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Medical Microbiology I > Innate Host Responses > Flashcards

Innate Host Responses Flashcards

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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
Q

TLRs sense the presence of microbial infection by

A
  • Binding to these characteristic patterns within molecules on the outside of bacteria, fungi and viruses
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26
Q

Immature dendritic cells located in

A
  • Blood and tissue

- Provide early cytokine-mediated warning system

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27
Q

Cytokine mediated warning system of iDCs

A
  • Cytokine-secreted proteins that function as mediators of immune and inflammatory responses
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28
Q

Types of immature dendritic cells

A
  • Langerhans cells in the skin
  • Dermal interstitial cells
  • Interdigitating cells (lymph node and spleen)
  • Splenic marginal DCs
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29
Q

iDCs present antigen to

A
  • T cells on MHC I and MHC II molecules
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30
Q

iDCs constantly acquiring antigenic material by

A
  • Macropinocytosis, pinocytosis, or phagocytosis of apoptotic cells, debris, and proteins in normal tissue and at sites of infection or tumor
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31
Q

Upon activation of the iDC by a TLR cascade in response to infection

A
  • The iDC matures into a DC and its role changes
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32
Q

TH1 function

A
  • First, early local response
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33
Q

TH1 inducer

A
  • IL12 by D
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34
Q

TH1 mediator

A
  • INF-gamma

- IL-2

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35
Q

TH1 response

A
  • Cellular, inflammatory reactions
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36
Q

TH1 targets

A
  • Intracellular viral, bacterial, fungal, parasitic infections
  • Tumors
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37
Q

TH2 function

A
  • 2nd to TH1

- Later, systemic

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38
Q

TH2 inducer

A
  • IL4
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39
Q

TH2 mediators

A
  • IL-4
  • IL-5
  • IL-6
  • IL-10
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40
Q

TH2 response

A
  • Humoral (antibody)
41
Q

TH2 targets

A
  • Blood borne microbes
  • Some viruses
  • Most bacteria
42
Q

Mature activated dendritic cells lose

A
  • Ability to phagocytize, preventing it from acquiring irrelevant antigenic material other than the microbial debris
  • Adhesiveness for epithelia
43
Q

Mature activated dendritic cells express

A
  • Surface receptor specific for chemoattractant cytokines produced in T cell areas of the lymph node
44
Q

Mature activated dendritic cells progress to

A
  • T cell areas of the lymph node

- Trigger the response to the microbial challenge

45
Q

Mature activated dendritic cells upregulate

A
  • Class II MHC molecules for antigen presentation
46
Q

DCs present antigenic material attached to MHC class I and CD1 molecules to

A
  • CD8 T and NKT cells
47
Q

DCs present antigenic material attached to MHC class II molecules to

A
  • CD4 T cells
48
Q

Natural killer cells

A
  • Large granular lymphocytes
  • Share characteristics with T cells
  • Target cell recognition different from T cells
49
Q

Natural killer cells are stimulated by

A
  • 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
Q

NK cells express

A
  • CD2, CD7, IL-2 receptor and Fas ligand

- Fc receptor for IgG (CD16)

51
Q

NK cells complement receptors for

A
  • ADCC
52
Q

Activated NK cells produce

A
  • IFN-γ
  • IL-1
  • Granulocyte-macrophage colony-stimulating factor (GM-CSF)
53
Q

Cytokines reinforce local initial protective responses (TH1) by

A
  • Encouraging the production of IL-12 by pre-DCs and activated macrophages
54
Q

NK cells characteristics different from T cells

A
  • 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
Q

Process of NK cells killing cells

A
  • 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
Q

Granules in an NK cell contain perforin and granzymes

A
  • A pore-forming protein and esterases

- Similar to the contents of the granules of a CD8 cytotoxic T lymphocyte (CTL)

57
Q

ADCC binding of NK cell to antibody-coated target cells

A
  • Also initiates killing
58
Q

Apoptosis

A
  • Process of cell death triggered by interaction of FasL on the NK cell with Fas protein on target cell
59
Q

NKT cells and γ / δ T cells reside in

A
  • 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
Q

NKT cells and γ / δ T cells are unlike other T cells because

A
  • Able to sense non-peptide antigens
  • Glycolipids of mycobacteria
  • Phosphorylated amine metabolites from some bacteria
61
Q

Bacteria activate

A
  • Innate protective response

- Inflammatory responses well

62
Q

Bacterial cell wall components

A
  • Teichoic acid
  • Peptidoglycan
  • Lipopolysaccharide (LPS)
63
Q

Bacterial cell walls contain

A
  • Repetitive structures easily recognized
  • PAMP receptors
  • Toll-like receptors (TLRs)
  • Strong activators of DCs, macrophages
64
Q

