Close
In basic terms, what is inflammation?
The changes in blood vessels and blood flow as a result of inflammation give rise to...?
Give a very brief overview of the inflammatory response, moving from the innate to the acquired aspects.
What are PAMPs?
What are DAMPs?
Where are DAMPs found?
How might loss of function develop in inflammation? How might this lead to amputation of tissue/a limb?
Soluble mediators of inflammation are released by damaged tissues and immune cells to recruit cells to the inflammatory response in order to fight infection and/or initiate healing of tissue damage. Which cytokines are released by macrophages? And which chemokine? Which complement proteins are activated directly by PAMPs with or without antibody? Which other vasodilating soluble mediators are involved?
Which soluble mediators do the auxillary cells (basophils, mast cells, and platelets) release?
What are the primary effects of soluble mediators of inflammation?
The vascular changes at the beginning of the inflammatory response include blood vessel wall activation and increased permeability. Describe this in more detail.
Which are the first leukocytes to be recruited in an inflammatory response?
True or false: cell recruitment is enhanced by activation of tissue macrophages near small blood vessels?
Are neutrophils antigen-presenting cells?
Natural killer cells and eosinophils are both cytotoxic - but to which organisms/cells?
Sometimes when there should be inflammation, it is absent, and there is a lack of resolution. List three situations in which this occurs.
Absence of inflammation causes pathology, but so does excess inflammation. What is the most common disease caused by excess inflammation? What is the most fatal disease caused by excess inflammation?
Which cells and soluble mediators is inflammation controlled by to avoid excess inflammation?
How soon after tissue injury is there an increase in vascular diameter (vasodilation) resulting in a rise in blood volume in the area?
How soon after tissue injury to leukocytes adhere to vascular endothelium in order to extravasate into the damaged tissue?
Can the N-formyl bacterial peptides act as chemoattractants?
Before adhesins are expressed on the endothelial wall and integrins are expressed on the neutrophil membrane in order to strongly tether the leukocyte to the vascular endothelium and facilitate extravasation, which glycoproteins are expressed on the vascular endothelium and neutrophils which allow them to form weak interactions which are easily broken by blood flow force?
Other than holding bodily cells together and allowing leukocytes to extravasate, what other (immune) function do cell adhesion molecules (CAMs) have?
What is leukocyte adhesion deficiency (LAD)?
