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PHARM 310 > Body's Defenses Against Infection > Flashcards

Body's Defenses Against Infection Flashcards

1
Q

What are the 4 types of Body Defenses against Infection

A
  1. Physical Barriers to prevent infection
  2. Innate Immune mechanisms of defense
  3. Adaptive Immune responses
  4. Immunological memory that lessen the impact of subsequent encounters of same pathogens
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2
Q

Direct Pathogen Mechanisms of Tissue Damage

A
  1. Exotoxin Release
    - Acts at cell surface
  2. Endotoxin Release
    - Released after phagocytic digestion
    - Results in cytokine secretion (Causing pyrogenic leaky vessels)
  3. Direct Cell Killing
    - Results in cell loss
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3
Q

Indirect Pathogen Mechanisms of Tissue Damage

A
  1. Antigen:Antibody Immune Complexes
    - Results in Kidney, Blood Vessel, and Joint damage through inflammation
  2. Autoimmune Conditions caused by self-antibodys
    - Cross specificity of pathogen antigens with self antigens
  3. Tissue damage
    - Inflammatory cells release damaging mediators and debris
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4
Q

Extracellular Host Defenses
- Interstitial spaces, Blood, Lymph

A
  • Antibodies (IgG)
  • Complements
  • Phagocytosis
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5
Q

Extracellular Host Defenses
- Epithelial Spaces

A
  • IgA antibodies
  • Cells secreting antimicrobial peptides
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6
Q

Intracellular Host Defenses
- Cytoplasmic

A
  • Cytotoxic T-Cells
  • NK Cells
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7
Q

Intracellular Host Defenses
- Vesicular

A
  • Activated Macrophages
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8
Q

What are the different kinds of Epithelium as a barrier?

A

Mechanical
- Tight junctions
Chemical
- Enzymes and pH modulations
Microbiological
- Bacterial Commensalism, where bacteria in body competes with foreign bacteria for nutrients

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9
Q

Where are Mechanical Barriers found

A

Epithelial Cells joined by tight junctions
- Skin, Gut, Lung, Eye/Nose

Longitudinal flow of air or fluid
- Skin, Gut

Movement of mucus by cilia
- Lung

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10
Q

Where are Chemical Barriers found

A

Fatty Acids
- Skin

Low pH
- Gut

Enzymes (Pepsin)
- Gut

Antibacterial Peptides (Defensins)
- Skin, Gut, Lungs

Salivary Enzymes (Lysozymes)
- Eye/Nose

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11
Q

Where are microbiological barriers found

A

Normal Flora
- Skin, Gut

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12
Q

What happens when a macrophage receptor is activated

A

Triggers cytokine production

Triggers further leukocyte recruitment

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13
Q

What kinds of Cytokines are secreted by Macrophages

A

IL-1 Beta
TNF-Alpha
IL-6
CXCL8
IL-12

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14
Q

Function of IL-1 Beta

A

Local Effects
- Activates Vascular Endothelium
- Activates Lymphocyte
- Local Tissue destruction
- Increases access of effector cells

Systemic Effects
- Fever
- Production of IL-6

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15
Q

Function of TNF-Alpha

A

Local Effect
1. Increases vascular permeability
2. Increased entry of IgG, Complement, and Cells to tissues
3. Increased drainage of fluid to lymph nodes

Systemic Effects
- Fever
- Mobilization of metabolites
- Shock

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16
Q

Function of IL-6

A

Local Effects
- Lymphocyte activation
- Increased Antibody production

Systemic Effects
- Fever
- Induces acute-phase protein production by hepatocytes

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17
Q

Function of CXCL8

A

Local Effects
- Chemotactic factor that recruits neutrophils, basophils, and T-Cells to site of infection

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18
Q

Function of IL-12

A

Local Effects
- Activates NK Cells
- Induces differentiation of CD4 T Cells into T-Helper 1 Cells

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19
Q

Induction of Last Pathway of Complement Process

A
  1. Bacteria binds to Macrophage’s receptors
  2. Macrophage secretes IL-1 beta cytokine
  3. IL-1 produces IL-6
  4. IL-6 induces the liver to produce acute-phase proteins
  5. Acute-phase proteins induce the last pathway of complement
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20
Q

