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Inflammation Flashcards

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1
Q

What is inflammation?

A

A complex response process triggered by infection, tissue injury or irritants enabling specific host cells and interacting chemicals (cytokines) to coordinate and attempt their neutralisation and removal

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2
Q

What is the difference between inflammation and swelling?

A

Swelling is an abnormal enlargement of a part of the body usually as a result of fluid accumulation
Inflammation and swelling are connected but not the same

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3
Q

What are the types of inflammation?

A

Acute
Chronic

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4
Q

Describe acute inflammation

A

Rapid onset (mins, hours)
Short duration (days)
Initiated by non-specific innate immune responses
Refined and prolonged by adaptive immune responses

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5
Q

Describe chronic inflammation

A

Slow or insidious onset
Long duration (weeks, months)
Initiated by inadequate acute inflammatory responsiveness or host susceptibility
Attempts to repair damaged tissue more likely to cause scarring/fibrosis

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6
Q

What is the outcome of acute inflammation?

A

Resolution
Fibrosis
Scarring
Persistence

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7
Q

What is the outcome of chronic inflammation?

A

Tissue destruction
Fibrosis
Scarring
Necrosis

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8
Q

Describe the course of acute inflammation

A

Non self antigens or damage signals trigger response
Immune cells and mediators are attracted and retained at the initiating site
Immune cells commit by differentiating and activating mechanisms able to kill pathogens, limit the spread of infection and further injury and protect damaged tissue from becoming infected
Infectious agents/dead cells/tissue are deconstructed
Conditions are created for tissue repair e.g. TGF-b

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9
Q

How are PAMPs and DAMPs involved in acute inflammation?

A

PAMPs/DAMPs are recognised by PRRs on cell surfaces initially involving resident macrophages
PRR activation triggers cell signalling pathways to secrete pro-inflammatory cytokines and type I IFNs

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10
Q

What type of inflammation do PAMPs cause?

A

Infectious

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11
Q

What type of inflammation do DAMPs cause?

A

Sterile

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12
Q

What causes releases of DAMPs?

A

Endogenous cell damage/stress

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13
Q

Describe recruitment in acute inflammation

A

Resident tissue macrophages and mast cells recognise pathogens and secrete cytokines and histamine
Cytokine activate integrins, capturing neutrophils attracted by chemotaxis which then migrate into tissue
Neutrophils capture bacteria then release more vascular permeability and monocyte recruitment mediators
Differentiated monocytes remove bacteria and release cytokines for further recruitment or repair

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14
Q

Describe the response stage of acute inflammation

A

Short lived neutrophils phagocytose pathogens
Cytokine release
Neutrophils expand and burst, sending out neutrophil extracellular traps (nets) to capture and immobilise other pathogens

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15
Q

Describe the removal and repair stages of acute inflammation

A

Monocytes initially differentiated into killing M1 convert to resolving M2 macrophage types
M1 has highly phagocytic activated killing and is able to clear the inflammation site
M2 secretes growth factors e.g. TGF-b for repair involving angiogenesis, fibroblast proliferation and collagen synthesis

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16
Q

Describe the course of chronic inflammation

A

Macrophage activation or direct innate encounters by other leukocytes of non-self antigens or host cell damage signals
Macrophages, neutrophils, T cells, eosinophils and mast cells are recruited
T cell activation feeds back directly to activate macrophages, both secrete pro-inflammatory cytokines and stimulate broader adaptive responses
Persistent pathogens or long term non-specific antigen exposure are not removed, prolonging the response
Tissue repair signalling is compromised (may form granulomas) and can lead to tissue destruction. Cell proliferation needs specialised regulatory cells to resolve

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17
Q

What are the triggers of chronic inflammation?

A

Failure to activate or resolve acute inflammatory reaction - persistent infections (viruses, Mycobacteria, parasites, fungi)
Misdirected inflammatory reactivity - harmless environmental substances (allergies), self antigens (autoimmune diseases)
Underlying disorders prolong immune activity - cancer, atherosclerosis, Alzheimer’s, T2D

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18
Q

What happens if there is persistent build up of endogenous substances?

