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Microbiology > CH 14 - Innate Immune Response > Flashcards

CH 14 - Innate Immune Response Flashcards

1
Q

Apoptosis
(definition)

A

Programmed death of “self” cells that does not cause inflammation

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2
Q

Complement system
(definition)

A

Series of proteins in blood & tissue fluids that can be activated to help destroy & remove invading microbes

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3
Q

Cytokines
(definition)

A

Proteins that function as chemical messengers, allowing cells involved in host defenses to communicate

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4
Q

Inflammatory response
(definition)

A

Coordinated innate response with purpose of:

  1. Containing site of damage
  2. Localizing the response
  3. Eliminating the invader
  4. Restoring tissue function
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5
Q

Innate immunity
(definition)

A

Host defenses involving:

  1. Anatomical barriers
  2. Sensor systems that recognize patterns associated with microbes or tissue damage
  3. Phagocytic cells
  4. Inflammatory response
  5. Fever
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6
Q

Macrophage
(definition)

A

Type of phagocytic cell that wanders or resides in tissues

Has multiple roles including: scavenging debris & producing pro-inflammatory cytokines

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7
Q

Membrane attack complexes (MACs)
(definition)

A

Complement system components assembled to form pores in membranes of invading cells

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8
Q

Neutrophil
(definition)

A

Major type of phagocytic cell in blood

Quickly move to infected tissues, where they use multiple mechanisms to destroy invading microbes

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9
Q

Opsonization
(definition)

A

Coating of an object with molecules for which phagocytes have receptors, making it easier for phagocytosis to occur

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10
Q

Pattern recognition receptors (PRRs)
(definition)

A

Proteins on or in cells that recognize specific compounds unique to microbes or tissue damage

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11
Q

Phagocyte
(definition)

A

Cell type that specializes in engulfing & digesting microbes & cell debris (phagocytosis)

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12
Q

Innate Immunity

  1. Response time
  2. Specificity
  3. Diversity
  4. Memory responses
  5. Self/non-self discrimination
  6. Soluble components of blood/tissue fluids
A
  1. Minutes/hours
  2. Specific for molecules/molecular patterns associated with pathogens
    (non-specific)
  3. Limited # of germ line-encoded receptors
  4. NO memory responses
  5. Perfect self/non-self discrimination
    (NO microbe-specific patterns in host)
  6. Many antimicrobial peptides & proteins
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13
Q

Adaptive Immunity

  1. Response time
  2. Specificity
  3. Diversity
  4. Memory responses
  5. Self/non-self discrimination
  6. Soluble components of blood/tissue fluids
A
  1. Days
  2. Highly specific
  3. Highly diverse (genetic recombination of receptor genes)
  4. Persistent memory (faster + greater response on subsequent infection)
  5. Very good self/non-self discrimination (occasional failures = autoimmune disease)
  6. Antibodies
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14
Q

Innate Immunity:
Major Cell Types

A
  1. Phagocytes
    - Monocytes
    - Macrophages
    - Neutrophils
  2. Natural killer (NK) cells
  3. Dendritic cells
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15
Q

Adaptive Immunity:
Major Cell Types

A
  1. T cells
  2. B cells
  3. Antigen-presenting cells (APCs)
    - Dendritic cells
    - B cells
    - Macrophages
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16
Q

1st Line of Defense

A
  1. Physical barriers
    - Skin
    - Mucous membranes
  2. Antimicrobial substances
    - Lysozyme
    - Peroxidase
    - Iron-binding proteins
    - Defensins
    - Complement proteins
  3. Normal flora
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17
Q

Physical Barriers:
Skin

A
  1. Dermis
    - Under epidermis
    - Tightly woven fibrous CT
    - Extremely tough
  2. Epidermis
    - Exposed to outside
    - Layers of epithelial cells
    - Keratin (water-repellant) embedded in outermost sheets of cells
    - Outer layers slough off
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18
Q

Physical Barriers:
Mucous Membranes

A

Lines digestive tract, respiratory tract, genitourinary tract
- Where exchanges occur (only 1 cell separates)