What are the two kinds of Chemokinds

A

CC Chemokines
- Produced by leukocytes
- Recruits monocytic cells like NK and T-Cells

CXC Chemokines
- Produced by a wide variety of cells
- Recruits primarily Neutrophils

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21
Q

Sepsis Process

A
  1. Bacteria enters systemic blood (Bacteremia)
  2. Liver Macrophages (Kupffer Cells) are activated by LPS
  3. Liver Macrophages start to secrete pro-inflammatory cytokines into bloodstream
  4. Causes widespread coagulation and organ failure (Septic Shock)
22
Q

Local vs Systemic Infection

A

Local Infection
- Macrophages in tissue are activated and release TNF-alpha
- Release of plasma proteins
- Increased Phagocytosis
- Increased Platelet adhesion to blood vessel wall
–> Infection if contained and antigens are drained/carried to lymph node

Systemic Infection
- Macrophages in liver are activated and release TNF-alpha
- Fluids leak into tissue (systemic edema), less blood volume in central compartment causing collapse of vessels
- Disseminated Intravascular Coagulation (DIC) leads to wasting and multiple organ failure (Septic Shock)

23
Q

Condition which is the main cause of Septic Shock

A

Disseminated Intravascular Coagulation (DIC)
- Basically widespread intravascular coagulation

24
Q

What are the two types of phagocytes

A

Macrophages
- Long Lived
- Tissue Resident
- Secretes Cytokine Mediators

Neutrophils
- Short Lived
- More abundant in numbers
- Recruited by cytokine mediators released at site of infection

25
Q

Neutrophil Recruitment Process

A
  1. Cytokines induce selectin expression on vascular endothelium
  2. These selectins hook on to sialyl-Lwisx glycoproteins on neutrophil
  3. Induces leukocyte rolling
  4. ICAMs on endothelium bind to cellular integrins (LFA-1) on neutrophils
  5. Neutrophils migrate to infection through CXC chemokine gradient
26
Q

Neutrophil Effector Functions

A

Binds to microbes and induces phagocytosis and microbial killing

Myeloperoxidase
- Uses Respiratory Burst where NADPH oxidase reduce O2 to Oxygen Free Radical and then H2O2
- Myeloperoxidase combines H2O2 with Cl- to produce hypochlorite/hypohalite

Phagosomes
- Phagosome fuses with neutrophil granules and lysosomes packed with enzymes and peptides that help disrupt microbes

27
Q

Fate of Neutrophil

A
  1. Dies by apoptosis
  2. Throws out a DNA NETs (Neutrophil Extracellular Traps)
  3. These DNA NETs are decorated with cationic proteins that trap and kill pathogens
  4. Macrophages clean up dead neutrophils and any debris from phagocytosis
    5.Activated macrophage then secretes cytokines producing lots of different systemic/local effects
28
Q

Inflammatory Cytokines Body Heat Mechanism

A

Acts on hypothalamus to raise body temperature (IL-1, TNF-alpha) causing fever (pyrogenic)
- Increases metabolism to burn more energy creating heat

29
Q

Inflammatory Cytokines Activating Liver Production of Acute Phase Proteins Mechanism

A
  1. IL-1 increases production of IL-6
  2. IL-6 activates hepatocytes causing production of acute-phase proteins
    - C-reactive protein (CRP)
    - Mannose Binding Lectin (MBL)
30
Q

C-Reactive Protein function

A
  1. Binds phosphorylcholine on bacteria surfaces
  2. Acts as an opsonin (tags the bacteria) and as a complement activator
31
Q

Mannose-Binding Lectin function

A
  1. Binds to residues on bacterial surface
  2. Acts as an opsonin (tags the bacteria) and as a complement activator
32
Q

Complement Pathway
- Lectin Pathway vs other pathways

A
  1. MBL binds foreign surface
  2. MASP1 and MASP2 binds MBL
  3. Generates C1-like complex
  4. C1 cleaves C4 just like in Classical/Alternative Pathway pathway
33
Q