A

Become target crystals of cholesterol and urate
Cholesterol = atherosclerosis
Urate = gout

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19
Q

What can chronic inflammation result in?

A

Large accumulations of T cells at inflamed sites
e.g. Rheumatoid arthritis

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20
Q

Describe recruitment of T cells in chronic inflammation

A

Activated naive T cells migrate and become effectors in lymphoid organs
Effector T cells return to inflammatory sites and increase response

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21
Q

Describe recruitment of eosinophils in chronic inflammation

A

Recruited and activated by parasites and IgE responsiveness

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22
Q

Describe recruitment of mast cells in chronic inflammation

A

Activated by injury or IgE mediated allergy

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23
Q

Describe recruitment of neutrophils in chronic inflammation

A

Several diseases influenced by over recruitment of neutrophils
e.g. COPD

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24
Q

Describe the resolution stage of chronic inflammation

A

Phases of incomplete resolution gradually increase the magnitude of inflammation

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25
What cells are involved in resolution of CI?
Macrophages Treg cells Innate lymphoid cells Myeloid derived suppressor cells (MDSC)
26
Describe the role of macrophages in resolution of CI
Killing, removal or apoptotic/spent immune cells Type shift to M2 drives repair
27
Describe the role of Treg cells in resolution of CI
Derived from CD4 lineages Use various cytokines (IL-10, TGF-b, IL-17) to deactivate many cell types exhibiting inflammatory cell responses (mast, eosinophils)
28
Where is lack of Tregs found?
In IBD Particularly IL-17
29
Describe the role of innate lymphoid cells in resolution of CI
e.g. NK cells Help to reduce activation of proinflammatory cells such as eosinophils (asthma)
30
Describe the role of MDSCs in resolution of CI
Aid in efferocytosis Induce Treg cell expansion Promote IL-10 and TGF-b production
31
What is chronic granulomatous inflammation?
Granulomas form when the causative agent cannot be eradicated to try and isolate/prevent its spread
32
What do granulomas comprise of?
Macrophages Lymphocytes - mostly T cells, some B cells Fibroblasts and collagen Necrotic tissue (sometimes)
33
What are the causes of chronic granulomatous inflammation?
Immune granulomas Foreign body granulomas Diseases of unknown aetiology - Sarcoidosis, Crohn's disease
34
What are immune granulomas associated with?
Persistent T cell activation due to specialist chronic infectious agents - M.tb - M.leprae - Treponema pallidum - Schistosoma sp.
35
What are foreign body granulomas associated with?
Inert materials but no T cell activation - talc - sutures - fibres - silica
36
Describe the course of chronic granulomatous inflammation
Macrophages take up agent but initial killing is ineffective T cell activation begins helping to activate macrophages Activated macrophages still do not kill agents Macrophages become epitheloid with large cytoplasms Macrophages fuse into giant multinucleate cells Inflammation is persistent and granulomas are formed Often causes significant tissue destruction
37
What are the outcomes of M. tb granulomatous inflammation?
MTB is eradicated MTB becomes latent
38
What does eradication of MTB lead to?
Tissue healing but with scarring/fibrosis and tissue damage Calcium deposits associate with scars and can be seen on xray
39
What happens when MTB becomes latent?
Leads to 'walling off' by fibrous tissue TB kept from dissemination by persistent T cell activation and surrounding activated macrophages However once immunity wanes (age/HIV) MTB reactivates
40
What does too little inflammation lead to?
Opportunistic or persistent infections e.g. Cryptococcus fungal infection in HIV
41
What does excessive inflammation cause?
Can produce fatal tissue damage e.g. excessive neutrophil activity associated with COVID-19 acute respiratory distress syndrome
42
What does undirected inflammation do?
