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R&C; Chapter 2: Acute and Chronic Inflammation
Terms in this set (189)
What are the 3 major components of acute inflammation?
1. alterations in vascular caliber that lead to an increase in blood flow
2. structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation
3. emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
What are 5 general ways that acute inflammatory reactions may be triggered?
2. tissue necrosis
4. foreign bodies
5. immune reactions
How does hypoxia induce inflammation?
HIF-1a made by cells deprived of O2--> many genes involved in inflammation induced (including VEGF--> increased vascular permeability)
What is one of the earliest manifestations of acute inflammation?
What is the resulting change in vascular flow after vasodilation?
increased blood flow
What are the 2 main mediators responsible for vasodilation in acute inflammation?
Vasodilation---> ______---> ________-->______
vasodilaton--> increased permeability--> stasis/vascular congestion---> margination of leuks
What are the mechanisms responsible for increased vascular permeability in acute inflammation?
- contraction of endothelial cells
- endothelial injury--> endothelial cell necrosis and detachment
- leukocyte-mediated vascular injury
- increased transcytosis
What are 4 examples of mediators that cause contraction of endothelial cells during vascular leakage in acute inflammation?
histamine, bradykinin, LTs, substance P
Is retraction of endothelial cells typically short or long-lived?
Leukocyte-mediated vascular injury is short/long-lived and lasts minutes/hours.
Increased transcytosis in increased vascular permeability in acute inflammation is induced by ___.
What are the steps in leukocyte migration through the blood vessels?
Margination, rolling, stable adhesion, migration through endothelium
Initial rolling interactions in leukocyte migration is mediated by _____.
What are the 3 types of selectins and which cells express them?
P-selectin-- platelets and endothelium
What are the leukocyte ligands for P and E selectin?
Sialyl-Lewis C-modified proteins
What are the endothelial ligands for leukocyte L-selectin?
What are the leukocyte ligands for endothelial cell ICAM-1?
CD11/CD18 integrins (LFA-1, Mac-1)
What is the leukocyte ligand for endothelial cell VCAM-1?
What are the cytokines that trigger expression of adhesion molecules in endothelial cells near sites of infection?
TNF and IL-1
Firm adhesion of leukocytes to endothelial cells is mediated by _____.
What cytokines induce endothelial expression of ligands for integrins VCAM-1 and ICAM-1?
TNF and IL-1
What is responsible for the transformation of low-affinity state leukocyte integrins to high affinity state and activation of rolling leukocytes?
Chemokines from site of infection bind endothelial cell proteoglycans and are displayed on the endothelial surface where they bind and activate rolling leukocytes-- now VLA-4 and LFA-1 integrins on leukocytes are in a high-affinity state
What mediators are responsible for causing redistribution of P-selectin from intracellular stores to the cell surface?
histamine, thrombin, PAF
What adhesion molecule is present between endothelial cells and involved in migration of leukocytes?
PECAM-1 (interacts with itself between leukocytes and endothelial cells)
In the connective tissue, the luekocytes are able to adhere to the ECM by ____ and ___ binding to matrix proteins.
CD44 and integrins
LAD-1 is a defect in the biosynthesis of ____. LAD-2 is a is caused by absence of ___ as a result of a defect in ______.
LAD-1 is a defect in the biosynthesis of the B2 chain shared by LFA-1 and Mac-1 integrins. LAD-2 is a is caused by absence of sialyl-Lewis X (contains fucose) as a result of a defect in fucosyl transferase (attaches fucose to protein backbones).
What are the 3 main chemoattractants?
1. cytokines (esp IL-8)
2. complement proteins (esp C5a)
3. AA metabolites (esp LTB4)
What happens in leukocytes when chemoattractants bind their G-protein coupled receptors?
signals initiate second mesesengers--> increased cytosolic Ca--> activation of Rac/Rho/cdc42 family and kinases--> polymerization of actin at front of cell--> filapodia form
Neutrophils predominate in acute inflammation during the first __ to ___ and are replaced by monocytes in ___ to ____.
What are the 2 things that need to happen once leukocytes arrive at the site of inflammation?
