Inflammation Research Paper

Inflammation is defined as the presence of edema fluid and the invasion of tissue by leukocytes. Inflammation is characterized by heat, redness, pain, and swelling. These characteristics are the result of the release of various chemical mediators during an immune response. Cytokines and other inflammatory mediators act on local blood vessels causing dilation of blood vessels and an increase in vascular permeability. Blood flow is increased and there is an increase in the leakage of fluid and proteins from blood vessels into tissues. This increase in blood flow and vascular permeability is produced so that immune cells can leave blood vessels, enter blood cells and fight infection.
During the innate immune response, pathogen-associated molecular patterns(PAMP) that are parts of invading
Upon pathogen recognition, macrophages will proceed to phagocytose the bacteria and release chemokines and cytokines. Cytokines act on blood vessels causing dilation and increase in vascular permeability. Cytokines also act on vascular endothelium, causing endothelial cells to express adhesion molecules. The action of cytokines on blood vessels and endothelial cells helps immune cells to leave the blood vessels and enter the infected tissue. Chemokines released by macrophages attract cells which have chemokine receptors such as neutrophils and monocytes. Neutrophils and monocytes may also be recruited by C3a and C5a which are generated through the complement system when a pathogen is encountered by complement protein. Apart from serving as chemo-attractant, C5a can also activate phospholipase A2 in neutrophils. This ultimately leads to the production of prostanoids such as PGE2, which potentiate the effects of histamine and bradykinin.