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Infection and Immunity > Innate immunity and inflammation > Flashcards

Innate immunity and inflammation Flashcards

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

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

A

Sense viral mRNA in cytoplasm

25
Q

PAMP binding with RIG-I-helicases causes…

A

Activation of IRF-3 resulting in the production of IFN-α & -β

26
Q

Explain the PRRs acting via the complement system post activation

A

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
Q

What are the three pathways and 3 main consequences of complement activation?

A
  • Inflammation: recruitment of inflammatory cells
  • Phagocytosis: opsonisation of pathogens
  • Cell membrane disruption: killing of pathogens
27
Q

What are the three pathways and 3 main consequences of complement activation?

A
  • Inflammation: recruitment of inflammatory cells
  • Phagocytosis: opsonisation of pathogens
  • Cell membrane disruption: killing of pathogens
28
Q

Diagram of pathways that lead to complement activation and their consequences

A
29
Q

Which receptors can induce phagocytosis (5)

A
  • Lipid receptors – bind to lipid components of pathogens
  • Complement receptors – bind to complement coated microbes
  • Mannose receptors
  • Glucan receptors (dectin-1)
  • Scavenger receptors
30
Q

What occurs upon the binding of pathogen to the receptor? (phagocytosis)

A

The phagocyte internalises the pathogen and then other enzymes, defensins, reactive oxygen intermediates & reactive nitrogen intermediates break down the pathogen within the phagosome.

31
Q

What happens when some of the pathogens bind to the PRR in phagocytosis?

A

Induces gene expression for secretion of cytokine, activating the process of inflammation. (meaning that macrophages and dendritic cells activated by pathogens secrete cytokines)

32
Q

What are cytokines?

A

Small proteins released by cells that induce responses in other cells by binding to specific receptors.

33
Q

Effect of IL-1

A
  • 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
Q

Effects of IL-8 (CXCL 8)

A

Attracts cells expressing chemokines receptors eg. neutrophils to site of infection

35
Q

Effects of IL-12

A
  • 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
Q

Effects of IFN-α & IFN-β (Anti-viral cytokines)

A
  • 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
Q

What is the function of the innate immune system?

A

Causes inflammation

38
Q

What are the mechanisms used by the body to prevent the entrance of pathogens?

A
  • Mechanical barriers
  • Chemical barriers
  • Microbiological
39
Q

What are mechanical barriers ?

A

Mucus membrane and tight junctions between cells.

40
Q

What are the chemical barriers?

A
  • Acidic pH in stomach
  • Defensins
  • Mucins to prevent adherence
  • Antibacterial and antifungal peptides
  • Surfactants which coat pathogens to facilitate phagocytosis
41
Q

What is the microbiological aspect that helps as a protection barrier?

A

The normal flora of the gut (microbiota) competes with the pathogens for nutrients and for attachment sites on the epithelium.

42
Q

What are toll-like receptors

A

Single membrane spanning, non-catalytic receptors.

43
Q

What are toll-like receptors

A

Single membrane spanning, non-catalytic receptors.

44
Q

Where are toll-like receptors usually found?

A

On macrophages and dendritic cells.

45
Q

What to TLRs recognise?

A

Structurally conserved molecules derived from microbes ep, lipids, lipoproteins, HSPs, LPS

46
Q

What does TLR binding activate?

A

Transcription factors: NF-kB , AP-1 and IRF

47
Q

Function of NF-kB and AP-1

A

They induce the transcription of cytokines

48
Q

IRF function

A

Activates interferon alpha and beta to inhibit viral replication

49
Q

What are interferons? (incl function)

A

Signalling proteins released by host cells in response to pathogens and tumour cells to stimulate other cells to heighten their defences.

50
Q

How many TCRs are there in humans?

A

10

51
Q

Which TCRs exist on the inner surface of endosomes?

A

3,7,9 - the rest are on the cell surface

52
Q

Function of NOD1 and NOD2

A

Recognise bacterial peptidoglycans and activate NF-kB in response

53
Q

RIG-I-like helicases function

A

Sense viral mRNA in the cytoplasm to activate IRF3 to stimulate IFN and .

54
Q

Serum receptors (mannose binding lectin) function

A

Trigger complement activation

Infection and Immunity (3 decks)

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