1. recognize the offending agent so they can send signals to
2. activate leukocytes to ingest and destroy the offending agent and amplify the inflammatory response
What are 4 types of receptors that leukocytes express that can recognize external stimuli and deliver activating signals?
1. TLRs- see microbial products
2. G-protein coupled receptors-- can see bacterial proteins (N-formyl-methionyl peptides) or chemokines, C5a, lipid mediators (PAF, PGs, LTs)
3. Opsonin receptors (ex FcyRI and complement receptors)- see IgG, C3, or plasma lectins
4. Cytokine receptors- see IFN-y secreted by NK cells and activated Ts
What is the major macrophage activating enzyme made by NK cells or activated Ts?
What receptor is present on phagocytes that recognize IgG coated particles?
What receptor is present on phagocytes that recognizes breakdown products of C3 on opsonized particles?
type 1 complement receptor (CR1)
What happens after leukocytes see antigen at site of inflammation?
They are activated by signaling pathways and there is an increase in cytosolic Ca which activates enzymes like protein kinase C and PLA2--> phagocytosis and intracellular killing
What are the 3 steps in phagocytosis?
1. recognition and attachment
What 4 receptors on phagocytes function to bind and ingest microbes?
1. mannose receptors
2. scavenger receptors
3. receptors for various opsonins (IgG, C3b, and lectin)
4. Mac-1 macrophage integrin may
What do scavenger receptors on phagocytes bind?
microbes and modified LDL particles
What are the 2 major functional outcomes of G-protein coupled receptor activation on leukocytes?
1. Increased integrin avidity--> adhesion to endothelium
2. Chemotaxis--> migration into tissues
What is the major functional outcomes of TLR activation on leukocytes?
Amplification of the inflammatory reaction and killing of microbes
What is the major functional outcomes of phagocytic receptor activation on leukocytes?
killing of microbes
The generation of ROS is due to assembly of the _____ which _____ and in the process, reduces ___ to ____.
The generation of ROS is due to assembly of the NADPH oxidase which oxidizes NADPH and in the process, reduces oxygen to superoxide anion.
Superoxide anion, generated by the ____ is converted to ___ by ____. ____ converts this to ____ which destroys microbes by halogenation.
Superoxide anion, generated by the NADPH oxidase is converted to H2O2 by spontaneous dismutation. MPO converts this to hypochlorite which destroys microbes by halogenation.
Describe the H2O2-MPO-halide system for killing bacteria in lysosomes.
Superoxide anion, generated by the NADPH oxidase is converted to H2O2 by spontaneous dismutation. MPO converts this to hypochlorite which destroys microbes by halogenation (requires a halide like Cl-)
NO, made from ____ by the action of ____ reacts with ____ to generate highly reactive free radical ____.
NO, made from arginine by the action of nitric oxide synthase reacts with superoxide to generate highly reactive free radical ONOO.
What are examples of neutrophil granules that help kill microbes and what are their mechanisms of action?
Lysozyme- hydrolyzes the muramic acid-N-acetylglucosamine bone in the coat of all bacteria
Lactoferrin- iron-binding protein
MBP- cytotoxic to many parasites
bactericidal/permeability increasing protein- binds endotoxin
Classically activated macrophages respond to what 2 things?
Microbial products (TLR-ligands)
IFN-y (secreted by T cells)
What are the 2 outcomes of classically activated macrophages?
Microbicidal actions (phagocytosis and killing)
What are the substances secreted by classically activated macrophages that are responsible for the microbicidal actions?
ROS, NO, and lysosomal enzymes
What are the substances secreted by classically activated macrophages that are responsible for pathologic inflammation?
IL-1, IL-12, IL-23, chemokines
Alternatively activated macrophages respond to what 2 cytokines?
IL-13 and IL-4 (secreted by Th2 cells)
What cells are responsible for the secretion of cytokines that activate alternatively activated macrophages?
What are the 2 outcomes of alternatively activated macrophages?
Wound repair and fibrosis
What are the substances secreted by alternatively activated macrophages that are responsible for the anti-inflammatory effects?
IL-10 and TGF-B
What are the substances secreted by alternatively activated macrophages that are responsible for wound repair and fibrosis?
arginase, proline polyaminases, TGF-B
What is an example of an inherited defect in phagolysosome function?
