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Microbiology > 2. Inflammation > Flashcards

2. Inflammation Flashcards

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1
Q

a complex array of interactions among soluble biologically active factors and cells of the immune system that arise in any tissue in response to trauma, infections, post-ischemic, or toxic injury

A

definition of inflammation

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2
Q

why is inflammation a double-edged sword

A

essential for normal immune response (allows tissues to return to homeostasis) but can be pathogenic when unresolved

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3
Q

___ plays a major role in pathogenesis of most chronic diseases (periodontal disease, endocarditis, autoimmunity, heart disease, Alzheimer’s, allergies, obesity, cancer)

A

inflammation

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4
Q

5 signs of inflammation

A
  1. heat
  2. redness
  3. swelling
  4. pain
  5. loss of function
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5
Q

acute inflammation

A

occurs immediately after injury (lasts for a few days)

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6
Q

__ __ starts after injury that will cause soluble mediators like cytokines, acute phase proteins, and chemokines to promote the migration of neutrophils and macrophages to the area of inflammation. These cells are part of innate immunity that have an active role in __ __.

A

acute inflammation

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7
Q

subacute inflammation

A

transformational period from acute to chronic (lasts 2 to 6 weeks)

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8
Q

if this inflammation does not resolve after 6 weeks, chronic form develops with migration of T lymphocytes and plasma cells to site of inflammation

A

subacute inflammation

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9
Q

chronic inflammation

A

lasts for months or even years when acute inflammation fails to resolve; occurs with persistence of antigen (viruses, autoimmunity, cancer)

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10
Q

if this persists with no recovery, then tissue damage and fibrosis will ensue. There are other varieties of cells such as the macrophages and monocytes that play a role in both acute and chronic inflammation.

A

chronic inflammation

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11
Q

true or false: inflammation may be localized or systemic

A

true

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12
Q

steps of local infection with gram-negative bacteria

A
  1. macrophage activated to secrete TNFalpha in the tissue
  2. increased release of plasma proteins into tissue; increased phagocyte and lymphocyte migration into tissue; increased platelet adhesion to blood vessel wall
  3. phagocytosis of bacteria; local vessel occlusion; plasma and cells drain to local lymph node
  4. removal of infection; adaptive immunity
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13
Q

steps of systemic infection with gram-negative bacteria (sepsis)

A
  1. macrophages activated in the liver and spleen secrete TNFalpha into the bloodstream
  2. systemic edema causing decreased blood volume, hypoproteinemia, and neuropenia, followed by neutrophilia; decreased blood volume causes collapse of vessels
  3. disseminated intravascular coagulation leading to wasting and multiple organ failure
  4. death
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14
Q

under homeostatic conditions, what does inflammation promote?

A

clearance of microbes and tissue healing

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15
Q

3 steps of homeostatic conditions of inflammation

A
  • mobilization of immune effector cells and molecules to the site of infection or tissue damage to mediate destruction of microbes
  • clot formation to control bleeding and prevent spreading of infection into bloodstream
  • promotes remodeling and healing of damaged tissues
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16
Q

causes of inflammation (2 types of inducers)

A
  • endogenous inducers
  • exogenous inducers
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17
Q

endogenous inducers

A
  • released by tissues that are either dead, damaged, or stressed
  • referred to as damage associated molecular patterns (DAMPs)
  • inflammation caused by our own tissues!
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18
Q

exogenous inducers: microbial and nonmicrobial

A

microbial: two classes
- pathogen-associated molecular patterns (PAMPs)
- virulence factors restricted to pathogens

nonmicrobial
- causes include allergens, toxic compounds, irritants, and foreign bodies that are too large to be digested or cause phagosomal damage in macrophages (foreign bodies such as silica and asbestos) – derived from environment
- also classified as exogenous DAMPs

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19
Q

generation of inflammation requires

A

receptor activation

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20
Q

in order to generate inflammation, cells must first be able to recognize a specific stimulus (___ or ___). This recognition is mediated by ___ expressed on the cells. These receptors are located on the cell ___ and ___ the cell.

