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Fever, clinically known as pyrexia, is an abnormal increase in body temperature, usually due to an illness. Commonly thought as an undesirable side effect of diseases, fever is actually an effective way the body uses to fight infections. Patients usually recover faster when they allow fever to run its course rather than suppressing it with fever-reducing medications. This is because a higher temperature slows down the growth of most pathogens, as well as boosts the effectiveness of the body’s immune response. It also increases metabolic rates and thereby accelerating tissue repair.
Normally, the hypothalamus keeps the body’s temperature within a narrow range around 37 degrees Celsius, or 98.6 degrees Fahrenheit. The hypothalamus acts like a thermostat. It receives inputs from heat and cold receptors throughout the body, and activates heating or cooling, accordingly. When the body is too hot, the hypothalamus sends instructions for it to cool down, for example, by producing sweat. On the other hand, when temperature drops, the hypothalamus directs the body to preserve and produce heat, mainly via the release of norepinephrine. Norepinephrine increases heat production in brown adipose tissue and induces vasoconstriction to reduce heat loss. In addition, acetylcholine stimulates the muscles to shiver, converting stored chemical energy into heat.
Fever is part of the inflammatory response. When immune cells detect the presence of a pathogen, for example, upon binding to a component of bacterial cell walls, they produce inflammatory cytokines. Some of these cytokines are fever-inducers, or pyrogenic. Pyrogenic cytokines act within the hypothalamus to induce the synthesis of prostaglandin E2, PGE2, the major fever inducer. PGE2 acts on thermoregulatory neurons of the hypothalamus to raise the body’s temperature set point. In other words, PGE2 tricks the hypothalamus into thinking that the body is cold, while in fact the temperature did not change. In response, the hypothalamus instructs the body to actively produce heat to raise body temperature above normal. Fever-reducing medications, such as aspirin and ibuprofen, work by suppressing PGE2 synthesis.
Once infection is cleared, pyrogens are no longer produced and the hypothalamic thermostat is set back to normal temperature. Cooling mechanisms, such as sweating and vasodilation, are activated to cool the body down.
While fever is usually beneficial and need not be treated, precaution should be taken to prevent body temperature from running too high, which may cause confusion, seizures and irreversible damage to the brain.
Finally, it is important to differentiate between fever and hyperthermia, the latter is often caused by extended exposures to extreme heat, or heat stroke. Unlike fever, the body’s temperature set point in hyperthermia is unchanged and the body does not produce the extra heat; its cooling system is simply exhausted and fails to compensate for the excessive external heating. Hyperthermia is always harmful and must be treated with various cooling methods. Fever-reducing medications have no effect on hyperthermia as pyrogens are not involved.

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Inflammation is the body’s protective response against infections or injuries. Inflammation mobilizes defensive cells to the site of injury, limits the spread of pathogens, eliminates them, and initiates tissue repair. Inflammation can occur in any organ, but is most common, and also most easily observable in the skin and underlying tissues. Typical signs include redness, heat, swelling and pain.
Inflammation is an important defense mechanism, but it can be a double-edged sword when things go wrong. An autoimmune disease may result when inflammation targets and destroys the body’s own cells. An acute inflammation that fails to stop after the original insult is cleared, can become chronic and damaging to healthy tissues.
Acute inflammation is initiated when tissue-resident immune cells, such as macrophages, encounter an inflammatory stimulus. This stimulus can be a pathogen, a toxin, or an injured host cell. Binding of the stimulus to its receptor on the immune cell triggers a signaling cascade that activates production of cytokines and other inflammatory mediators.
Inflammatory chemicals dilate blood vessels, increasing blood flow and enhancing vessel permeability, allowing plasma fluid and more immune cells to seep through and accumulate in the inflamed tissue. This vasodilation is responsible for clinical signs of inflammation such as redness, heat and swelling.
The infiltration of blood components into the injured tissue occurs in 3 phases. The first phase is the exudation of plasma fluid containing various antimicrobial mediators, platelets and blood clotting factors. These factors can destroy microbes and stop any bleeding that may have occurred.
