Unit 4 - Immune System PART F & G Flashcards
Innate Immunity – Inflammation
Inflammation is hallmark reaction of the innate immune response.
Functions of inflammation:
- ATTRACTING IMMUNE CELLS AND CHEMICAL MEDIATORS to the site
- PRODUCING a PHYSICAL BARRIER to SLOW DOWN the SPREAD of infections
- PROMOTING TISSUE REPAIR once the infection is under control
(function in fighting infection in damaged tissue)
4 Signs of inflammation:
- Redness (rubor)
- Heat (calor)
- Swelling (tumor)
- Pain (dolor)
All created when activated immune cells release cytokines
- these cytokines attract add. immune cells, increase capillary permeability, & cause fever
Innate Immunity – Inflammation
Requires:
Requires RECOGNITION OF BACTERIA by local macrophages, neutrophils, mast cells
- All have Toll-like Receptors (TLRs) capable of detecting bacterial cell wall components, lipopolysaccharide, flagella, etc.
Toll-like Receptors (TLRs)
capable of detecting bacterial cell wall components, lipopolysaccharide, flagella, etc.
Innate Immunity – Inflammation
Steps:
- Pathogen crosses physical barrier and enters body tissue
- Complement system is activated
a. activation of phagocytosis (C3b as opsonin, flags microbe for phagocytosis)
b. Activation of mast cells
c. Production of membrane attack complex
d. Some complement proteins are chemotaxins - Phagocytosis of microbe by RESIDENT MACROPHAGES
a. Macrophages release cytokines such as INTERLEUKIN 1 (IL-1) and TUMOR NECROSIS FACTOR-α (TNF- α) - several functions:
1) cause blood vessel endothelial cells to express adhesion molecules (e..g. SELECTINS), that help leukocytes to emigrate from blood vessels;
2) Stimulate liver to produce ACUTE PHASE PROTEINS (some are opsonins)
3) Both also act as endogenous pyrogens and cause fever (higher temp increases macrophage activity)
b. Macrophages release INTERLEUKIN 8 (IL-8), a cytokine that acts as a chemotaxin (it is also known as neutrophil chemotactic factor). It is recognized by the IL-8 receptor on neutrophils and helps attracts them to the infected area. - Mast cells release Histamine (among other proinflammatory
cytokines including bradykinin, IL-1, etc.)
a. A potent vasodilator that causes localized vasodilation – increase of amount of blood present causes redness and head (rubor and calor)
b. Increases capillary permeability – so much so that plasma proteins can leave blood and enter ISF, which increases the colloid osmotic pressure of the ISF (πI.). Fluid moves into the ISF causing the are to swell = localized edema. - Pain is caused by local distension within the swollen tissue.
a. Swelling can cause loss of function.
b. Locally produced cytokines (e.g. BRADYKININ) stimulate pain
receptors. - Leukocytes emigrate from blood vessels into tissue
(chemotaxis). Neutrophils come first (within 1 hour,
attracted by chemotaxins). Blood monocytes follow
and mature into macrophages over 8-12 hours.
a. Steps of emigration:
i. Margination
ii. Rolling
iii. Diapedesisiv.
Migration - Phagocytosis by neutrophils (& recruited macrophages)
- Neutrophil elimination
a. Phagocytosis of used neutrophils (once they have ingested 5-20 microbes,
they no longer work). - Macrophages
a. Recruited and resident macrophages activated via Toll-like receptors, or opsonization by antibodies or complement proteins , continue eating
b. Antigen presentation to Helper T cell occurs (link to Adaptive Immunity) - Local inflammatory response acts to separate infected tissue from
healthy tissue so that infection cannot spread.
- Complement system is activated
a. activation of phagocytosis (C3b as opsonin, flags microbe for phagocytosis)
b. Activation of mast cells
c. Production of membrane attack complex
d. Some complement proteins are chemotaxins
- Phagocytosis of microbe by RESIDENT MACROPHAGES
a. Macrophages release cytokines such as INTERLEUKIN 1 (IL-1) and TUMOR
NECROSIS FACTOR-α (TNF- α) - several functions:
1) cause blood vessel
endothelial cells to express adhesion molecules (e..g. SELECTINS), that
help leukocytes to emigrate from blood vessels;
2) Stimulate liver to produce ACUTE PHASE PROTEINS (some are opsonins)
3) Both also act as endogenous pyrogens and cause fever (higher temp increases macrophage activity)
b. Macrophages release INTERLEUKIN 8 (IL-8), a cytokine that acts as a chemotaxin (it is also known as neutrophil chemotactic factor). It is recognized by the IL-8 receptor on neutrophils and helps attracts them to the infected area.
- Mast cells release Histamine (among other proinflammatory cytokines including bradykinin, IL-1, etc.)
a. A potent vasodilator that causes localized vasodilation – increase of amount of blood present causes redness and head (rubor and calor)
b. Increases capillary permeability – so much so that plasma proteins can leave blood and enter ISF, which increases the colloid osmotic pressure of the ISF (πI.). Fluid moves into the ISF causing the are to swell = localized edema.
- Pain is caused by local distension within the swollen tissue.
a. Swelling can cause loss of function.
b. Locally produced cytokines (e.g. BRADYKININ) stimulate pain receptors.
- Leukocytes emigrate from blood vessels into tissue
(chemotaxis). Neutrophils come first (within 1 hour,
attracted by chemotaxins). Blood monocytes follow
and mature into macrophages over 8-12 hours.
a. Steps of emigration:
i. MARGINATION – Neutrophils and Monocytes stick to
endothelium of blood vessel
ii. ROLLING – SELECTINS indicate to neutrophils and
monocytes to slow down and “roll” along the
interior of the vessel.
iii. DIAPEDESIS – neutrophils and monocytes leave the
blood vessel using amoeba-like movement
(squeeze themselves out through spaces between
endothelial cells).
iv. MIGRATION – newly recruited phagocytes move
through the tissue toward the injury site
- Neutrophil elimination
a. Phagocytosis of used neutrophils (once they have ingested 5-20 microbes, they no longer work).
- Macrophages
a. Recruited and resident macrophages activated via Toll-like receptors, or opsonization by antibodies or complement proteins , continue eating
b. Antigen presentation to Helper T cell occurs (link to Adaptive Immunity)
Innate Immunity is the…
First line of defense, acts within minutes, lasts for hours.
Innate Immunity occurs…
Occurs INDEPENDENTLY of antibody presence (although some antibodies can help mediate the process if present)
