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Microbiology and Immunology - SGUL (Sem 4) > Hypersensitivity reactions (asthma and allergy) > Flashcards

Hypersensitivity reactions (asthma and allergy) Flashcards

1
Q

How is hypersensitivity classified

A
  • Type 1: Immediate hypersensitivity
  • Type 2: Cytotoxic hypersensitivity
  • Type 3: Serum sickness and Arthus reaction
  • Type 4: Delayed-type hypersensitivity, contact dermatitis
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2
Q

Describe how type 1: Allergy mechanism works

A
  • Mediated by IgE
  • There is an interaction between mast cells, IgE and the allergens
  • causes degranulation and releases cytokines for an allergic response
  • Consequences are allergic rhinitis, Asthma and anaphylaxis
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3
Q

Describe what happens with systemic anaphylaxis

A
  • Severe localised oedema
  • Vey progressive reaction
  • Occlusion of airways and causes asphyxia
  • Treated with adrenaline (Epi-pen)
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4
Q

Describe how type 2 hypersensitivity mechanism works

A
  • Mediated by IgG (anti-drug antibodies)
  • Drug binds red blood cells or platelets and antibodies bind to the drug
  • Antibody-bound cells are cleared by macrophages and form complements
  • Leads to inflammation and disease
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5
Q

Explain how graves disease is an example of Type 2 hypersensitivity

A
  • IgG antibodies are made against the TSH receptor
  • IgG blocks receptor binding which results in the inhibition of the negative feedback cycle
  • Excess thyroid hormone is produced
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6
Q

Give some other examples of type 2 hypersensitivity

A
  • Myasthenia gravis
  • Newborn haemolytic disease
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7
Q

Describe how type 3 hypersensitivity mechanism works

A
  • Mediated by IgG
  • A soluble antigen comes in contact with antibodies
  • IgG and antigen form immune complexes
  • Immune complexes cleared by phagocytes
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8
Q

Describe how serum sickness is type 3

A
  • Caused by large
    intravenous doses of
    soluble antigens (e.g.
    drugs)
  • IgG antibodies produced
    form small immune
    complexes with the antigen
    in excess.
  • Immune complexes
    deposited in tissues e.g.
    blood vessel walls.
  • Iissue damage is caused
    by complement activation
    and the subsequent
    inflammatory responses
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9
Q

Describe how farmers lungs is an example of type 3

A
  • Hay or grain dust is inhaled into farmers lungs
  • Causes a type 3 hypersensitivity reaction
  • Inflamed lungs
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10
Q

Describe how type 4 hypersensitivity mechanism works

A
  • T-cell mediated response to antigens
  • T cell gets activated and activates macrophages which release chemokine, cytokine and cytotoxins
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11
Q

Explain the time-delayed nature of type 4 hypersensitivity

A
  • Takes time for T cell activation to happen and differentiate into effector cells to carry out the response
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12
Q

List some examples of type 4 hyper sensitivity reactions

A
  • Mantoux test
  • Tuberculoid leprosy
  • Contact dermatitis
  • Poison ivy
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13
Q

Describe the characteristic of the IgG antibody

A
  • First line of defence against worms
  • Binds FcεR1 receptor on mast cells
  • Pre-arms mast cells to react when in the
    presence of antigen
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14
Q

Describe the allergen-specific IgE production model

A
  • There is initial exposure to pollen
  • IL-4 drives B cells to produce IgE in response to pollen antigens
  • Pollen specific IgE binds to mast cells
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15
Q

What factors determine allergen sensitivity

A
  • Nature of allergen
  • Dosage of Allergen
  • Timing
  • Location of priming
  • Role of pro-allergic dendritic cells and cytokines
  • genetic predisposition to allergy
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16
Q

What are some characteristics of common allergens

A
  • Examples include: dust mites, pollens and cockroaches
  • Named after the source organism and the order of discovery
  • Allergens have common functionalities such as proteases
  • Normally received in small doses
  • High-dose exposure may lead to tolerance
17
Q