The second phase is the infiltration of neutrophils – the major phagocytes involved in first-line defense. Once activated by inflammatory mediators, endothelial cells of blood vessels become adhesive, they attach to neutrophils in blood flow, slowing them down, before getting them to squeeze through the vessel wall. Chemical cues guide neutrophils to the battle field, where they engulf bacteria and destroy them with enzymes or toxic peroxides. Neutrophils may also release highly reactive oxygen species in a phenomenon known as oxidative burst, which kills pathogens faster and more efficiently. The pathogen-laden neutrophils then die via apoptosis.
In the third phase arrive monocytes. Monocytes differentiate into macrophages, which then remove pathogens, injured cells and dying neutrophils by phagocytosis. Macrophages that have completed their mission are cleared from the tissue by the lymphatic system. Accumulation of fluid increases pressure on lymphatic capillaries, forcing open their one-way valves, facilitating lymphatic drainage. Lymph containing debris-laden macrophages passes through a number of lymph nodes and is filtered clean before it returns to the bloodstream.
Once the site is cleared from the original insult, immune cells stop producing pro-inflammatory chemicals and, instead, start producing anti-inflammatory mediators, which actively drive the termination of inflammation. Many of these anti-inflammatory molecules are lipids, some of which are synthesized from dietary omega-3 fatty acids. This step is essential in ensuring the favorable outcome of inflammation. Failure to resolve inflammation leads to development of chronic inflammation which continuously deals damage to healthy tissues. Chronic inflammation is a known contributing factor to pathogenesis of a wide variety of conditions including cardiovascular diseases, asthma, diabetes, arthritis, and even cancer.

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In a nutshell, the lymphatic system is a drainage system that removes excess fluid from body tissues and returns it to the bloodstream. It is actually a subsystem of both the circulatory and immune system.
The major purpose of the circulatory system is to bring oxygen and nutrients to body tissues and remove wastes. This exchange happens in the smallest blood vessels called the capillaries. Blood plasma containing nutrients moves out of capillaries at the arterial end of capillary beds, while tissue fluid containing wastes reabsorbs back in at the venous end. However, not all of the fluid is drawn back to the bloodstream at this point. About 15% of it is left in the tissues and would cause swelling if accumulated. This is where the lymphatic system comes into play, it picks up the excess fluid and returns it to the circulatory system.
Unlike the blood circulatory system, which is a closed loop, the lymphatic system is a one-direction, open-ended network of vessels. Lymphatic vessels begin as lymphatic capillaries made of overlapping endothelial cells. The overlapping flaps function as a one-way valve. When fluid accumulates in the tissue, interstitial pressure increases pushing the flaps inward, opening the gaps between cells, allowing fluid to flow in. As pressure inside the capillary increases, the endothelial cells are pressed outward, closing the gaps, thus preventing backflow. Unlike blood capillaries, the gaps in lymphatic capillaries are so large that they allow bacteria, immune cells such as macrophages, and other large particles to enter. This makes the lymphatic system a useful way for large particles to reach the bloodstream. It is used, for example, for dietary fat absorption in the intestine.
Once inside lymphatic vessels, the recovered fluid is called lymph. Lymph flow is enabled by the same forces that facilitate blood flow in the veins. It goes from lymphatic capillaries to larger and larger lymphatic vessels and eventually drains into the bloodstream via the subclavian veins. On the way, it passes through a number of lymph nodes, which serve as filters, cleansing the fluid before it reaches the bloodstream.
Lymph nodes are small bean-shaped structures scattered throughout the lymphatic network. They are most prominent in the areas where the vessels converge. Lymph nodes contain macrophages and dendritic cells that directly “swallow up” any pathogens, such as bacteria or viruses, that may have been taken up from an infected tissue. They also contain lymphocytes: T-cells and B-cells, which are involved in adaptive immune response, a process that produces activated lymphocytes and antibodies specific to the invading pathogen. These are then carried by the lymph to the bloodstream to be distributed wherever they are needed.
The lymphatic system also includes lymphoid organs. Primary lymphoid organs – the thymus and bone marrow, are the sites of lymphocyte production, maturation and selection. Selection is the process in which lymphocytes learn to distinguish between self and non-self, so they can recognize and destroy pathogens without attacking the body’s own cells. Mature lymphocytes then leave the primary for the secondary lymphoid organs – the lymph nodes, spleen, and lymphoid nodules – where they encounter pathogens and become activated.