Mucous protects surface from infections
- Secretions wash microbes from surface

Mechanisms that move microbes toward elimination areas:
1. Peristalsis
2. Ciliated cells (mucociliary escalator)
3. Turnover/shed of mucosal epithelial cells

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19
Q

Physical Barriers:
Antimicrobial Substances

A
  1. Lysozyme
  2. Peroxidase
  3. Iron-binding proteins
  4. Defensins
  5. Complement proteins
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20
Q

Lysozyme

A

Enzyme that degrades PTG (cleaves)

More effective on G+ bacteria

Found in:
1. Tears
2. Saliva
3. Blood
4. Phagocytes

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21
Q

Peroxidase

A

Breaks down hydrogen peroxide to produce ROS
- Kills microbes on contact

Found in:
1. Saliva
2. Body tissues
3. Phagocytes

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22
Q

Iron-binding proteins

A

Sequesters iron from microorganisms
- Require iron to survive

  1. Lactoferrin
    - Saliva & phagocytes
  2. Transferrin
    - Blood & tissue fluid
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23
Q

Defensins

A

Antimicrobial peptides inserted into microbial membrane
- Kill on contact

Found in:
1. Mucous membranes
2. Phagocytes

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24
Q

Physical Barriers:
Normal Flora

A

Microorganisms found growing on body surfaces of healthy individuals
- NOT technically part of immune system

Provide protection through competitive exclusion:
1. Covers binding sites
2. Competes for nutrients
3. Stimulates immune response (exercise)
4. Directly kills other microbes (release toxic substances)

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25
Q

General Categories of Blood Cells

A
  1. Red blood cells (RBCs)
    - Non-living (no nucleus)
    - Carry O2 in blood
  2. Platelets
    - Fragments of megakaryocytes
    - Non-living (no nucleus)
    - Blood clotting
  3. White blood cells (WBCs)
    - Host defenses
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26
Q

4 Categories of WBCs

A
  1. Granulocytes (contain granules)
    - Eosinophils
    - Basophils
    - Neutrophils
  2. Mononuclear phagocytes
    - Monocytes
    - Macrophages
  3. Lymphocytes
    - B cells
    - T cells
  4. Dendritic cells
    (sentinels - 1st to notice infection & alert)
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27
Q

Macrophages

A

Derived from blood monocytes
- Migrate to tissue & differentiate
- Various names based on tissue found
- Present in nearly all tissues

Part of reticuloendothelial system (RES)

Phagocytize & digest engulfed material
- Clear microorganisms out of host
- Destruction of old/imperfect cells
- Often 1st to respond to invaders

2 major functions:
1. Phagocytosis
2. Antigen presentation (MHC II)

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28
Q

Macrophages:
Morphological Forms

A
  1. Kupffer cells - liver
  2. Alveolar macrophages - lungs
  3. Splenic macrophages - spleen
  4. Peritoneal macrophages - peritoneum
  5. Microglial cells - brain
  6. Osteoclasts - bone
  7. Mesangial cells - kidneys
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29
Q

Steps of Phagocytosis
(macrophages)

A
  1. Bacterium becomes attached to pseudopodia (membrane envaginations)
  2. Bacterium ingested, forming phagosome
  3. Phagosome fuses with lysosome
  4. Lysosomal enzymes digest captured material
  5. Digestion products released from cell (exocytosis)
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30
Q

Modes of Phagocyte Intracellular Killing:

A
  1. Antimicrobial species generated from O2 & N
    - ROS
    - RNS
  2. Acidification
    - pH within phagosome = 3.5-4.0
  3. Antimicrobial peptides (toxic)
    - Defensins
    - Cationic peptides
  4. Enzymes (cleave)
    - Lysozyme
    -Acid hydrolases
  5. Competitors (keep out nutrients)
    - Lactoferrin
  6. Vitamin B12 binding protein
31
Q

