inflammatory mediator

Examples of inflammatory mediator in the following topics:

• Inflammation

  • An inflammatory response can be caused by any of numerous inflammatory mediators released from innate immune system cells.
  • After an inflammatory mediator is released in the bloodstream, a period of transient vasoconstriction, lasting only a few seconds, occurs.
  • Then blood vessels expand to undergo vasodilation from the stimulus of the vasoactive inflammatory mediator, which increases blood flow to the area.
  • Other inflammatory mediators, such as TNF-alpha and IL-1, increase the expression of adhesion molecules on vascular endothelial cells.
  • When acute inflammation ends (typically by release of anti-inflammatory mediators such as IL-10 or an end to the release of inflammatory mediators) resolution will occur if the problem is alleviated.

• Types of Cytokines Participating in Immune Response

  • Some of the more important ones include inflammatory mediators such as IL-1, IL-4, and IL-6, the potent anti-inflammatory IL-10, and other interleukins involved with T and B cell signaling following antigen presentation.
  • One common interferon is IFN-gamma, a pyrogen involved in inflammatory response and macrophage and NK cell activation.
  • By definition, inflammatory mediators in other classes of cytokines are also considered chemokines.
  • This long-lasting inflammatory mediator and pyrogen can cause fever and inflammation for up to 24 hours.

• Respiratory Distress Syndrome

  • It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange with concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia, and frequently resulting in multiple organ failure.
  • If the underlying disease or injurious factor is not removed, the amount of inflammatory mediators released by the lungs in ARDS may result in a systemic inflammatory response syndrome (or sepsis if there is lung infection).

• Fever

  • Fever is an elevation of body temperature above the regulatory set point, mediated through the release of prostaglandin E2.
  • PGE2 release comes from the arachidonic acid pathway, which also produces inflammatory mediators such as thromboxane and leukotriene.
  • This pathway is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase.
  • These enzymes ultimately mediate the synthesis and release of PGE2.
  • For example, septic shock is a severe bacterial infection in which bacterial toxins stimulate pyrogen and inflammatory mediator activity causes high fever.

• Vascular Spasm

  • This is because as tissues are damaged during an injury, inflammation occurs as a result of inflammatory mediator release from immune system cells (such as mast cells or NK cells) that receive cell stress cytokines from damaged enothelial cells or vasoactive amines (serotonin) that are secreted by activated platelets.

• Types of Adaptive Immunity

  • The adaptive immune response is mediated by B and T cells and creates immunity memory.
  • There are two subdivisions of the adaptive immune system: cell-mediated immunity and humoral immunity.
  • Cell mediated immunity is controlled by type 1 helper T cells (Th1) and cytotoxic T cells.
  • This binding will cause degranulation and release of inflammatory mediators that start an immune response against the antigen.
  • This process is the reason why memory B cells can cause hypersensitivity (allergy) formation, as circulating IgE from those memory cells will activate a rapid inflammatory and immune response.

• Stress and Immunity

  • Cortisol has numerous effects on the body, such as sympathetic nervous system activation, increasing blood sugar for energy purposes, and anti-inflammatory effects that include the inhibition of certain inflammatory mediators that are important in innate immunity.
  • Other studies show that the weakened inflammatory effect makes pathogen-caused diseases more likely to lead to infection.
  • Over time, immune cells may become desensitized to cortisol and express fewer cortisol receptors, so chronic inflammation can develop as the anti-inflammatory effect of cortisol is weakened.
  • Erythema nodosum—lesions that occur in some patients suffering from inflammatory bowel syndrome.

• Types of WBCs

  • They may also cause granule dependent cell-mediated apoptosis through the release of perforins, granzymes, and proteases.
  • Neutrophils defend against bacterial or fungal infection and other very small inflammatory processes.
  • They are also the predominant inflammatory cells in allergic reactions.
  • Mast cells function similarly to basophils in that they often mediate inflammation, but are more common and arise from a different hemopoeitic lineage.
  • T-lymphocytes participate in the cell-mediated immune response.

• Specific T-Cell Roles

  • The different categories of T cells are the basis for cell-mediated immune system activity.
  • Cytotoxic T cells recognize their antigen on pathogens through their T cell receptor, and will kill the pathogen through degranulation and cell-mediated apoptosis.
  • Through IL-10 - adenosine and other anti-inflammatory cytokines secreted by regulatory T cells - the CD8+ cells can be inactivated to an anergic state, which can prevent or reduce the severity of autoimmune diseases.
  • The secondary immune response mediated by memory T cells is much faster and more effective at eliminating pathogens compared to the initial immune response.
  • There is an association between NKT cell deficiency and development of autoimmune diseases, or chronic inflammatory diseases like asthma, however the exact mechanism of this association is not fully understood.

• Abscesses and Ulcers

  • The cytokines trigger an inflammatory response, which draws large numbers of white blood cells to the area and increases the regional blood flow.
  • Many researchers view the causes of aphthous ulcers as a common end product of many different disease processes, each of which is mediated by the immune system.