Inflammatory Cytokines Actions and Result
- Liver

A

IL-1/IL-6/TNF-alpha causes production of acute phase proteins
- CRP and MBP

  • Activates the complement system
  • Also opsonizes bacteria
34
Q

Inflammatory Cytokines Actions and Result
- Bone-Marrow Endothelium

A

IL-1/IL-6/TNF-alpha causes Neutrophil mobilization

  • Neutrophils then phagocytosis bacteria
35
Q

Inflammatory Cytokines Actions and Result
- Hypothalamus

A

IL-1/IL-6/TNF-alpha causes an increase in body temperature

  • Decreases bacterial/viral replication
  • Increased antigen processing
  • Facilitates adaptive immune response
36
Q

Inflammatory Cytokines Actions and Result
- Fat, Muscle

A

IL-1/IL-6/TNF-alpha causes protein and energy to mobilize to generate more body heat

  • Decreases bacterial/viral replication
  • Increased antigen processing
  • Facilitates adaptive immune response
37
Q

Inflammatory Cytokines Actions and Result
- Dendritic Cells

A

TNF-alpha stimulates migration to lymph nodes and maturation

  • Initiates the adaptive immune response
38
Q

What are Virally-Induced Cytokines

A

When human cells are infected by a virus they are then stimulated to produce Type 1 Interferons

39
Q

Type-I Interferons vs Type-II Interferons

A

Type-II Interferons are secreted by effector lymphocytes

Type-I Interferons are secreted by virally infected human cells

40
Q

Type I Interferon Function

A

Two types
- Interferon-alpha
- Interferon-beta

  • Interferes with viral replication
  • Sends signals to IFN Type 1 Receptors on adjacent cells to prepare their defenses (Both autocrine and paracrine)
41
Q

What cells have IFN Type 1 Receptors

A

All cells

42
Q

Interferon I Response

A
  • Induces resistance to viral replication in all cells
  • Increases MHC Class I Expression and Antigen presentation in all cells (Cytotoxic Cells)
  • Activate NK cells to kill virus-infected cells
43
Q

Time it takes for each defense mechanism in viral infection

A

1st: Production of IFN-Alpha, IFN-Beta, TNF-alpha, and IL-12

2nd: NK Cells kill infected cells

3rd: T-Cell kill infected cells
- Has the longest lag phase

44
Q

B1 B Cells Function

A

Subpopulation of B-Cells
- Has a nonconventional surface phenotype

More for rapid response to infection (Does not have gene switching so can have a faster response)

B1 cells have a general affinity for bacterial polysaccharide antigens

45
Q

Gamma:Delta T-Cells Function

A

Subpopulation of T-Cells
- Has a nonconventional surface phenotype

More for rapid response to infection (Does not have gene switching so can have a faster response)

γ:δ T-Cells secrete cytokines and develops cytotoxic function

46
Q

B1 Cell Process

A
  1. B1 B Cell binds to bacteria cell wall (polysaccharide)
  2. B1 Cell is then activated by IL-5
  3. B1 Cell then secretes IgM anti-polysaccharide antibody
    4.IgM then binds to polysaccharide capsule
  4. Activation of complement and removal of bacteria
47
Q

What produces Immunological Memory

A
  • Clones of long-lived B and T Cells
  • Circulating Antibodies
48
Q

What is immunological memory

A

After the primary immune response has cleared the infection a long-term protective immunity is established
- Provokes a faster and stronger secondary immune response when encountering the same infection

49
Q

Immunological memory process

A
  1. Naive B and T cells are activated by an infecting pathogen
  2. Most activated cells become short-lived effector cells
  3. Some activated cells become long-lived memory cells
50
Q

What is Original Antigenic Sin

A

When the body first encounters a viral antigen for the first time it will focus on any antigens it has seen before and constrain any new processing of unknown antigens
- Will ignore all other antigens and only make antibodies for the original antigen

Antigens you first see will constrain your ability for highly mutable viruses later

51
Q

What kind of organisms can evade adaptive immunity

A

Highly mutable viruses only present very little of the original antigen
- However, the body will prioritize antigens it has seen before and will constrain any processing for new antigens

52
Q

When will the immune system make antibodies for new epitopes

A

When any of the original epitopes are present
- Minimal response to new epitopes

When all of the original epitopes are present
- Primary response to new epitopes

PHARM 310 (7 decks)

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