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Infection and Immunity > Innate immunity and inflammation > Flashcards

Innate immunity and inflammation Flashcards

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1
Q

Inflammation defn

A

The local accumulation of fluid, plasma proteins & WBCs in response to injury or infection

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2
Q

What are the 5 characteristics of inflammation

A
  • Redness
  • Swelling
  • Pain
  • Heat
  • Loss of function
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3
Q

Function of heat in inflammation

A

Increased temp can kill pathogen

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4
Q

Function of pain in inflammation

A

Draws attention to infection & may immobilise that part of the body

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5
Q

Function of redness in inflammation

A

Vasodilation allows increased blood flow to site of infection, facilitating delivery of effector molecules and cells

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6
Q

Function of swelling in inflammation

A

Movement of leukocytes into infected tissues eg. blisters full of pus are dead leukocytes

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7
Q

What occurs in the initiation of inflammation

A

When the pathogen binds to cells which causes the release of inflammatory mediator

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8
Q

What are the inflammatory mediators released

A
  • Lipid mediators - prostaglandins, leukotrienes and platelet activation factor
  • Chemokines
  • Cytokines - TNFs
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9
Q

What is the function of chemokines in inflammation?

A

Attract other cells; chemoattractant

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10
Q

What is the function of cytokines in inflammation?

A

It activates other cells

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11
Q

What does injury to blood vessels cause?

A

Activates enzymes cascades in the blood
- Kinin system
- Blood clotting system (prevent spread of bacteria)

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12
Q

What does the binding of complement proteins to pathogens cause?

A

Bacterial cell lysis, phagocyte activation and inflammation

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13
Q

Which cells have pathogen recognition receptors (PRRs)?

A

Cells of in the innate immune system eg macrophages, neutrophils and dendritic cells.

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14
Q

Where are pathogen-associated molecular patterns (PAMPs) present?

A

In microorganisms but not host’s cells

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15
Q

What do PAMPs trigger?

A

Triggers infectious pathogen-induced inflammatory response

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16
Q

When are DAMPs produced?

A

In response to cell damage

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17
Q

What do DAMPs trigger?

A

Non-infectious inflammatory response

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18
Q

Give four examples of major PAMPs

A
  1. Lipopolysaccharide (LPS)
  2. dsRNA
  3. Bacterial DNA
  4. Bacterial Flagellin
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19
Q

3 examples of DAMPs

A
  • HMGB1
  • Presence of DNA/RNA outside nucleus or mitochondrion
  • Extracellular purine metabolites – ATP, adenosine uric acid
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20
Q

8 pathogen recognition receptors

A
  • Cell-surface & intracellular signaling receptors – initiate immune responses to deal with specific pathogens
  • Toll-like receptors
  • NOD-like receptors
  • RIG-I-like receptors
  • Serum receptors – trigger complement activation
  • Mannose binding lectin
  • Receptors that induce phagocytosis
  • Dectin-1
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21
Q

Give the process of the activation of TLR-4 (Toll-like receptor 4) (Pathogenic components binding to TLR-4)

A
  1. LPS (found on pathogens), together with the help of LPS-binding protein & CD14, is recognised by TLR-4 present on macrophages or dendritic cells.
  2. Activation of macrophages or dendritic cells
  3. Activation of transcription factors eg. NFKB, AP-1 & IRF
    a. NFKB and AP-1 (activation factor-1)
    - Transcription of cytokines that stimulate inflammation
    b. IRFs (interferon regulatory factors)**
    - Cytokines production (eg. interferon-α and –β) to inhibit viral replication
  4. Innate immune response – inflammation where activated macrophages/dendritic cells produce
    a. Chemokines: attract other cells to site of infection
    b. Cytokines: activate vascular endothelium & neutrophil production, raise body temperature, promote blood clotting, activate the adaptive immune system
    c. Costimulatory molecules: activate the adaptive immune system
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22
Q

Function of NOD1 and NOD2 (types of NOD-like receptors)

A

Recognise bacterial peptidoglycans and activate NFkB

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23
Q

NALP3 function and when

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A

Forms the inflammasome complex in response to cellular stress (efflux of K+), such as infection, & proteolytically activates IL-1β and IL-18