Can drive chronic inflammation e.g. gut mucosal granulomas of unknown aetiology arising from chronic inflammatory dysregulation
43
What are the mediators of inflammation?
Vasoactive amines Lipid-derived mediators Complement Inflammatory cytokines Chemokines
44
Name some vasoactive amines
Histamine Seratonin
45
Name some lipid-derived mediators
Prostaglandins; COX-1/2 Leukotriens; lipoxygenases Lipoxins are anti-inflammatory
46
What are the complement inflammation mediators?
C3a C5a
47
What are some other inflammation mediators?
Kinins (bradikinin) Neuropeptides
48
What is a cytokine?
A molecule inter-signalling between cells of the immune system
49
What is a chemokine?
A chemotactic (attractant) cytokine
50
What are the cytokine families?
Il-1 family Class 1 Class 2 IL-17 family TNF family TGF family Chemokines
51
Describe the IL-1 family
Pro-inflammatory Includes IL-1 (alpha and beta), IL-18 and IL-33
52
Describe class 1 cytokines
Cell proliferation, differentiation and Ab secretion Includes IL-2, 3, 4, 5, 6, 7, 12, GM-CSF
53
Describe class 2 cytokines
Response to viruses, macrophage activation Includes type I IFN (alpha and beta) and type II IFN (gamma), IL-10
54
Describe IL-17 family
Pro-inflammatory Includes IL-17-A, B, C, D, F
55
Describe the TNF family
Induce differentiation, survival, proliferation, apoptosis Includes TNF alpha and beta
56
Describe the TGF family
Inflammatory regulators Includes TGF-B
57
Describe chemokines
Chemoattractants Includes CXCL8, CCL2, MCP-1
58
How are chemokines given their names?
Based on the number and location of N-terminal cysteine residues
59
What are the types of chemokines?
Type CC - expressed by monocytes and eosinophils Type CXC - expressed by neutrophils, Th1 cells and macrophages
60
What are the roles of chemokines?
Recruiting immune cells to infection sites Regulating traffic/recirculation through lymphoid organs Regulating DC migration from infection sites to lymph node Attracting effector T cells to specific sites of infection Migrating memory T cells
61
What are some additional roles of chemokines?
Regulating angiogenesis and tissue healing (fibrosis) Driving development of lymphoid organs Activating cell proliferation Regulating susceptibility to apoptosis Driving development of non-lymphoid organs (heart and cerebellum)
62
What do chemokines bind to?
7TM-spanning G-protein-coupled receptors on leucocytes AND GAGs (glycosaminoglycans) on epithelial cells
63
What are decoy chemokine receptors?
Non-signalling chemokine receptors used to dampen or scavenge chemokine responses and fine tune inflammatory reactions
64
What cells secrete IL-1b?
Monocytes/macrophages DCs Neutrophils Epithelial cells Endothelial cells
65
What induced IL-1b release?
PAMPs and DAMPs
66
What are systemic effects of IL-1b?
Pyrogen (fever)
67
What are immune effects of IL-1b?
Activated endothelial cells with TGF-b Induces Th17 differentiation
68
What cells secrete TNF-alpha?
Macrophages DCs Th1 cells
69
What induces TNF-a release?
PAMPs and DAMPs
70
What are systemic effects of TNF-a?
Pyrogen (fever) Acute phase protein release from hepatocytes Catabolism of muscle and fat
71
What are immune effects of TNF-a?
Activates neutrophils Induces apoptosis in some cells Activates endothelial cells
72
What cells secrete IL-6?
Macrophages Endothelial cells Fibroblasts
73
What induces IL-6 release?
PAMPs IL-1b TNF-a
74
What are systemic effects of IL-6?
Acute phase protein release from hepatocytes Catabolism of muscle and fat
75
What are immune effects of IL-6?
Increases neutrophil production Proliferates B cells With TGF-b induces Th17 differentiation
76
What cells secrete type 1 IFNs?
Macrophages DCs Virally infected cells
77
What induces release of type 1 IFNs?
PAMPs IL-1b TNF-a TLR3 TLR7 TLR9
78
What are the effects of type 1 IFNs?
Inhibit viral replication Induce MHC 1 expression/presentation Promotes Th1 differentiation
79
What cells secrete IGN gamma?
NK cells Th1 cells CD8+ T cells
80
What induces release of IFN-g?
IL-12 IL-18 T cell activation to Th1/CD8+
81
What are the effects of IFN-g?
Activates macrophages Induces MHC 1 and 2 expression/presentation Promotes Th1 differentiation and inhibits Th2 Controls Ab switching (promotes IgG2a, inhibits IgE and IgG1)

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