What is an example is inherited defects in microbicidal activity and what is its mechanism?
Chronic granulomatous disease-- inherited defects in the genes encoding components of phagocyte oxidase which generates superoxide anion-- the neutrophils response is deficient so macs try to make up for it
What are 4 active termination mechanisms of acute inflammation?
1. switch from production of pro-inflammatory LTs to anti-inflammatory lipoxins
2. release of anti-inflammatory cytokines TGF-B and IL-10
3. Production of anti-inflammatory lipid mediators resolvins and protectins
4. cholinergic impulses that inhibit TNF production in macs
What are the principal cell-derived mediators of acute inflammation (9)?
Cytokines (TNF, IL-1)
What are the principal plasma protein-derived mediators of inflammation?
Proteases activated during coagulation
What are the main actions of histamine in acute inflammation (3)?
Vasodilation, increased vascular permeability, endothelial activation
What are the main actions of serotonin in acute inflammation (2)?
Vasodilation, increased vascular permeability
What are the main actions of PGs in acute inflammation (3)?
Vasodilatin, pain, fever
What are the main actions of LTs in acute inflammation (3)?
Increased vascular permeability, chemotaxis, leukocyte adhesion and activation
What are the main actions of PAF in acute inflammation (6)?
Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst
What are the main actions of ROS in acute inflammation (2)?
Killing of microbes, tissue damage
What are the main actions of NO in acute inflammation (2)?
Vascular smooth muscle relaxation, killing of microbes
What are the main actions of cytokines in acute inflammation (6)?
Local endothelial activation (expression of adhesion molecules), fever, pain, anorexia, hypotension, decreased vascular resistance (shock)
What are the main actions of chemokines in acute inflammation (2)?
chemotaxis, leukocyte activation
What are the main actions of complement products in acute inflammation (2)?
Leukocyte chemotaxis and activation, vasodilation (mast cell stimulation)
What are the main actions of kinins in acute inflammation?
Increased vascular permeability, smooth muscle contraction, pain (also bronchoconstriction, starts the AA cascade)
What are the main actions of proteases activated during coagulation in acute inflammation (2)?
Endothelial activation, leukocyte recruitment
Which of the mediators of inflammation are responsible for fever?
prostaglandins, cytokines TNF and IL-1
Which of the mediators of inflammation are responsible for pain?
prostaglandins, cytokines TNF and IL-1, kinins
What 6 things can cause mast cell degranulation?
1. physical injury (cold, hot, trauma)
2. binding of antibodies to mast cells
4. histamine- releasing proteins from LTs
5. neuropeptides like substance P
6. cytokines (IL-8 and IL-1)
Histamine causes dilation/constriction of arterioles and increases/decreases the permeability of vessels.
Release of serotonin and histamine from platelets is stimulated when?
When platelets aggregate after contact with collagen, thrombin, ADP, and antigen-ab complexes
How does platelet release in clotting cause increased vascular permeability, therefore linking clotting and inflammation?
When platelets aggregate after contact with collagen, thrombin, ADP, and antigen-ab complexes, serotonin and histamine are released--> increased vascular permeability
What cell is rich in serotonin storage?
Are histamine and serotonin preformed or do they need to be synthesized after mast cell activation?
How is AA stored in the cell?
esterified in the membrane phospholipids
How does AA get released from the cell membrane?
What kind of cells make PGs?
mast cells, macrophages, endothelial cells, etc
AA----(COX)---> ____ ---> ____----> ____, ____, ___, and ____
AA----(COX)---> PGG2 ---> PGH2----> PGI2, TXA2, PGD2, and PGE2
What are PGI2's effects on vessels and platelets?
Causes vasodilation and inhibits platelet aggregation
Is PGI2 pro or anti-coagulant?
anti (inhibits platelet aggregation)
What are TXA2's effects on vessels and platelets?
Causes vasconstriction, promotes platelet aggregation
Is TXA2 pro or anti coagulant?
pro (promotes platelet aggregation)
What are PGD2 and PGE2's effects on vessels?
vasodilation and increased vascular permeability
Is PGI2 a vasodilator or vasoconstrictor?