Inflammasome

A
  • Multiprotein complex present in epithelial cells, DCs, and macrophages
65
Q

Inflammasomes activated by

A
  • Several proteins induced by response to the PAMPS, tissue damage or indications of intracellular infection
66
Q

Activated inflammasome can initiate

A
  • Apotosis-like cell death for cells with intracellular infections
67
Q

Chemokines

A
  • Cytokines that stimulate leukocyte movement & regulate the migration of leukocytes from blood to tissues
68
Q

Chemotaxis

A
  • Movement of a cell directed by a chemical concentration gradient
69
Q

Neutrophils respond to

A
  • Inflammatory signals

- C3a, C5a, TNF-α

70
Q

Diapedesis

A
  • Process by which PMNs extravasate the capillary wall to the site of inflammation
71
Q

Phagocytic responses

A
  • PMNs, monocytes: 1st responders at site of infection, macrophages follow later
  • Provide a major antibacterial response
  • Contribution to inflammation
72
Q

Bacterial infection indicated by

A
  • Increased number of neutrophils (“polys”) in the blood, body fluids (cerebrospinal fluid), or tissue
73
Q

Left shift

A
  • Accompanies mobilization of neutrophils

- An increase in the number of immature band forms released from the bone marrow

74
Q

Phagocytosis of bacteria by macrophages and neutrophils involves 3 steps:

A
  • Attachment
  • Internalization
  • Digestion
75
Q

Attachment step of phagocytosis

A
  • Macrophages - mediated by receptors for bacterial carbohydrates receptors for opsonins - C3b, mannose-binding protein, Fc portion of antibody
76
Q

Internalization step of phagocytosis

A
  • A section of plasma membrane surrounds the particle to form a phagocytic vacuole around the microbe
77
Q

Digestion step of phagocytosis

A
  • Vacuole fuses with the primary lysosomes (macrophages) or granules (PMNs) to allow inactivation and digestion of the vacuole contents
78
Q

Activation of macrophages promoted best by

A
  • IFN – γ, also by TNF-α

- Activation required for killing

79
Q

2 mechanisms of killing bacteria

A
  • Oxygen dependent or oxygen independent

- Depends on the antimicrobial chemicals produced by the granules

80
Q

Oxygen dependent mechanism of killing bacteria

A
  • Powerful oxidative burst
  • Formation of H2O2
    neutrophil
  • Myeloperoxidase transforms chloride ions into hypochlorus ions to kill
81
Q

Oxygen independent mechanism of killing bacteria

A
  • 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
Q

Neutrophils contribute to inflammation response in several ways

A
  • 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
Q

Innate responses are constantly stimulated by

A
  • Normal flora of the skin, nose, mouth, urogenital and GI tracts
84
Q

PAMPRs on the intestine “see” the LPS, LTA, flagella, and other components of

A
  • Bacteria of the gut lumen

- An equilibrium is maintained between the innate response & immunoregulatory responses & the microbes

85
Q

Disruption of the established equilibrium between innate and immunoregulatory responses can occur by

A
  • Altering the species with antimicrobial treatment or disruption of the innate response
  • Can result in inflammatory bowel disease, autoimmune disease or gastroenteritis
86
Q

LPS & other bacterial cell wall components stimulate immature DCs & macrophages to release

A
  • Interleukins IL-1, IL-6
  • TNF-α (cachetin)
  • Chemokines
87
Q

Endogenous pyrogens

A
  • 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
Q

Acute-phase response

A
  • 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
Q

Acute phase response promotes changes that support host defenses

A
  • Fever
  • Anorexia
  • Sleepiness
  • Metabolic changes
  • Production of proteins
90
Q

Acute phase proteins

A
  • C-reactive protein
  • Complement components
  • Coagulation proteins
  • LPS-binding proteins
  • Protease inhibitors
  • Adherence proteins
91
Q

C-reactive protein (CRP)

A
  • Complexes with the polysaccharides of bacteria & fungi
  • Activates the complement pathway
92
Q

Acute-phase proteins reinforce

A
  • Innate defenses against infection

- But excessive production during sepsis can cause serious problems, such as shock

93
Q

Acute inflammation

A
  • Early defense mechanism to contain an infection, prevent its spread, & signal subsequent specific immune responses
94
Q

3 major events of acute inflammation

A
  • 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
Q

Cytokine storm

A
  • Overwhelming release of cytokines in response to bacterial cell wall components, toxic shock toxins, and viremia
96
Q

Vascular leakage of fluids into tissue

A
  • Causes shock
97
Q

Septic shock

A
  • Form of cytokine storm caused by systemic action of large amounts of TNF-a
98
Q

Bridge to antigen-specific responses

A
  • 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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