Reactive Oxygen Species (ROS):
Generated within Phagosome

A
  1. Superoxide anion (O2-)
  2. Hydroxyl radical (OH-)
  3. Hydrogen peroxide (H2O2)
  4. Hypochlorite anion (ClO-)
32
Q

Reactive Nitrogen Species (RNS):
Generated within Phagosome

A
  1. Nitric oxide (NO)
  2. Nitrogen dioxide (NO2)
  3. Peroxynitrite (ONOO-)
33
Q

Pattern Recognition Receptors:
Types

A
  1. Toll-like receptors (TLR)
  2. NOD proteins
34
Q

Toll-like Receptors (TOLR)

A

Located inside & outside cell

Recognize specific components of foreign invaders:
1. LPS
2. PTG
3. Flagellin
4. Bacterial nucleotide sequences

TLR engagement & induction sends signal to cell nucleus
- Gene expression
- Cytokines, chemokines, etc.

Present on phagocytes, endothelial cells, etc.

35
Q

Outside TLRs Recognize:

A
  1. Bacterial parasites (TLR1 & 2)
  2. G+ bacteria & fungi (TLR2 & 6)
  3. G- bacteria (TLR4)
  4. Flagellated bacteria (TLR5)
36
Q

Internal TLRs Recognize:

A
  1. Viral dsRNA (TLR3)
  2. Viral ssRNA (TLR7 & 8)
  3. Bacterial DNA elements (TLR9)
37
Q

NOD Proteins

A

Intracellular pathogen-recognition molecules

Recognize bacterial cell wall components (bacteria replicating in cytoplasm)

Mutation in NOD2 = predisposing factor in development of Crohn’s disease (inflammatory bowel disease)

38
Q

Receptors of the Innate Immune System

A
  1. Complement
  2. Mannose-binding lectin (MBL)
  3. C-reactive protein (CRP)
  4. Lipopolysaccharide (LPS) receptor & LPS-binding protein
  5. Toll-like receptors (TLR)
  6. NOD family receptors
  7. Scavenger receptors
39
Q

Complement Receptor
(location, target, effect)

A

Located in bloodstream & tissue fluids

Target microbial cell wall components

Effect of recognition:
1. Complement activation
2. Opsonization
3. Lysis

40
Q

Receptors of the innate immune system

Mannose-Binding Lectin (MBL) Receptor

(location, target, effect of recognition)

A

Located in bloodstream & tissue fluids

Targets mannose-containing microbial carbohydrates (cell walls)

Effect of recognition:
1. Complement activation
2. Opsonization

41
Q

Receptor of innate immune system

C-Reactive Protein (CRP)

(location, target, effect of recognition)

A

Located in bloodstream & tissue fluids

Targets phosphatidylcholine & pneumococcal polysaccharide
(microbial membranes)

Effect of recognition:
1. Complement activation
2. Opsonization

42
Q

LPS Receptor & LPS-Binding Protein
(location, target, effect of recognition)

A

Located in bloodstream & tissue fluids

LPS bound at cell membrane by complex of proteins (CD14, MD-2, TLR)

Targets bacterial LPS (G- cell wall)

Effect of recognition:
1. Delivery to cell membrane

43
Q

TLRs

A

Cell surface or internal compartments

Targets microbial components (NOT found in hosts)

Induces innate responses

44
Q

NOD Family Receptors

A

Intracellular

Targets bacterial cell wall components

Induces innate responses

45
Q

Receptors of the innate immune system

Scavenger Receptors (SRs)

(location, target, effect of recognition)

A

Located in cell membrane

Targets G-/G+ bacteria & apoptotic host cells

Induces phagocytosis or endocytosis

46
Q

Cytokines

A

Protein “messages”
- Bind to surface receptors
- Regulate cell function

Cytokine classes:
1. Chemokines
2. Colony-stimulating factors
3. Interferons
4. Interleukins
5. Tumor necrosis factor

47
Q

Chemokines

A

Chemotaxis

Enhance cell ability to migrate to infection site

48
Q

Colony Stimulating Factors

A

Important in multiplication & differentiation

Directs immature WBCs to correct maturation pathway (developmental factor)

