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Medical Microbiology I > Innate Host Responses > Flashcards

Innate Host Responses Flashcards

1
Q

Cellular components of innate responses

A
  • Phagocytes
  • Cells of the Monocyte-Macrophage Lineage
  • Immature Dendritic Cells
  • Dendritic Cells
  • Natural Killer, γ / δ T Cells, and NKT Cells
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2
Q

3 lines of protection from microbial world

A
  • Natural barriers
  • Innate, antigen-nonspecific immune defenses
  • Adaptive, antigen-specific immune responses
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3
Q

Natural barrier examples

A
  • Skin
  • Mucosal surfaces
  • Stomach acid
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4
Q

Soluble innate components

A
  • Complement components

- Type 1 interferons

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5
Q

Cellular innate components

A
  • Phagocytes
  • Monocytes
  • Macrophages
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6
Q

Neutrophils have a major role in

A
  • Antibacterial and antifungal protection

- Lesser role in antiviral protection

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7
Q

Phagocyte (neutrophils) features

A
  • Reptors to bind microbes
  • Granules
  • Terminally differentiated cells
  • Component of “pus” at the site of infection
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8
Q

Phagocyte (neutrophil) life span

A
  • Spend less than 3 days in the blood

- Die rapidly in tissue

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9
Q

Macrophages mature from

A
  • Monocytes
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10
Q

Macrophage similarities to neutrophils

A
  • Opsonin receptors to promote phagocytosis
  • Receptors for PAMPS to initiate activation
  • Cytokine receptors to promote activation
  • Express MHC II proteins
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11
Q

Macrophages differences from neutrophils

A
  • Live longer and can divide
  • Must be activated to kill phagocytosed microbes
  • Remain at site of infection or inflammation
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12
Q

M1 macrophages

A
  • Classical Activation” – mediated by IFN-γ produced by NK cells and CD4 and CD8 T cells
  • Part of TH1 response
  • Able to kill phagocytosed bacteria
  • Produce cytokines and enzymes
  • Reinforce local inflammation by producing cytokines
  • Activation makes them more efficient to kill
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13
Q

M2 macrophages

A
  • “Alternatively Activated” by cytokines IL-4 and IL-13
  • Part of the TH2 response
  • Anti-parasitic responses
  • Wound repair
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14
Q

M2 macrophages form

A
  • Granulomas to surround chronic infections such as unresolved mycobacterial infections
  • Macrophages fuse to become multinucleated giant cells and enlarge to become epitheloid cells
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15
Q

Effects of binding & ingestion of microbes by monocytes and macrophages

A
  • Promote the release of interleukin-1 (IL-1), IL-12, and tumor necrosis factor (TNF), which initiate inflammatory reactions
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16
Q

IFN-γ made by NK or T cells activates

A
  • Killing mechanisms in macrophage

- Creating “activated macrophage”

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17
Q

Activation of the macrophages makes them more efficient killers of

A
  • Phagocytosed microbes
  • Virally infected cells
  • Tumor cells
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18
Q

Immature dendritic and dendritic cells

A
  • Bridge between innate and the adaptive immune responses
  • Octopus-like arms (dendrites)
  • Antigen-sticky cell surface
  • Produce cytokines
  • Present antigen to T and B Cells
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19
Q

Protein antigens of microbes that enter the body are captured mainly by

A
  • Dendritic cells

- Concentrated in the peripheral lymphoid organs, where immune responses are initiated

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20
Q

Microbes enter the body through

A
  • Skin by contact
  • Gastrointestinal tract by ingestion
  • Respiratory tract by inhalation
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21
Q

Interfaces between the body and external environment are lined by

A
  • Continuous epithelia

- Function is to provide a physical barrier to infection

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22
Q

Toll-like receptors (TLRs)

A
  • Cell surface and endosomal receptors

- Pattern recognition receptors for many different pathogen-associated molecular patterns

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23
Q

Pathogen-associated molecular patterns (PAMPs) for TLRs

A
  • LPS
  • Peptidoglycan
  • Fungal glycans
  • Microbial nucleic acids
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24
Q

