5: Inflammation Flashcards
Inflammation is
non-specific response to cellular injury
Inflammation clears
infectious material
toxins
dead or damaged cells
How does inflammation clear dead or damaged cells
Remove causative material
Resolve the issue
Repair damaged tissue
Cellular damage releases
damage associated molecular patterns (DAMPs)
+cytokines and chemokines
Cellular damage in case of infection releases
Pathogen associated molecular patterns (PAMPs)
Process of inflammation
DAMAGE - release of inflammatory triggers 1.(DAMPS / PAMPS) + chemokines/cytokines
2VASODILATORS RELEASED - nitric oxide + histamine
VASCULAR CHANGES
1.cause white cells to migrate to site
2.incr. amount of cells that arrive by affecting blood supply to site
clears trigger and resolution
3 Vascular changes of inflammation
Vasodilation - incr. blood flow, reduced speed of flow
Permeability - exudate
Loss of fluid from vessels - reduced speed of flow
= increased blood volume traveling through area at slower rate
Four cardinal signs of inflammation
Rubour - incr. amount of RBCs = redness
Calor - warm and metabolically active cells = heat
Tumor - fluid build up = swelling
Dolor - swelling presses on nerve endings, histamines and cytokines act on nerve endings
loss of function
Exudate
Fluid, proteins and cells that have seeped out of a blood vessel into tissue
- forms a barrier
Process of white cells leaving blood and entering tissue at site of inflammation
1) Chemo-attraction -‘glue’ placed to catch white cells
2) Rolling Adhesion - gentle sticking to blood vessel
3) Tight Adhesion - tight sticking to wall
4) Transmigration - goes through wall
Molecules used in white cell entrance to inflamed tissue
PECAM1
selectins
PSGL1
Once at site of inflammation, neutrophils have 3 functions
Recognise pathogen - receptors: TLR4, CD14
Remove pathogen - phagocytosis (elastase, lysozyme) , Netosis- neutrophils lay extracellular trap
Secrete cytokines - more neutrophils accumulate
(reactive oxygen species - O2 forms free radicals which kill cells,
Antimicrobial peptides secreted - if bacteria or microbe)
Process of resolution
Wound repair - macrophages, engulf any apoptotic cells, supress inflammation via anti-inflammatory mediators
Chronic inflammation
Occurs when stimulus/antigen is still present
continuous tissue destruction
continuous attempts to repair
adaptive immune cells
What arises as a result of chronic inflammation
Granulomas
- focal aggregate of immune cells
- form in response to a chronic/persistent inflammatory stimulus
-forms a barrier
3 cell types in chronic inflammation
Macrophages
Tcells
Bcells
Positives of Macrophages in chronic inflammation
Phagocytic
Cytotoxic
Anti-inflammatory
Wound repair (help build collagen matrix/ cause angiogenesis)
Negatives of macrophages in chronic inflammation
Indiscriminate what they target
Excessive ECM deposition
Positives of T cells in chronic inflammation
Specific
Guide other immune cells to site
3 types = range of functions
Positives of B cells in chronic inflammation
Generate specific antibodies
Clear infection
Local action or remote
Negatives of B cells in chronic inflammation
Can generate self antibodies leading to chronic inflammation
Acute inflammation
Resolves quickly
Minimal tissue damage
Neutrophils are main inflammatory cell
Mainly innate immunity
Chronic inflammation
Can last for months/years
Scarring and loss of tissue function
Monocytes and macrophages predominate
Adaptive immune cells recruited
Outcome of chronic inflammation
causes angiogenesis and fibrosis
Outcome of acute inflammation
pus formation and vasculature may need to be reformed
Antigens
molecule or molecular structure that can be recognised by an antibody
- any substance which your immune system can mount and antibody or adaptive immune response
4 types of antigens
Foreign antigen
Self antigen
Immunogen - causes immune response by itself
Hapten - needs to be processed before eliciting immune response