A

DAMP, PAMP, receptors, surface, within

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21
Q

DAMPs bind specific receptors to generate inflammation. Many different types of endogenous molecules can act as DAMP:

A
  • proteoglycans/glycosaminoglycans
  • proteins/peptides
  • nucleic acids/protein nucleic acid complexes
  • fatty acids/lipoproteins
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22
Q

DAMPs bind to specific cellular receptors. Many types of receptors recognize DAMP:

A
  • toll-like receptors (TLRs) bind diverse ligands (proteoglycans and nucleic acids)
  • inflammasomes bind self DNA
  • P2X7 receptor binds ATP
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23
Q

toll-like receptors (TLR)

A
  • type of pattern recognition receptor
  • expressed on cell surface and intracellularly
  • bind diverse ligands such as proteoglycans and nucleic acids
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24
Q

AIM2 and NLRP3

A

types of inflammasomes

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25
true or false: self-derived DAMP bind to our own receptors to cause inflammation
true
26
Inflammation is also generated by PAMPs that bind to the same receptors as DAMPs. Many types of receptors recognize PAMPs:
- TLRs: bind bacteria, fungi, viruses - inflammasomes: bind viral DNA - NOD receptors: bind bacterial components
27
true or false: pathogens do not bind to the same receptors as DAMP to cause inflammation
false: they do
28
what happens following binding of the DAMP or PAMP to its cognate receptor?
1. activation of signaling cascades leads to translocation of transcription factors (TFs) from the cytoplasm to the nucleus 2. TFs bind to DNA in nucleus and initiate transcription of inflammatory genes 3. leads to production of proteins integral to immune response - pre-formed mediators are also important in immune response
29
cell-derived mediators of inflammation that are pre-formed mediators in secretory granules
- histamine: mast cells, basophils, platelets - serotonin: platelets *these are fast
30
cell-derived mediators of inflammation that are newly synthesized
- prostaglandins: all leukocytes, mast cells - leukotrienes: all leukocytes, mast cells - platelet-activating factor: all leukocytes, endothelium - reactive oxygen species: all leukocytes - nitric oxide: macrophages, endothelium - cytokines: macrophages, endothelium - neuropeptides: lymphocytes, mast cells, leukocytes, nerve fibers *these are slow
31
plasma-protein derived mediators of inflammation by complement activation
- C3a: anaphylatoxins - C5a: anaphylatoxins - C3b - C5b-9: membrane attack complex *liver is major source!
32
plasma-protein derived mediators of inflammation by factor XII activation (Hageman factor)
- kinin system (bradykinin) - coagulation/fibrinolysis system *liver is major source!
33
what mediate inflammation through diverse effects?
cytokines and chemokines; they can have synergistic or additive effects
34
true or false: multiple receptors can be activated simultaneously during an immune response
true
35
__ between different receptors and pathways facilitates effective response
crosstalk
36
depending on nature of inflammatory stimulus, distinct receptors can be activated ___
contemporaneously
37
multiple receptors activated simultaneously during immune response results in production of __ __ __ by different cell types
specific inflammatory mediators
38
engagement of multiple receptors and cell types ensures a __, __ response that leads to clearance of the inflammatory insult
rapid, robust
39
how is inflammation regulated?
initiation, activation, amplification, termination
40
true or false: only immune cell types mediate inflammation
false: both immune and non-immune cell types mediate inflammation
41
innate immune cells are activated ___ in immune response and provide signals to activate adaptive immunity
first
42
types of innate immune cells
- monocytes/macrophages - dendritic cells - neutrophils - mast cells - NK cells - eosinophils
43
types of nonimmune cells
- epithelial cells - endothelial cells - fibroblasts
44
types of adaptive immune cells
- T cells - B cells
45
innate immune cells interact to mediate which type of inflammation?
acute
46
kinetics of primary (innate) and memory (adaptive) immune responses
- innate immune response is fairly linear - adaptive immune response has two peaks: primary and secondary responses - innate can engage adaptive - memory cells sit around waiting to be used, then have a fast immune response when they're needed - adaptive response maintains the cells that were recognized by the immune system
47
5 R's in resolution of the inflammatory response
- removal of microbes, dead cells, and debris - restoration of vascular integrity and perfusion - regeneration of tissue - remission of fever - relief of pain
48
high immune activity leads to __ homeostasis
adapted
49
low immune activity leads to __ homeostasis
maladapted (chronic inflammation and autoimmunity)
50
true or false: inflammation is a component of physiologic aging
true: it's called inflamm-aging!
51
inflamm-aging