Is TXA2 a vasodilator or vasoconstrictor?
AA--(5-lipoxygenase)-->____---(12-lipoxygenase)-->____ and _____
AA--(5-lipoxygenase)-->HPETE---(12-lipoxygenase)-->LXA4 and LXB4
Which enzyme leads to the production of lipoxins in the AA pathway?
What are the main roles of lipoxins in inflammation?
inhibit neutrophil adhesion and chemotaxis
What are the main effects of LTC4, LTD4 and LTE4 in inflammation? (3)
Vasoconstriction, bronchospasm, and increased vascular permeability
What is the main effect of LTB4 in inflammation?
Which AA metabolites are vasoconstrictors?
LTC4, LTD4, LTE4
Which AA metabolites are vasodilators?
PGI2, PGD2, PGE1&2
Which AA metabolites cause bronchospasm?
LTC4, LTD4, LTE4
Which AA metabolites cause increased vascular permeability?
PGD2, PGE2, LTC4, LTD4, LTE4
Steroids inhibit which part of the AA pathway?
The phospholipases that cleave AA from cell membrane phospholipids
Which cells have a lot of thromboxane synthetase and therefore make a lot of TXA2?
Which cells have a lot of prostacyclin synthetase and therefore make a lot of PGI2?
What is the major PG made by mast cells?
What is responsible for cytokine-induced fever during infections?
Which 2 AA mediators are chemoattractants for neutrophils?
PGD2 and HPETE
Which are more potent in increasing vascular permeability and causing bronchospasm, LTs or histamine?
Which leukocyte is a primary producer of intermediate lipoxins and which cell converts them to lipoxins?
LOX inhibitors are useful in the treatment of what clinical condition?
In addition to platelet aggregation, PAF causes vasodilation/vasconstriction and bronchodilation/bronchoconstriction, and at extremely low concentrations it induces vasodilation/vasoconstriction and increased/decreased venular permeability with a potency 100 to 10,000 times greater than that of _____.
In addition to platelet aggregation, PAF causes vasconstriction and bronchoconstriction, and at extremely low concentrations it induces vasodilation and increased venular permeability with a potency 100 to 10,000 times greater than that of histamine.
How does secretion of ROS amplify the inflammatory response?
release of low levels can increase expression of chemokines (IL-8), cytokines, and endothelial leukocyte adhesion molecules.
What are 3 sequelae to extracellular release of ROS?
1. endothelial damage, with resultant increased vascular permeability
2. injury to other cell types
3. inactivation of antiproteases
What are the 5 major antioxidant mechanisms used to protect against harmful ROS?
1. superoxide dismutase
3. glutathione peroxidase
What ROS does catalase detoxify?
Is the half-life of NO long or short?
Only seconds (it's a gas)
What are the 3 different types of NOS and which are constituitively expressed and which are expressed after macrophages and other cells are activated by cytokines or microbial products?
eNOS and nNOS constituitively expressed
What are the dual actions of NO in inflammation?
1. relaxes vascular smooth muscle and promotes vasodilation
2. inhibitor of the cellular component of the inflammatory response
How does NO inhibit the cellular component of the inflammatory response?
it reduces platelet aggregation and adhesion, inhibits features of mast cell-induced inflammation, and inhibits leukocyte recruitment
Which ROS is an endogenous mechanism for controlling inflammation?
TNF and IL-1 are made mainly by activated _____.
macrophages (but also made by mast cells and T lymphs)
What are the principal actions of TNF in acute inflammation?
stimulate expression of endothelial adhesion molecules and secretion of other cytokines, chemokines, GFs, eicosanoids, and NO, augments neut response to endotoxin
What are the principal actions of IL-1 in acute inflammation?
similar to TNF-- greater role in fever
What are the principal actions of IL-6 in acute inflammation?
What component of the cell is in control of IL-1?
What are the principal actions of IL-12 in chronic inflammation?
increased production of IFN-y
What are the principal actions of IFN-y in chronic inflammation?
activation of macrophages (can kill better)
What are the principal actions of IL-17 in chronic inflammation?
recruitment of neutrophils and monocytes
C-X-C chemokines attract primarily ____ and ___ is the prototype in this category. It is secreted by ____, ___ and other cells. It is induced mainly by ____ and other cytokines like ___ and ____.