TLRs are linked to

A
  • Signal transduction pathways

- Activate genes that promote inflammation

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25
TLRs sense the presence of microbial infection by
- Binding to these characteristic patterns within molecules on the outside of bacteria, fungi and viruses
26
Immature dendritic cells located in
- Blood and tissue | - Provide early cytokine-mediated warning system
27
Cytokine mediated warning system of iDCs
- Cytokine-secreted proteins that function as mediators of immune and inflammatory responses
28
Types of immature dendritic cells
- Langerhans cells in the skin - Dermal interstitial cells - Interdigitating cells (lymph node and spleen) - Splenic marginal DCs
29
iDCs present antigen to
- T cells on MHC I and MHC II molecules
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iDCs constantly acquiring antigenic material by
- Macropinocytosis, pinocytosis, or phagocytosis of apoptotic cells, debris, and proteins in normal tissue and at sites of infection or tumor
31
Upon activation of the iDC by a TLR cascade in response to infection
- The iDC matures into a DC and its role changes
32
TH1 function
- First, early local response
33
TH1 inducer
- IL12 by D
34
TH1 mediator
- INF-gamma | - IL-2
35
TH1 response
- Cellular, inflammatory reactions
36
TH1 targets
- Intracellular viral, bacterial, fungal, parasitic infections - Tumors
37
TH2 function
- 2nd to TH1 | - Later, systemic
38
TH2 inducer
- IL4
39
TH2 mediators
- IL-4 - IL-5 - IL-6 - IL-10
40
TH2 response
- Humoral (antibody)
41
TH2 targets
- Blood borne microbes - Some viruses - Most bacteria
42
Mature activated dendritic cells lose
- Ability to phagocytize, preventing it from acquiring irrelevant antigenic material other than the microbial debris - Adhesiveness for epithelia
43
Mature activated dendritic cells express
- Surface receptor specific for chemoattractant cytokines produced in T cell areas of the lymph node
44
Mature activated dendritic cells progress to
- T cell areas of the lymph node | - Trigger the response to the microbial challenge
45
Mature activated dendritic cells upregulate
- Class II MHC molecules for antigen presentation
46
DCs present antigenic material attached to MHC class I and CD1 molecules to
- CD8 T and NKT cells
47
DCs present antigenic material attached to MHC class II molecules to
- CD4 T cells
48
Natural killer cells
- Large granular lymphocytes - Share characteristics with T cells - Target cell recognition different from T cells
49
Natural killer cells are stimulated by
- IFN-α and IFN-β - produced early in response to viral and other infections - TNF-α - IL-12, IL-15, and IL-18 - produced by pre-DCs and activated macrophages - IL-2 - produced by CD4 TH1 cells
50
NK cells express
- CD2, CD7, IL-2 receptor and Fas ligand | - Fc receptor for IgG (CD16)
51
NK cells complement receptors for
- ADCC
52
Activated NK cells produce
- IFN-γ - IL-1 - Granulocyte-macrophage colony-stimulating factor (GM-CSF)
53
Cytokines reinforce local initial protective responses (TH1) by
- Encouraging the production of IL-12 by pre-DCs and activated macrophages
54
NK cells characteristics different from T cells
- Do not express a TCR or CD3 - Cannot produce IL-2 - Do not recognize a specific antigen - Do not require presentation of antigen by MHC molecules - NK system does not involve memory - Cannot be enhanced by specific immunization
55
Process of NK cells killing cells
- See every cell as potential victim - Cells that appear in distress are targeted - Class I MHC on target cell interacts with KIR inibitory receptor on NK cells - If all is normal with the target cell (then it provides an inhibitory signal to prevent killing) - “stress related receptors” – expressed by virally infected cells and tumor cells as signal (often depleted of Class I MHC – become NK target)
56
Granules in an NK cell contain perforin and granzymes
- A pore-forming protein and esterases | - Similar to the contents of the granules of a CD8 cytotoxic T lymphocyte (CTL)
57
ADCC binding of NK cell to antibody-coated target cells
- Also initiates killing
58
Apoptosis
- Process of cell death triggered by interaction of FasL on the NK cell with Fas protein on target cell
59
NKT cells and γ / δ T cells reside in
- Tissue and blood - Differ from other T cells because they have a limited repertoire of T-cell receptors - Produce IFN- γ - which activates macrophages and DCs to enforce a TH1 response
60
NKT cells and γ / δ T cells are unlike other T cells because
- Able to sense non-peptide antigens - Glycolipids of mycobacteria - Phosphorylated amine metabolites from some bacteria
61
Bacteria activate
- Innate protective response | - Inflammatory responses well
62
Bacterial cell wall components
- Teichoic acid - Peptidoglycan - Lipopolysaccharide (LPS)
63
Bacterial cell walls contain
- Repetitive structures easily recognized - PAMP receptors - Toll-like receptors (TLRs) - Strong activators of DCs, macrophages
64
Inflammasome
- Multiprotein complex present in epithelial cells, DCs, and macrophages
65
Inflammasomes activated by
- Several proteins induced by response to the PAMPS, tissue damage or indications of intracellular infection
66
Activated inflammasome can initiate
- Apotosis-like cell death for cells with intracellular infections
67
Chemokines
- Cytokines that stimulate leukocyte movement & regulate the migration of leukocytes from blood to tissues