- progressive tendency towards proinflammatory phenotype with age, found in association with age-related diseases - several pathways trigger release of inflammatory cytokines, stimulate NF-kB related signaling networks - not inevitable -- modulate inflammaging with diet, exercise, etc.
52
pro-inflammatory cytokines
IL-1, IL-6, TNF-alpha
53
anti-inflammatory cytokines
IL-10, TGF-beta, IL-37
54
failure to resolve inflammation leads to pathologies such as
- multiple sclerosis - asthma - myocardial infarction - liver fibrosis - scleroderma - rheumatoid arthritis - cancer
55
examples of chronic inflammation in oral disease
- periodontal disease - autoimmunity (Sjogren's syndrome, vesiculoerosive disease)
56
vesiculoerosive disease
- patients produce autoantibodies that bind to constituents of the hemidesmosomes - hemidesmosomes anchor the epithelium to the underlying connective tissue - results in tissue sloughing - due to chronic inflammation - epithelium and CT are not tightly joined as they should be - very painful
57
examples of therapeutic approaches to mitigate inflammation
- NSAIDs (non selective/selective cyclooxygenase COX inhibitors) - aspirin - ibuprofen - celebrex - corticosteroids - biologic therapies
58
NSAIDs mechanism of action
- traditional NSAIDs (aspirin, ibuprofen) exhibit non-selective COX inhibition and are some of the most widely prescribed NSAIDs to relieve short term fever, pain and inflammation - tissue injury --> epithelial cell -phospholipase A-> arachidonic acid - arachidonic acid -COX1/2-> prostaglandins (fever, pain, inflammation) - arachidonic acid -5/12/15LOX-> leukotrienes (inflammation)
59
aspirin mechanism of action
- 2 COX enzyme systems controlling the production of prostanoids: prostaglandins (PGs) and thromboxane (TtxA2) - COX-1: produces PGs and TxA2 that regulate gastrointestinal, renal, vascular and other physiological functions - COX-2: regulates production of PGs involved in inflammation, pain and fever - aspirin initiates the biosynthesis of novel anti-inflammatory mediators from arachidonic acid
60
aspirin inhibits __ and acetylates __
COX-2, COX-1
61
increase in aspirin-triggered ATL will cause
anti-inflammation and pro-resolution
62
decrease in thromboxane will cause
anti-thrombotic
63
corticosteroids mechanism of action
- glucocorticoids and glucocorticoid receptor reside at the apex of a regulatory network that blocks several inflammatory pathways - glucocorticoids can inhibit PG production through 3 independent mechanisms: 1. induction and activation of annexin I 2. induction of MAPK phosphatase 1 3. repression of transcription of cyclooxygenase phospholipase A2alpha (cPLA2alpha)
64
_____ are a class of steroid hormones released by the adrenal cortex, which includes glucocorticoids and mineralcorticoids
corticosteroids
65
both ___ and ___ corticosteroids are given for inflammatory conditions, including for oral mucosal disease
topical, systemic
66
what is a biological product?
biological products include wide range of products such as blood and blood components, gene therapy, tissues, and recombinant therapeutic proteins - typically monoclonal antibody-based
67
what can biologic therapies reduce?
- reduce inflammatory mediators - diminish immune cell activation - reduce numbers of specific types of immune cells (biologic therapies can target specific aspects of the immune system based on what the patient needs)
68
generation of and naming scheme for monoclonal antibodies is __
complex - all names end in -mab (think antibody, ab)
69
monoclonal antibody naming for mouse
-omab
70
monoclonal antibody naming for chimeric
-ximab
71
monoclonal antibody naming for humanized
-zumab
72
monoclonal antibody naming for human
-umab
73
examples of types of biologic therapies: inhibition of T cell activation
- anti-CD40, anti-B7RP1, anti-CD28, CTLA4 fusion protein (don't need to memorize) - this dampens the interactions between dendritic cells and T cells
74
examples of types of biologic therapies: inhibition of immune cell chemotaxis
- therapeutics target integrin receptors: - natalizumab targets subunit of VLA-4 - vedolizumab targets alpha4beta7 integrin
75
examples of types of biologic therapies: targeted depletion of B cells
anti-CD20 (rituximab RTX) has multiple mechanisms: - induces B cell killing by NK cells through antibody-dependent cellular cytotoxicity (ADCC) - direct cross-linking of CD20 on B cell tumor cell lines sufficient for the induction of apoptosis - may induce complement-dependent cytotoxicity on target B cells - opsonization of B cells by RTX may also induce clearance of B cells in circulation through phagocytosis by the reticulo-endothelial system (phagocytosis by macrophages)
76
examples of types of biologic therapies: inhibition of cytokine signaling
- anti-BAFF/APRIL (belimumab) - anti-BAFFR (ianalumab) - anti-IL-17 (secukinumab, ixeizumab, bimekizumab) - anti-IL-17R (brodalumab) - anti-IL-1R (anakinra) - anti-TNFalpha (infliximab, etanercept) - anti-IL-12/23 (ustekinumab) - anti-IL-6R (tocilizumab)
77
4 caveats of biologic therapies
- inhibition of inflammation also makes host more susceptible to microbial infection - biologics can be targeted by the patient's immune system (immunogenic) - biologics can be immunogenic - biologics are extremely expensive

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