mother cell. Some daughter cells initiate the immunological response, while others are kept in reserve, as "immunological" memory". There are three types of lymphocytes:
Besides the functions referred to above, antibodies may also trigger other mechanisms: they can activate the complement cascade (thereby leading to pathogen lysis), they may complex toxins (and form extensive antibody-toxin-antibody-toxin-etc. comlpexes) in order to allow their phagocytosis, and they can also act as opsonins.
The surface of erythrocytes contains a high number of glycoproteins, grouped in families called "blood groups". The most imoprtant groups are the ABO and Rhesus systems.
ABO system - It includes carbohydrate H and two similar variants, known as A and B. An individual may therefore be A, AB, B or O (if it only carries antigen H). Every individual carries specific antibodies against those carbohydrates it lacks: an A person carries anti-B antibodies, an O person carries anti-A and anti-B antibodies, and an AB person carries neither (there are no anti-H antibodies, since the H antigen is the core carbohydrate of both A and B antigens, and an anti-H antibody would also react against the A and B carbohydrates). During a blood transfusion, the donor's antibodies quickly get diluted in the receptor's blodstream, and (in)compatibility effects arise from the interaction between the receptor's antibodies and the antigens present in the donor's blood. If the receptor carries specific antibodies against the donor's erythorocytes, they will agglutinate (cross-linked through the receptor's antibodies) and form a thrombus. Rhesus system- This system is dependent on the presence or absence of the D antigen. Unlike the ABO system, no anti-D antibodies exist in the bloodstream of an individual wo has never been exposed to the antigen. This becomes relevant during mother-fetus interaction. In parturition, the rupture of placental blood vessels leads to contact between the mother and the baby's blood. Should the mother be Rh- and the baby be Rh+, this leads to exposure of the mother to the D antigen, and she will start to produce anti-D antibodies. In future pregnancies, these antibodies may cross the placenta and lead to agglutination of the erythocytes of a Rh+ baby, leading to sever anemia, or even death. Nowadays, this is prevented through inffusion of anti-D antibodies to the Rh- mother immediatlly after the birth of a Rh+ baby. These antibodies bind to the D antigens of the baby's erythocytes that are present in the mother's bloodstream, thereby preventing them to induce the mother to synthesize antibodies. These problems do not arise in the ABo system because anti-A and anti-B antibodies are IgM antibodies, too large to cross the placenta.