49
Q

Interferons

cytokines

A

Important in control of viral infections

Associated with inflammatory response

Changes way cells respond to infection
(to enhance killing)

50
Q

Interleukins

cytokines

A

Produced mainly by WBCs

Important in innate & adaptive immunity

Changes way cells respond to infection
(to enhance killing)

51
Q

Tumor Necrosis Factor

A

Kills tumor cells

Initiation of inflammatory response

Changes way cells respond to infection
(to enhance killing)

52
Q

Chemotaxis:
Adhesion molecules

A

Allow cells to adhere to each other
- Responsible for recruitment of phagocytes to area of injury

Produced by endothelial cells in blood vessels
- Catch passing phagocytes
- Cause phagocytes to slow & leak out of vessels to area of injury

Neutrophils = 1st to arrive

53
Q

Initiation of Extravasation
(image)

A
  1. Selectin-mucin interactions mediate rolling
  2. Chemokines/chemoattractants induce change in integrins
  3. Integrins adhere firmly to ICAMs
54
Q

Functions of Complement Pathway

A
  1. Lysis of cells
    - MAC
  2. Opsonization
    - Promotes phagocytosis
    (enhances macrophage recognition)
  3. Binding to specific complement receptors on cells of immune system
    - Inflammation
    - Secretion of immunoregulatory molecules (ex: cytokines, chemokines, etc.)
    - Degranulation
    - Extravasation
  4. Immune clearance
    - Removes immune complexes from circulation & deposits in spleen/liver for disposal
55
Q

3 Pathways of Complement Activation

A
  1. Classical
  2. Alternative
  3. Lectin
56
Q

Classical Pathway

A

1st pathway discovered

Initiated by antigen-antibody complex
(Ab binding to microbe)
- Ag-Ab dependent (IgG or IgM)
- Requires suitable Ab bound to Ag & complement proteins 1, 4, 2, 3

Abs interact complement C1 (C1qrs)
- Activates protein & leads to activation of all complex proteins
- Activity limited by C1-esterase inhibitor (C1INH); prevents inappropriate activation of complement

Part of adaptive response

57
Q

Alternative Pathway

A

Initiated by binding of C3b to cell surfaces
- Regulatory proteins protect host cell surfaces
- Initiates activation of other complement proteins

Non-specific resistance against infection without antibody participation

Requires preformed C3b & factors B & D
- C3 always cleaving at low level
- Properdin helps stabilize complex

58
Q

Lectin Pathway

A

Initiated by binding of mannan-binding lectins to cell surfaces

3 proteins involved:
1. Mannan-binding lectin (MBL)/mannan-binding protein (MBP)
- Pattern recognition molecule
- Detects mannan found in microbial cells
2 & 3. Mannan-binding lectin-associated serine proteases
- MASP
- MADSP2

MBL interacts with MASP & MADSP2 (analogous to C1r & C1s)
- Generates complex analogous to C1qrs
- Leads to antibody-independent activation of classical pathway

59
Q

Complement System

A

Composed of 9 main proteins (C1-9)
- Numbered in order of discovery
(NOT activation)

Proteins split int a & b fragments after activation
- C3 spontaneously splits –> C3a & C3b
- C4a & C4b
- C5a & C5b

60
Q

Membrane Attack Complex (MAC)

A

Complexes of C5b, C6, C7, C8, & multiple C9
- Spontaneously assemble
- Donut shape

Creates pores in membranes
- Lysis of foreign cells
- Most effect on G- (little effect on G+)
- NON-SPECIFIC

61
Q

Biologically Active Components of Complement Activation

A
  1. Anaphylotoxins
    - C4a, C3a, C5a
    - Cause basophil/mast cell degranulation & smooth muscle contraction (anaphylaxis)
  2. Chemotactic factors
    - C5a & C3a
    - Potent activators of neutrophils, basophils, & macrophages
    - Causes induction of adhesion molecules on vascular endothelial cells
  3. Opsonins
    - C3b & C4b (on microorganism surface)
    - Attach to complement receptor 1 (CR1) on phagocytic cells
    - Promote phagocytosis
62
Q

