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Semester 2 Infection > L4: Innate Immunity > Flashcards

L4: Innate Immunity Flashcards

1
Q

What factors determine the outcome of host-pathogen relationship?

A

Infection require patient and pathogen
Pathogen- infectivity –> ability of microbe to establish on or within the host
Patient- host immune response–> Essential in determining outcome of pathogen invasion
Mechanism of action- virulence –> capacity of microbe to do damage to the host

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2
Q

Which groups are most at risk of infection?

A

Elderly
Children
Pregnant women

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3
Q

Define immune system?

A

Cells and organs that contribute to the immune defences against infectious and non-infectious conditions (self vs non-self)

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4
Q

Define infectious disease?

A

When a pathogen suceeds in evading and/or overwhelming the host’s immune defences

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5
Q

What are the key roles of the immune system? How does it do this?

A

Pathogen recognition–> cell surface and soluble receptors
Containing/ eliminating the infection–> killing and clearance mechanisms
Regulating itself–> minimise damage to host
Remembering pathogens–> prevent disease from recurring

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6
Q

What are the two methods of response in the immune system?

A 
Innate--> Immediate --> prevent microorganisms getting in
--> fast (within seconds)
--> non specific
--> no memory 
--> no change in sensitivity 
Adaptive --> long lasting 
--> Slow (days)
--> Specific
--> Immunological memory 
--> Changes in sensitivity
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7
Q

What are the main first lines of defence?

A 
Physical barriers 
Physiological barriers
Chemical barriers 
Biological barriers
--> prevent entry and limit growth
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8
Q

What are the physical barriers?

A

Skin –> water tight, 1-2m surface area
Mucous membrane–> mouth, respiratory tract, GI tract and urinary tract–> traps pathogens
Bronchial cilia–> trap bacteria in mucous, mucocillary escalator up to mouth

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9
Q

What are the physiological barriers?

A

Symptoms that the patient presents with

  • Diarrhoea
  • Vomiting
  • Coughing
  • Sneezing

In response to pathogen to eliminate pathogen from body

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10
Q

What are the chemical barriers?

A 
Low pH --> point of entry
-Skin pH 5.5
-Stomach pH 1-3
-Vagina pH 4.4
Antimicrobial factors
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11
Q

What are the antimicrobial factors?

A
  • IgA (tears, saliva, mucous
  • Lysosomes (sebum, perspiration, urine)
  • Mucus (mucous membrane)
  • Beta-defensins (epithelium)
  • Gastric acid + pepsin
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12
Q

What are the biological barriers?

A

Normal flora

  • -> absent from internal organs/tissues
  • Compete with pathogens for attachment sites and resources
  • Produce antimicrobials and chemicals
  • Synthesis vitamins (K, B12 and other B vitamins)
  • Immune maturation –> stops immune system producing wrong response
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13
Q

What is the normal flora?

A

–> non pathological (unless they enter a new environment in the body)
–> strategic locations (nasopharynx, mouth/throat, skin, GI tract, vagina)
Helps normal body functions

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14
Q

What are the normal flora that inhabit the skin?

A 
Staphylococcus aureus
Staphylococcus epidermis
Streptoccoccus pyogenes
Candiba albicans 
Clostridium perfringens
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15
Q

What are the normal flora that inhabit the nasopharnyx?

A

Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus species

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16
Q

How does the normal flora lead to infection?

A

If it become displaced and enters a new body compartment –> infection
e.g. breaching the skin (burns, cuts, tattoos, injections, surgery), fecal-oral route (foodborne infection), Fecal-perineal-urethral route, poor dental hygiene (gets in through gums)

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17
Q

Which patients are at highest risk of serious infection?

A

Patients

  • without a spleen (asplenic or hyposplenic)
  • damaged or prosthetic valves
  • previous ineffective endocarditis
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18
Q

What else can causes normal flora to become pathogenic?

A

Overgrowth and host becomes immuno-compromised (diabetes, AIDS, malignant diseases, chemotherapy)
or
Flora is depleted in mucosal surfaces by antibiotic therapy –> intestine (severe colitis), vagina (thursh)

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19
Q

What is the second line of defence after the barriers have been breached?

A

Phagocytes and chemicals

–> contain and clear infection

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20
Q

What are the names of the main phagocytes?

A 
Macrophages
Monocytes 
Neutrophils 
Basophils
Eosinophils 
Natural killer cells 
Dendritic cells
21
Q

What are the key features about macrophages?

A

Present in all organs
Ingest and destroy microbes (phagocytosis)
Present microbial antigens to T cells (adaptive immunity)
Produce cytokines/chemokines

22
Q

What are monocytes? What is there function?

A

Precursor to macrophages
Present in blood (5-7%)
Recruited at infection site and differentiate into macrophages

23
Q

What is the main function of neutrophils?

