inflammation Flashcards
What are the four main signs of acute inflammation?
Colour
heat
pain
swelling
four factors of inflammation being a universal process
immunity and infection
genetic
cell biology
hameatology
What is inflammation
a rapid non specific response to cellular injury
what three things occur during acute inflammation
change in blood flow
structural changes in the microvasculature (capillaries, venules and arterioles)
recruitment/accumulation of immune cells and proteins
what cells are typically found in the interstitium?
mast cells
macrophages
what cells are typically found in the vascular endothelium?
.leukocytes
.neutrophils
inflammatory signals results in …
. non apoptotic cell death
.detection of foreign material
what are the 2 vasodilators released during infection?
histamine
Nitric oxide
what vascular changes are observed during inflammation?
Increased permeability
. dilation
.reduced flow
.plasma leakage
Give 3 sources of histamines
source: Mast cells, basophils, platelets
Give 2 sources of prostaglandins
mast cells, leukocytes
Give three sources of cytokines (TNF, IL-1)
.Macrophages
.endothelial cells
mast cells
give two sources of chemokines
leukocytes
activated macrophages
Give a source of Complement. (C5a, C3a, C4a)
plasma
what does histamine do?
Vasodilation, increased vascular permeability, endothelial activation
actions of prostaglandins
vasodilation, pain, fever
action of cytokines
endothelial activation, fever
action of chemokines
chemotaxis, leukocyte activation
action of Complement (C5a, C3a, C4a)
LEUKOCYTE chemotaxis and activation, vasodilation, Oponisation (attach opsins for phagocytosis)
what is exudate
Fluid, proteins and cells that have seeped out of a blood vessel
Give an example of immune cell recruitment
Chemokine: CXCL8 otherwise known as IL-8
Receptors: CXCR1 and CXCR2, g-coupled 7-transmembrane proteins
Cell type: Neutrophils. Often the first cell type recruited to the site of inflammation
what are the four stages of neutrophile extravasition
1) Chemo attraction, cytokines lead to endothelial upregulation of adhesion molecules e.g selectin
2) rolling adhesion: carbohydrate low affinity ligand binds e.g PSGL binds P and E selectin
3) Tight adhesion: Chemokines promote higfh affinity switch in integrins e.g ICAM 1/2
4) TRANSMIGRATIO- cytoskeletal rearranges and pseudopodia occurs ( temp entension of cytoplasm)- mediated BY PECAM.
how to neutrophils work at sight of infection
. use of TLR4 and CD14 to identify lipopolysaccharides (LPS) present in gram-negative bacteria
Pathogen clearance via phagocytosis+netosis
.Cytokine secretion: recruit and activates other immune cells
Phagocytosis
Large particles engulfed into membrane bound vesicles (phagosomes)
Phagosome fuses with lysosome (vesicles containing enzymes e.g. elastase and lysozyme) -> phagolysosome
Ractive oxygen species (ROS) – phagocyte NADPH oxidase
Antimicrobial peptides – e.g. defensins.
define antigen
A molecule or molecular structure that can be recognised by an antibody
any substance to which your immune system can mount an antibody or adaptive immune response
what are the 4 types of antigen
Antigen types:
Foreign antigen: an antigen derived from molecules not found in the body
Self antigen: an antigen derived from molecules produced by our bodies
Immunogen: an antigen independently capable of driving an immune response in the absence of additional substances
Hapten: a small molecule that alone does not act as an antigen but when bound to a larger molecule can create an antigen
give some chronic diseseases
Asthma Hepatisis Inflammatory bowel disease Multiple sclerosis Rheumatoid arthritis Glomerulonephritis Psoriasis
give some dieases assoicated with granulomatous inflammation
Examples: Tuburculosis Leprosy Foreign body granuloma Tumor reactions Sarcoidosis Crohns disease ( a specific type of IBD)
chronic inflammation charactersitics:
. perisistent infection e.g hep B/c
unclearable particulates
autoimmunity
positives of macrophages
Phagocytic
cytotoxic
anti-inflammatory (e.g IL-10, TGF-beta)
Wound repair
Negatives of macrophages
cytotoxic
inflammatory
pro-fibrotic
T cells in inflammation:
.pro inflammatory e.g TNF, IFN-gamma)
Cytotoxic e.g granzymes, perforin
regulatory e.g TNF-beta
differences between acute and chronic inflammation
Acute: Immediate vasodilation neutrophils histamine release prominent necrosis complete resolution or progresses to chronic
Chronic: Delayed onset persistent inflammation Monocytes/macrophages cytokine release prominent scarring scarring/loss of function of tissues occurs
What are 3 advantages to acute and chronic inflammation?
. Clear inflammatory agent
.removes damaged cells
.restores normal tissue function
What are three negatives to chronic/acute inflammation
.Excess tissue damage
.scarring
.loss of organ function leading to organ failure
What causes scarring and excess tissue damage
excessive extracellular matrix deposition
give a consequence of inflammation
Bronco-pneumonia
