495
edits
Changes
→Exocytosis
<p>Oxygen dependant killing requires the production of reactive oxygen atoms that damage bacterial membranes. These atoms are generated during a burst of respiration following phagocytosis where increased amounts of oxygen are produced. Hydrochloric acid is also produced during this process.</p>
<p>Oxygen dependant killing requires the production of reactive oxygen atoms that damage bacterial membranes. These atoms are generated during a burst of respiration following phagocytosis where increased amounts of oxygen are produced. Hydrochloric acid is also produced during this process.</p>
<p>Oxygen independent killing uses lysosomes, cathepsin (a protease) and other mechanisms. Lysozymes are particularly effective against gram positive bacteria as they hydrolyse the glycopeptide coating of the bacterial organisms.</p>
<p>Oxygen independent killing uses lysosomes, cathepsin (a protease) and other mechanisms. Lysozymes are particularly effective against gram positive bacteria as they hydrolyse the glycopeptide coating of the bacterial organisms.</p>
===Exocytosis===
====Exocytosis====
This is the process of granule fusion with the plasma membrane, causing the release of the granule contents into the immediate vicinity. Contents can include vasoactive peptides, for example, histamine and bradykinin which, as their name suggests, activate the endothelium. This causes the endothelium to become more "leaky" causing a great increase in extravasation of blood granulocytes and monocytes, and the diffusion of plasma proteins to the site of infection. These peptides, released from other cells as well as neutrophils (e.g. [[Mast cells|Mast cells]], are responsible for the classical signs of inflammation: redness (rubor), heat (calor), swelling (tumor), and pain (dolor), often accompanied by loss of function.
This is the process of granule fusion with the plasma membrane, causing the release of the granule contents into the immediate vicinity. Contents can include vasoactive peptides, for example, histamine and bradykinin which, as their name suggests, activate the endothelium. This causes the endothelium to become more "leaky" causing a great increase in extravasation of blood granulocytes and monocytes, and the diffusion of plasma proteins to the site of infection. These peptides, released from other cells as well as neutrophils (e.g. [[Mast cells|Mast cells]], are responsible for the classical signs of inflammation: redness (rubor), heat (calor), swelling (tumor), and pain (dolor), often accompanied by loss of function.
===Further amplification of inflammation===
===Further amplification of inflammation===
Neutrophils have many mechanisms to increase inflammation. These include [[Cytokines|cytokine]] release and exocytosis of vasoactive peptides as mentioned above. Neutrophil activation in an inflammatory lesion can also result in the release of prostaglandins, through synthesis by cyclo-oxygenase 2, which are responsible for vasoactive changes and for pain (N.B. These are reduced with cyclo-oxygenase (COX) inhibition for example with the NSAID (non-steriodal anti-inflammatory drugs)'s Aspirin and Ibuprofen).
Neutrophils have many mechanisms to increase inflammation. These include [[Cytokines|cytokine]] release and exocytosis of vasoactive peptides as mentioned above. Neutrophil activation in an inflammatory lesion can also result in the release of prostaglandins, through synthesis by cyclo-oxygenase 2, which are responsible for vasoactive changes and for pain (N.B. These are reduced with cyclo-oxygenase (COX) inhibition for example with the NSAID (non-steriodal anti-inflammatory drugs)'s Aspirin and Ibuprofen).