It is triggered by the immune system, which is a cellular system within the body. If the immune system detects an injury or intruder, it mounts a response called an inflammatory response and signals cells to the site of injury or infection. You may hear the words infection and inflammation together, but they mean very different things. Infection refers to the invasion and multiplication of bacteria or viruses within the body, while inflammation is the body's protective response against infection.
Inflammation is a complex cellular process involving various types of immune cells, clotting proteins and signaling molecules. It can occur after an injury, such as a burn or a cut, and also when there is an infection present in the body. But, inflammation can sometimes also occur without an injury or infection. Sometimes, the immune system can over-react and can cause inflammation by attacking healthy tissues within the body.
When auto-inflammation occurs, there is a dysfunction within the immune system that triggers the body to mount an inflammatory response against itself. It is not known why this occurs, but it is thought that a virus or another trigger in the environment may be the initial cause.
When an injury occurs, the cells of our immune system immediately travel to the site of injury or irritation and the inflammatory response begins. This includes widening of local blood vessels to allow fluid and immune cells into surrounding injured tissue, which causes swelling, redness, warmth and pain at the site.
This process protects the injured area and signals other cells to the site to begin repairing and healing the injury. Normally, inflammation slowly goes away after the irritation has been removed and the body is adequately protected, as can be seen with the example of the splinter in the skin. During auto-inflammation, cells of the immune system also travel to certain sites in the body. However, there are no injuries or infections at these sites. Instead of repairing and healing, the auto-inflammatory response often ends up harming healthy tissues.
Auto-inflammation can cause damage and destruction to the body tissues or organs that it affects. An auto-inflammatory event can be a one-time occurrence or it may develop into a chronic long-term issue.
The exact cause of auto-inflammatory conditions is not known. Adult worms live in the lymphatic vessels, where their presence stimulates infiltration by lymphocytes, plasma cells, eosinophils, and thrombocytes a condition known as lymphangitis. Because of the chronic nature of the illness, granulomas, fibrosis, and blocking of the lymphatic system may eventually occur.
Over time, these blockages may worsen with repeated infections over decades, leading to skin thickened with edema and fibrosis. Lymph extracellular tissue fluid may spill out of the lymphatic areas and back into tissues, causing extreme swelling Figure 3.
Secondary bacterial infections commonly follow. Because it is a disease caused by a parasite, eosinophilia a dramatic rise in the number of eosinophils in the blood is characteristic of acute infection. However, this increase in antiparasite granulocytes is not sufficient to clear the infection in many cases. Lymphatic filariasis affects an estimated million people worldwide, mostly concentrated in Africa and Asia.
A fever is an inflammatory response that extends beyond the site of infection and affects the entire body, resulting in an overall increase in body temperature. Body temperature is normally regulated and maintained by the hypothalamus, an anatomical section of the brain that functions to maintain homeostasis in the body. Pyrogens may be exogenous or endogenous. In a cascading effect, these molecules can then lead to the release of prostaglandin E2 PGE 2 from other cells, resetting the hypothalamus to initiate fever Figure 4.
Figure 4. The role of the hypothalamus in the inflammatory response. Macrophages recognize pathogens in an area and release cytokines that trigger inflammation. The cytokines also send a signal up the vagus nerve to the hypothalamus. Like other forms of inflammation, a fever enhances the innate immune defenses by stimulating leukocytes to kill pathogens. In addition, some studies suggest that fever may also stimulate release of iron-sequestering compounds from the liver, thereby starving out microbes that rely on iron for growth.
During fever , the skin may appear pale due to vasoconstriction of the blood vessels in the skin, which is mediated by the hypothalamus to divert blood flow away from extremities, minimizing the loss of heat and raising the core temperature. The hypothalamus will also stimulate shivering of muscles, another effective mechanism of generating heat and raising the core temperature. The crisis phase occurs when the fever breaks. The hypothalamus stimulates vasodilation , resulting in a return of blood flow to the skin and a subsequent release of heat from the body.
The hypothalamus also stimulates sweating, which cools the skin as the sweat evaporates. Although a low-level fever may help an individual overcome an illness, in some instances, this immune response can be too strong, causing tissue and organ damage and, in severe cases, even death. The inflammatory response to bacterial superantigens is one scenario in which a life-threatening fever may develop. Superantigens are bacterial or viral proteins that can cause an excessive activation of T cells from the specific adaptive immune defense, as well as an excessive release of cytokines that overstimulates the inflammatory response.
For example, Staphylococcus aureus and Streptococcus pyogenes are capable of producing superantigens that cause toxic shock syndrome and scarlet fever , respectively. Patients with this genetic abnormality may have occasional episodes of swelling in various parts of the body. Please consult the latest official manual style if you have any questions regarding the format accuracy.
Acute inflammation is the early almost immediate response of a tissue to injury. It is nonspecific and may be evoked by any injury short of one that is immediately lethal. Acute inflammation may be regarded as the first line of defense against injury and is characterized by changes in the microcirculation: exudation of fluid and emigration of leukocytes from blood vessels to the area of injury. Acute inflammation is typically of short duration, occurring before the immune response becomes established, and it is aimed primarily at removing the injurious agent.
Until the late 18th century, acute inflammation was regarded as a disease. Clinically, acute inflammation is characterized by 5 cardinal signs: rubor redness , calor increased heat , tumor swelling , dolor pain , and functio laesa loss of function Figure The first four were described by Celsus ca 30 bc —38 ad ; the fifth was a later addition by Virchow in the nineteenth century.
Redness and heat are due to increased blood flow to the inflamed area; swelling is due to accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings; and loss of function is due to a combination of factors. These signs are manifested when acute inflammation occurs on the surface of the body, but not all of them will be apparent in acute inflammation of internal organs. Pain occurs only when there are appropriate sensory nerve endings in the inflamed site—for example, acute inflammation of the lung pneumonia does not cause pain unless the inflammation involves the parietal pleura, where there are pain-sensitive nerve endings.
The increased heat of inflamed skin is due to the entry of a large amount of blood at body core temperature into the normally cooler skin. When inflammation occurs internally—where tissue is normally at body core temperature—no increase in heat is apparent. Cardinal signs of acute inflammation. Note swelling and redness of the skin around an infected burn. Top Stories. Getting the data on homelessness. Hospital News.
MRT Week has started: Let's celebrate and recognize this essential role in health care. Ensuring patients and Essential Care Partners are heard in palliative care. Donor Impact.
0コメント