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"Inflammatory mediators" include molecules inside and outside your body that play a role in inflammation. A prime example of the latter, called an "exogenous" inflammatory mediator, is a molecule called endotoxin, or lipopolysaccharide (LPS). This substance is present in the outer covering of some types of bacteria, and signals to immune cells that there are bacteria present, causing an increase in inflammation. Your cells have sentinels on their surface called toll-like receptors (TLRs) that can sense the presence of several different microbial stimuli such as endotoxin. Occasionally, researchers studying inflammation can cause a minor acute inflammatory reaction by giving a small, safe amount of endotoxin to study volunteers. The scientists then measure changes in levels of body molecules to gain a deeper understanding of how inflammation works at a molecular level.

Monocyte/Macrophage Activation

During inflammation, monocytes and macrophages become activated by various immune system molecules (such as cytokines, including interferons, or IFNs), endotoxin, or by other microbial signals. Activated macrophages develop different properties, one of which is the capacity to stop dividing. Another feature of activated macrophages is the vigorous production of inflammatory molecules such as tumor necrosis factor (TNF) and interleukins (ILs), clotting factors, prostaglandins, free radicals, nitric oxide, and tissue remodeling enzymes. Activated macrophages also promote the growth of new blood vessels.

Neutrophil Activation

Chemokine action in injury and inflammation
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Neutrophils are among the most important cells in the first stage of an inflammatory response. These white blood cells are truly astonishing, if you consider their ability to roam through the body on demand. Neutrophils and other leukocytes can devour infectious organisms. By doing so, these cells buy time for the healing phase of an inflammatory response to begin. Neutrophils can kill because they carry molecular weapons called free radicals that are poisonous to bacteria. Typically, these poisons are hidden in specialized storage sacks kept separate from body tissues.

When a neutrophil senses an infection or injury, it undergoes a dramatic maneuver called a respiratory burst, gulping oxygen to make lots of free radicals, such as the molecule superoxide, along with protein-chewing enzymes that rip up the outer walls of bacterial cells. Neutrophils and other cells like macrophages continue to produce these toxins and loosen up the tissue to help the substances spread quickly through an injured site, or throughout the body in the case of systemic inflammation.

Lymphocyte Activation

Toll-Like Receptors (TLRs)
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There are two broad classes of lymphocytes: B cells and T cells. While all lymphocytes start out in the bone marrow, B cells develop in the marrow before entering the bloodstream whereas T cells travel to an organ called the thymus and mature there. B cells and T cells perform different roles. When activated, B cells acquire the ability to make antibodies that attack foreign substances. In contrast, T cells called "killer" T cells sense the presence of infected cells and do away with them directly. Other T cells called "helper" and "suppressor" T cells, assist killer T cells and also help to keep the immune response under control. Once activated (for example, by macrophage-produced cytokines), helper T cells produce immune substances that tell B cells to produce antibodies. T helper cells come in two varieties: TH1 and TH2. Most healthy people have more TH1 cells than TH2 cells, whereas this balance is often reversed in severely injured patients.

Platelet Activation

Platelets are essential components in blood. They are not actually cells, but rather cell fragments that become activated, changing their shape, in response to injury signals. Platelets are the parts of our blood that stimulate blood clotting to prevent us from losing blood when we are injured. Researchers now know that platelets are also an integral part of inflammation. Activated platelets shed certain molecules that directly activate inflammation inside blood vessels. Platelets also produce a variety of inflammatory mediators such as growth factors, adhesion molecules, and cytokines.