Why does the inflammatory response occur

My question is are we treating the underlying cause of hypoxemia? I feel that these patients should be hit with high dose antihistamines and an inhaled steroids such as pulmicort as frequently as possible. This may get the patient thru the massive inflammatory response which seems to be the culprit to so many deaths in H1N1.

Maybe it will buy the patients enough time to tackle the virus which is supposed to be self-limited in nature anyways if the hypoxemia did not get in the way so much. I know a mold victim with an immune level of 1, when is average. From what I ready in Times magazine, scientists at the Oxford Academy came up with a method of treating the inflammatory issues using anabolic steroids.

They're preparing a new drug that should be available for the public in A very informative article, thanks! And what are the differences? Thank you for any advice. It consists of fastidious material. Skip to main content Skip to primary sidebar During the earliest stages of a virus infection, cytokines are produced when innate immune defenses are activated.

Comments Very nice. I enjoyed reading this a great deal. Hi, albatross! Roids seem like a favorite, but long term effects are risky. 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. A dysfunction of the immune system causes auto-inflammation, but it is unknown why this dysfunction occurs. Various theories include exposure to a virus, possible environmental triggers, and genetics. The immune system is a cellular system within the body. White blood cells, also known as leukocytes, make up a large part of the cells of the immune system. White blood cells help fight infection by attacking invaders and consuming infected or dead cells.

The body has various types of white blood cells, all of which are produced in the bone marrow the soft middle part of our bones.

People with auto-inflammatory conditions may have higher levels of white blood cells in their blood, or they may have white blood cells present where white blood cells are not normally present. A tubercular granuloma is called a tubercle Figure 2.

Tuberculosis will be covered in more detail in Bacterial Infections of the Respiratory Tract. Chronic inflammation is not just associated with bacterial infections. Chronic inflammation can be an important cause of tissue damage from viral infections. The extensive scarring observed with hepatitis C infections and liver cirrhosis is the result of chronic inflammation. Figure 3. Elephantiasis chronic edema of the legs due to filariasis.

In addition to granulomas, chronic inflammation can also result in long-term edema. A condition known as lymphatic filariasis also known as elephantiasis provides an extreme example. Lymphatic filariasis is caused by microscopic nematodes parasitic worms whose larvae are transmitted between human hosts by mosquitoes.

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.