24
Q

Function of RIG-I-like helicases

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A

Sense viral mRNA in cytoplasm

25
PAMP binding with RIG-I-helicases causes...
Activation of IRF-3 resulting in the production of IFN-α & -β
26
Explain the PRRs acting via the complement system post activation
A series of plasma proteins are activated at the site of infection through a triggered enzyme cascade, where the product of one reaction is the catalyst for the next. Many are proteases and they are activated by proteolytic cleavage of precursor proteins.
27
What are the three pathways and 3 main consequences of complement activation?
- Inflammation: recruitment of inflammatory cells - Phagocytosis: opsonisation of pathogens - Cell membrane disruption: killing of pathogens
27
What are the three pathways and 3 main consequences of complement activation?
- Inflammation: recruitment of inflammatory cells - Phagocytosis: opsonisation of pathogens - Cell membrane disruption: killing of pathogens
28
Diagram of pathways that lead to complement activation and their consequences
29
Which receptors can induce phagocytosis (5)
- Lipid receptors – bind to lipid components of pathogens - Complement receptors – bind to complement coated microbes - Mannose receptors - Glucan receptors (dectin-1) - Scavenger receptors
30
What occurs upon the binding of pathogen to the receptor? (phagocytosis)
The phagocyte internalises the pathogen and then other enzymes, defensins, reactive oxygen intermediates & reactive nitrogen intermediates break down the pathogen within the phagosome.
31
What happens when some of the pathogens bind to the PRR in phagocytosis?
Induces gene expression for secretion of cytokine, activating the process of inflammation. (meaning that macrophages and dendritic cells activated by pathogens secrete cytokines)
32
What are cytokines?
Small proteins released by cells that induce responses in other cells by binding to specific receptors.
33
Effect of IL-1
* Stimulate production by liver of acute phase proteins, such as C-reactive protein (important reactive inflammatory marker), mannan-binding lectin & pulmonary surfactants * Bind to pathogens but not host cells * Opsonise pathogens for phagocytosis * Activate complement * Induce the release of neutrophils from bone marrow into blood and activation of lymphocytes * Induce vasodilation and increase vascular permeability, allowing recruitment of leukocytes * Promote energy metabolism to increase body temperature
34
Effects of IL-8 (CXCL 8)
Attracts cells expressing chemokines receptors eg. neutrophils to site of infection
35
Effects of IL-12
* Activates natural killer cells & cytotoxic lymphocytes * Kill virus-infected and tumour cells by releasing perforin which makes a pore in the target cell membrane. Granzymes enter this pore & induce cell death by apoptosis
36
Effects of IFN-α & IFN-β (Anti-viral cytokines)
* Produced by many cell types following infection by viruses * Produced in response to dsRNA * Bind to a common receptor which signals the synthesis of several proteins that disrupt viral replication * Induce expression of major histocompatibility complex (MH) class I, which presents the virus for specific recognition by the adaptive immune system * Activate NK cells
37
What is the function of the innate immune system?
Causes inflammation
38
What are the mechanisms used by the body to prevent the entrance of pathogens?
- Mechanical barriers - Chemical barriers - Microbiological
39
What are mechanical barriers ?
Mucus membrane and tight junctions between cells.
40
What are the chemical barriers?
- Acidic pH in stomach - Defensins - Mucins to prevent adherence - Antibacterial and antifungal peptides - Surfactants which coat pathogens to facilitate phagocytosis
41
What is the microbiological aspect that helps as a protection barrier?
The normal flora of the gut (microbiota) competes with the pathogens for nutrients and for attachment sites on the epithelium.
42
What are toll-like receptors
Single membrane spanning, non-catalytic receptors.
43
What are toll-like receptors
Single membrane spanning, non-catalytic receptors.
44
Where are toll-like receptors usually found?
On macrophages and dendritic cells.
45
What to TLRs recognise?
Structurally conserved molecules derived from microbes ep, lipids, lipoproteins, HSPs, LPS
46
What does TLR binding activate?
Transcription factors: NF-kB , AP-1 and IRF
47
Function of NF-kB and AP-1
They induce the transcription of cytokines
48
IRF function
Activates interferon alpha and beta to inhibit viral replication
49
What are interferons? (incl function)
Signalling proteins released by host cells in response to pathogens and tumour cells to stimulate other cells to heighten their defences.
50
How many TCRs are there in humans?
10
51
Which TCRs exist on the inner surface of endosomes?
3,7,9 - the rest are on the cell surface
52
Function of NOD1 and NOD2
Recognise bacterial peptidoglycans and activate NF-kB in response
53
RIG-I-like helicases function
Sense viral mRNA in the cytoplasm to activate IRF3 to stimulate IFN and .
54
Serum receptors (mannose binding lectin) function
Trigger complement activation

Infection and Immunity (3 decks)

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