Activation of Complement Leads to Major Protective Outcomes:

A
  1. Inflammation
  2. Lysis of foreign cells (MAC)
  3. Opsonization
63
Q

Unattended Activation of Complement Proteins Regulated by:

A
  1. Short half-life of some complement proteins
    - 100 us in fluid phase
  2. Specific host proteins that inactivate complement proteins
    - Serum proteins (DAF, Factor I, Factor H)
64
Q

4 Cardinal Signs of Inflammation

A
  1. Heat (calor)
  2. Pain (dolor)
  3. Redness (rubor)
  4. Swelling (tumor)

5 - loss of function (function laesa)

65
Q

Initiation of Inflammatory Process Leads to:

A
  1. Dilation of blood vessels
  2. Leakage of fluid from vessels
  3. Migration of leukocytes & phagocytes
66
Q

Rolling & Extravasation
(image)

A
  1. Rolling
  2. Activation
  3. Arrest/adhesion
  4. Transendothelial migration
67
Q

Inflammatory Process

A
  1. Pro-inflammatory mediators (cytokines) cause dilation of small blood vessels & increased blood flow
  2. Increased vascular permeability leads to leakage of fluid from blood vessels & accumulation of fluid in tissues (edema)
  3. Attraction of phagocytes causes cells to move to site of damage & inflammation
    - Diapedesis
    - Pus formation (dead neutrophils)
    - Clotting factors initiate clotting (entraps microbes)
68
Q

Factors that Initiate Inflammatory Response:

A
  1. Microbial products trigger TLRs of macrophages & other cells
    - Release of pro-inflammatory cytokines
    - TNF-alpha triggers liver synthesis of acute-phase proteins (C-reactive protein)
    - Facilitate complement activation & phagocytosis
  2. Microbial cell surface can trigger complement
    - Production of C3a & C5a
    - Mast cell release of pro-inflammatory cytokines & histamine
  3. Tissue damage
    - Enzymatic cascade initiates inflammation
    - Coagulation cascade
    - Kinin synthesis
    - Increased vascular permeability, endothelial cell adhesion, potent nerve stimulators (pain/itching)
69
Q

Inflammatory Response Triggered by Tissue Damage

A
  1. Tissue damage causes release of vasoactive & chemotactic factors
    - Trigger local increase in blood flow & capillary permeability
  2. Permeable capillaries allow influx of exudate & cells
  3. Phagocytes migrate to site of inflammation (chemotaxis)
  4. Phagocytes & antibacterial exudate destroy bacteria
70
Q

More Severe Consequences of Inflammation
(affects delicate systems)

A
  1. Arthritis
  2. Meningitis
    - Inflammation around brain/spinal cord
  3. Septic shock
    - Response to bloodstream infections with LPS (G- bacteria)
    - Fever, low BP, extensive tissue damage, wide-spread clot formation
    - Leads to disseminated intravascular coagulation (DIC)
71
Q

Fever

A

Host defense mechanism
- 1 of strongest indicators of infection (especially bacteria)

Temperature regulation center of body responds to fever-inducing cytokines
- Endogenous pyrogens (IL-1, TNF-alpha)

Inhibits growth of pathogens by:
1. Elevating body temp about max growth temp
2. Activating/speeding up other body defenses (immune response works better)

72
Q

Apoptosis

A

Programmed cell death
- Cells engulfed by macrophages
- Normally occurs during development

Cells undergo changes to signal macrophages:
1. Nuclear DNA degradation
2. Nuclear degeneration
3. Blebbing
4. Condensation

NO inflammatory response

73
Q

Necrosis

A

Death of tissue cells due to chemical/physical injury

Leaves extensive cellular debris
(must be removed by phagocytes)

Induces inflammation

Microbiology (15 decks)

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