C-X-C chemokines attract primarily neutrophils and IL-8 is the prototype in this category. It is secreted by macrophages, endothelial cells and other cells. It is induced mainly by microbial products and other cytokines like IL-1 and TNF.
C-C chemokines attract primarily ____, ___, ___, and ___ (NOT ____) and examples of C-C chemokines include ____, ___, ____, and ____.
C-C chemokines attract primarily monocytes, eosinophils, basophils, and lymphocytes (NOT neutrophils) and examples of C-C chemokines include eotaxin, MCP-1, RANTES, and MIP-1a.
C chemokines include _____ and attract ____.
CX3C chemokines include ___ as the only member and attracts ____ and ____.
monocytes and lymphocytes
Which chemokine family has both a endothelial cell induced and soluble form?
What are the systemic manifestations of TNF and IL-1 during inflammation?
fever, leukocytosis, increase acute-phase proteins, decreased appetite, increased sleep
What are the local effects of TNF/IL-1 on fibroblasts?
increased collagen synthesis
What are the local effects of TNF/IL-1 on leukocytes which lead to inflammation?
production of cytokines
What are the local effects of TNF/IL-1 on vascular endothelium which lead to inflammation?
increased expression of leukocyte adhesion molecules
production of IL-1 and chemokines
increased procoagulant and decreased anticoagulant activity
What are the 2 main functions of chemokines?
1. stimulate leukocyte recruitment in inflammation
2. control the normal migration of cells through various tissues
What do neutrophil specific/secondary granules contain?
lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and ALP
What do neutrophil azuophil/primary granules contain?
MPO, lysozyme, defensins, acid hydrolases, elastase, cathepsin G, nonspecific collagenases, proteinase 3
What keeps the destructive effects of lysosomal enzymes in check in serum and tissues?
antiproteases like a1-antitrypsin and a2-macroglobulin
What neuropeptides are released by sensory nerves and leukocytes that help transmit pain signals, regulate blood pressure, stimulate secretions from endocrine cells and increase vascular permeability?
substance P and neurokinin A
What is the critical step in complement activation? (going from circulating inactive complement to active)
proteolysis of C3
All 3 pathways of complement activation result in activation of _____ which cleaves ___.
C3 convertase, C3
The classical pathway of complement activation is triggered by fixation of ___ to ___ that has combined with the antigen.
fixation of C1 to antibody (IgM or IgG)
The alternative pathway of complement activation is triggered by ______, ____, ____, etc. It does not involve ____.
triggered by microbial surface molecules (endotoxin, LPS), complex polysaccharides, cobra venom. It does not involve antibodies.
In the lectin pathway of complement activation, _____ binds to _____ on microbes and directly activates ____.
mannose-binding lectin binds carbohydrates on microbes and directly activates C1
When C3 and C5 are split, C3__ and C5__ float away, and C3___ and C5__ stay stuck to cell/molecule.
When C3 and C5 are split, C3a and C5a float away, and C3b and C5b stay stuck to cell/molecule.
Which complement molecules make the MAC?
C5b binds C6-9 and then lots of C9 form a polymerized tube
What are the 3 biologic functions of the complement system?
3. cell lysis
How is complement involved in inflammation?
C3a, C5a and C4a stimulate histamine release from mast cells which increase vascular permeability and cause vasodilation
C5a chemotactic for neuts, monos, basos, and eos
C5a activates LOX path of AA metabolism
How is complement involved in phagocytosis?
C3b opsonizes to promote phagocytosis
What are the anaphylatoxins?
C5a and C3a
What 2 enzymes can cleave C3 and C5 at sites of inflammation, leading to a self-perpetuating cycle?
plasmin and lysosomal enzymes released from neuts
How is coagulation connected to inflammation?
Thrombin promotes inflammation by engaging PARs--> mobilization of P-selectin, production of chemo/cytokines, expression of adhesion molecules, induction of COX2 and PG production, production of PAF and NO, and change in endo shape
Kinins are vasoactive peptides made from ____ by the action of proteases called _____.
Kinins are vasoactive peptides made from kininogens by the action of proteases called kallikreins.