68
Chemotaxis
- Movement of a cell directed by a chemical concentration gradient
69
Neutrophils respond to
- Inflammatory signals | - C3a, C5a, TNF-α
70
Diapedesis
- Process by which PMNs extravasate the capillary wall to the site of inflammation
71
Phagocytic responses
- PMNs, monocytes: 1st responders at site of infection, macrophages follow later - Provide a major antibacterial response - Contribution to inflammation
72
Bacterial infection indicated by
- Increased number of neutrophils (“polys”) in the blood, body fluids (cerebrospinal fluid), or tissue
73
Left shift
- Accompanies mobilization of neutrophils | - An increase in the number of immature band forms released from the bone marrow
74
Phagocytosis of bacteria by macrophages and neutrophils involves 3 steps:
- Attachment - Internalization - Digestion
75
Attachment step of phagocytosis
- Macrophages - mediated by receptors for bacterial carbohydrates receptors for opsonins - C3b, mannose-binding protein, Fc portion of antibody
76
Internalization step of phagocytosis
- A section of plasma membrane surrounds the particle to form a phagocytic vacuole around the microbe
77
Digestion step of phagocytosis
- Vacuole fuses with the primary lysosomes (macrophages) or granules (PMNs) to allow inactivation and digestion of the vacuole contents
78
Activation of macrophages promoted best by
- IFN – γ, also by TNF-α | - Activation required for killing
79
2 mechanisms of killing bacteria
- Oxygen dependent or oxygen independent | - Depends on the antimicrobial chemicals produced by the granules
80
Oxygen dependent mechanism of killing bacteria
- Powerful oxidative burst - Formation of H2O2 neutrophil - Myeloperoxidase transforms chloride ions into hypochlorus ions to kill
81
Oxygen independent mechanism of killing bacteria
- Fusion of the phagosome with azurophilic granules containing cationic proteins (cathepsin G) & specific granules containing lysozyme and lactoferrin - Proteins kill gram-negative bacteria by disrupting their cell membrane integrity - Far less effective against gram-positive bacteria, killed principally through the oxygen-dependent mechanism
82
Neutrophils contribute to inflammation response in several ways
- Prostaglandins and leukotrienes, which increase vascular permeability, are released, causing swelling (edema) and stimulating pain receptors - During phagocytosis the granules may leak their contents to cause tissue damage - Neutrophils have short lives and become pus
83
Innate responses are constantly stimulated by
- Normal flora of the skin, nose, mouth, urogenital and GI tracts
84
PAMPRs on the intestine “see” the LPS, LTA, flagella, and other components of
- Bacteria of the gut lumen | - An equilibrium is maintained between the innate response & immunoregulatory responses & the microbes
85
Disruption of the established equilibrium between innate and immunoregulatory responses can occur by
- Altering the species with antimicrobial treatment or disruption of the innate response - Can result in inflammatory bowel disease, autoimmune disease or gastroenteritis
86
LPS & other bacterial cell wall components stimulate immature DCs & macrophages to release
- Interleukins IL-1, IL-6 - TNF-α (cachetin) - Chemokines
87
Endogenous pyrogens
- Released from macrophages in response to bacterial cell wall components - Promote fever production & enhance the inflammatory response - Causes further activation of macrophages, promoting acute phase response
88
Acute-phase response
- Occurs as part of the innate response to infections - Proteins are synthesized by the liver (C-reactive protein, fibrinogen) in response to inflammatory cytokines, especially IL-6 and TNF-α (C-reactive protein, fibrinogen)
89
Acute phase response promotes changes that support host defenses
- Fever - Anorexia - Sleepiness - Metabolic changes - Production of proteins
90
Acute phase proteins
- C-reactive protein - Complement components - Coagulation proteins - LPS-binding proteins - Protease inhibitors - Adherence proteins
91
C-reactive protein (CRP)
- Complexes with the polysaccharides of bacteria & fungi - Activates the complement pathway
92
Acute-phase proteins reinforce
- Innate defenses against infection | - But excessive production during sepsis can cause serious problems, such as shock
93
Acute inflammation
- Early defense mechanism to contain an infection, prevent its spread, & signal subsequent specific immune responses
94
3 major events of acute inflammation
- Expansion of capillaries to increase blood flow (redness or a rash, releasing heat) - Increase in permeability of microvasculature to allow escape of fluid, plasma proteins, & leukocytes from the circulation (swelling or edema) - Recruitment of neutrophils & their accumulation & response to infection at the site of injury
95
Cytokine storm
- Overwhelming release of cytokines in response to bacterial cell wall components, toxic shock toxins, and viremia
96
Vascular leakage of fluids into tissue
- Causes shock
97
Septic shock
- Form of cytokine storm caused by systemic action of large amounts of TNF-a
98
Bridge to antigen-specific responses
- Innate response is often adequate to control an infection - An infection can also stimulate antigen-specific immunity - Dendritic cells are the key to the transition and determine the nature of the next response

Medical Microbiology I (8 decks)

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