A

Present in blood (60% of leukocytes)
Increased during infection
Recruited by chemokines to infection
Ingest and destroy progenitor bacteria (Staph aureus and Strep progenies)

24
Q

What are the functions of basophil/ mast cells?

A

Inflammation (vasomodulation)

Allergic response

25
Q

What are eosinophils used for?

A

Defence—> multicellular parasites(worms)

26
Q

What is the function of natural killer cells?

A

Kill abnormal host cells

27
Q

What do dendritic cells do?

A

Present microbial antigens to T cells (acquired immunity)

28
Q

How are pathogens (microbes) recognised?

A

Pathogen Associated Molecular pattern (PAMPs)
- Carbs, lipids, proteins, nuclei acids on surface
- 100 PAMPs (shared)
- Not in host
Phagocytes - Pathogen recognition receptors (PRRs)
- Best = Toll like receptor

29
Q

What is significant about PRRs?

A

Can recognised more than one PAMP

E.g. TLR4 (toll like receptor 4) —> lipopolysaccharide (LPS) Gram -ve bacteria and lipoteichoic acids gram +ve bacteria

30
Q

What other molecule helps with pathogen recognition?

A

Opsonins
Increase recognition ability
Opsonins receptor on phagocyte bind —> kill microbe

31
Q

Give some examples of the classes of opsonins? Give a few examples of each?

A

Complement proteins
- C3b , C4b

Antibodies
- IgG, IgM

Acute phase proteins

  • C reactive proteins
  • Mannose binding proteins
32
Q

What microbes is opsonisation essential for?

A

Encapsulated bacteria

33
Q

Why is the spleen so important for clearing infection?

A

Blood borne pathogens recognised and removed

Specialised macrophages attack encapsulated bacteria

34
Q

Describe the process of phagocytosis?

A

Chemotaxis and adherence of microbe to phagocyte
Microbe ingested
Forms phagosome
Phagosome fuses with lysosome —> phagolysosome
Digestion by enzyme
Residual body—> indigestible material
Discharge of waste material

35
Q

What are the two mechanisms for killing a microbe? Which one is the major pathway?

A 
Oxygen dependent pathway 
- major pathway 
- respiratory burst 
- Toxic o2 products for pathogens —> H2O2, OH•, NO, O•, hypohalite
Oxygen independent pathway 
- lysosomes 
- lactoferrin or transferrin 
- Cationic proteins (cathepsin)
- Proteolytic and hydrologic enzymes
36
Q

What is the final stage of the innate immune response?

A

Inflammation

- factors that will contain and clear the infection

37
Q

What are the complement pathways?

A

Contains 20 serum proteins
Activated by enzymatic cascade
Produces–> C1-C9 –> antimicrobial action

38
Q

What are the two activating pathways?

less important

A

2 activating pathways for the complement system
- Alternative pathway
(—> initiated by cell surface microbial constituents- endotoxins)
- MBL pathways
(—> initiated when MBL binds to mannose containing residues of proteins found on many microbes)

39
Q

What are the main products of the complement pathways?

A

C3a and C5a—> recruitment of phagocytes
C3b- C4b: opsonisation of pathogens
C5-C9: Killing of pathogens, membrane attack complex

40
Q

What cytokines are produced by macrophages?

A

TNFalpha
IL-1
IL-6

41
Q

What are the systemic effects of the cytokines?

A 
Liver (opsonins)
--> CRP
--> MBL (--> complement actvation)
Bone marrow
--> neutorphil mobilization 
Hypothalamus
--> ↑ body tempterature
42
Q

What are the local inflammatory actions?

A

Blood vessel–> vasodilation, vascular permeability and expression of adhesion molecules –> attraction of neutrophils

43
Q

Why do the vascular changes occur?

A 
Allow other cells to enter BV
- monocytes
-neutrophils
Increase blood flow to infection site
Allow more immune cells into tissue
44
Q

Give a brief summary of the innate immune system response?

A
  1. Innate barriers breached
  2. Complement, mast cells and macrophages activation (PRR)
  3. Vascular changes –> vasodilation/ ↑vascaular permeability, chemoattraction (neutrophils, monocytes (TNF, IL-8))
  4. Hypothalamus ↑thermostat= fever, Liver–> acute phase response
  5. Redness, heat, swelling and pain –> local inflammation
45
Q

What can cause decreased spleen function?

A

Asplenic patients

Hyposplenic patients

46
Q

What can cause the neutrophil number to reduce?

A

Cancer chemotherapy
Certain drugs (phenytoin)
Leukaemia and lymphoma

47
Q

What causes the neutrophil function to decrease?

A

Chronic granulomatous disease (No respiratory burst)

Chediak-Higashi syndrome (no phagolysosomes formation)

48
Q

Define the function of first lines of defence? and second lines of defence?

A

First line–> various barriers –> limit entry and growth of pathogens at portal of entry
Second line –> phagocytes/chemicals –> contain and eliminate the infection

Semester 2 Infection (20 decks)

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