What are filaggrin and atopic dermatitis

A
  • Filaggrin links skin integrity
    and allergy
  • When it is defective atopic dermatitis is greater
  • This is due to the access for allergens
18
Q

What makes dendritic cell pro-allergic

A

Not Known but One Candidate Protein is TSLP This may switch DC to a ‘pro- allergic’ state

19
Q

What happens to mast cells when activated by allergens

A
  • Resting mast cell contains granules containing histamine and other inflammatory mediators
  • Multivalent antigen cross-links bound IgE antibody causes release of granule contents
20
Q

What causes early and late phase allergic response

A
  • Early phase is immediate and mediated by mast cells
  • The late phase is delayed and is mediated by T cells
21
Q

What effector mediators are produced by mast cells in the early phase

A
  • Histamine - Increases vascular permeability and cause smooth muscle contraction
  • Leukotrienes - increase vascular permeability, smooth muscle contraction and stimulate mucus secretion
  • Prostaglandins - chemoattractant for T cells, eosinophils and basophils
22
Q

What effector mediators are produced by mast cells in the late phase

A

Cytokines:

  • IL-4 and IL-13 - promotes Th2 and IgE
  • TNF-a - promotes tissue inflammation
23
Q

what are the effects of mast cell activation the GI tract

A
  • Increased fluid secretion
  • Increased peristalsis
  • Causes expulsion of GI tract contents
24
Q

What are the effects of mast cell activation on the airways

A
  • Decreased diameter
  • Increased mucus secretion
  • Congestion and blockage of airways
  • Swelling and mucus secretion in nasal passages
25
Q

What are the effects of mast cell activation on blood vessels

A
  • Increased blood flow
  • Increased permeability
  • Increased fluid in tissues causing increased flow of lymph to lymph nodes
  • Increased cells and protein in tissue
  • Increased effector response in tissues
26
Q

what are the effector function of eosinophils

A
  • Release highly toxic granule proteins and free radicals upon activation to kill microorganisms/par sites and cause tissue damage in allergic reactions.
  • Synthesise and release prostaglandins, leukotrienes and cytokines in order to amplify the inflammatory response by activating epithelial cells and recruiting leukocytes.
27
Q

Describe the late phase of the IgE mediated allergic response

A
  • Late-phase reaction is dependent on
    allergen dose
  • Continued synthesis and release of
    inflammatory mediators
  • Chronic allergic inflammation caused by Th2 cells i.e. a type IV hypersensitivity
    reaction
28
Q

what is Asthma

A

A State of reversible bronchial hyper reactivity resulting from a persistent inflammatory process in response to a number of stimuli in a genetically susceptible individual

29
Q

List some characteristics of asthma

A
  • episodes of wheezy breathing
  • narrowing of the airways
  • rapid changes in airway obstruction
  • severity varies
  • slight wheeziness to asthma attack

common allergens causing asthma include:

  • pollen
  • HDM
  • plants
  • some foods
30
Q

Describe the acute response to allergic asthma

A
  • occurs within seconds of allergen exposure
  • results in airway obstruction and breathing difficulties
  • caused by allergen-induced mast cell degranulation in the submucosa of the airways
31
Q

Describe the chronic response to allergic asthma

A
  • chronic inflammation of the airways
  • caused by activation of eosinophils, neutrophils, T cells and other leukocytes
  • mediators released by these cells cause airway remodelling, permanent narrowing of the airways, and further tissue damage
32
Q

how can we treat asthma

A
  • inhibit effects of mediators on specific receptors: anti-histamine (block the histamine H1 receptor)
  • inhibit mast cell degranulation: mast cell stabilizer (e.g. chromoglycate)
  • inhibit synthesis of specific mediators: lipoxygenase inhibitors (e.g montelukast)

Microbiology and Immunology - SGUL (Sem 4) (30 decks)

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