How are the kinin and coagulation systems connected?
XIIa converts prekallikrein to kallikrein which cleaves HMWK to bradykinin
Kallikrein activates XIIa (amplification of original stimulus)
What are the effects of bradykinin?
increase in vascular permeability, contraction of smooth muscle, dilation of blood vessels, and pain on injection (also bronchoconstriction, starts the AA pathway, and hypotension)
Bradykinin and ____ have similar effects.
What inactivates bradykinin?
kininase mainly, some by ACE in lungs
How is kallikrein involved in the fibrinolytic system?
It cleaves plasminogen to make plasmin
Is kallikrein pro or anti thrombotic?
anti (cleaves plasminogen to make plasmin which breaks up clots)
How is plasmin directly tied to the complement system?
during inflammation it cleaves C3 to its fragments and can activate factor 12 to start the cascade
What are the 3 ways that C3a and C5a can be generated?
1. immunologic reactions (classical pathway)
2. alternative and lectin pathways without antibody
3. plasmin, kallikrein and serum proteases
Activated factor 12 initiates which 4 systems in the inflammatory response?
1. kinin system
2. clotting system
3. fibrinolytic system
4. complement system
What are all of the mediators that cause vasodilation in acute inflammation?
What are all of the mediators that cause increased vascular permeability in acute inflammation?
Histamine and serotonin
C3a and C5a (activate mast cells)
LTs C4, D4, and E4
What are all of the mediators that cause chemotaxis, leukocyte recruitment and activation in acute inflammation?
What are all of the mediators that cause fever in acute inflammation?
What are all of the mediators that cause pain in acute inflammation?
What are all of the mediators that cause tissue damage in acute inflammation?
Lysosomal enzymes of leukocytes
What are the 3 outcomes of acute inflammation?
1. complete resolution
2. healing by connective tissue replacement (scarring or fibrosis)
3. progression into chronic inflammation
Describe serous inflammation.
Exudation of cell poor fluid in damaged areas or body cavities
Describe fibrinous inflammation.
Large molecules slip through with increased permeability happens when vascular leaks are large or there's a local procoagulant stimulus
Describe purulent inflammation.
neutrophils liquefied debris of necrotic cells, and edema fluid
What are the 3 main causes of chronic inflammation?
1. persistent infections
2. immune-mediated inflammatory diseases
3. prolonged exposure to potentially toxic agents
What are the morphologic features of chronic inflammation?
infiltration with mononuclear cells, tissue destruction, attempts at healing (angiogenesis and fibrosis)
What is the dominant cell in most chronic inflammatory responses?
How do macrophages play a dominant role in inflammation?
they secrete cytokines and GFs that destroy invaders and tissues, activate other cells, especially T lymphs
How do lymphocytes play a role in chronic inflammation?
TNF, IL-1 from macs calls in antigen-stimulated Ts and Bs--> CD4 Ths promote inflammation and influence the nature of the reaction by secreting cytokines--> amplification of initial response (Th1,Th2, Th17)
Th1--> make ___ which activates ___ macs
Th2--> make __, ___, ___ which call in ___ and activates ___ macs
Th17--> make ___ which call in ___ and ____
Th1--> make IFN-y which activates M1 macs
Th2--> make IL-4, IL-5, IL-13 which call in eos and activates M2 macs
Th17--> make IL-17 which call in neuts and monos
Which type of granuloma does not have a T cell component to it?
Foreign body granulomas
Describe immune mediated granulomas.
Persistent T cell response--> macs tell Ts to make cytokines like IL-2-->activates more Ts and IFN-y (activates more macs)
What are the mediators involved in the acute phase response?
TNF, IL-1, IL-6 mediate it, type 1 IFNs contribute
How does fever develop in the acute phase response?
bacterial products--> leuks make IL-1 and TNF--> increase COX enzymes--> AAs made into PGs-->PGE2 made in vascular/perivascular cells of hypothalamus stimulate NT production that resets the temperature
What are 4 important acute phase proteins?
C-reactive protein, fibrinogen, SAA, hepcidin
How does leukocytosis develop in the acute phase response?
TNF & IL-1 cause accelerated release out of BM
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