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CVR Lectures > Host Defence in the lung 1 > Flashcards

Host Defence in the lung 1 Flashcards

1
Q

How do we maintain a healthy lung?

A
  • The airways are not sterile
  • We inhale particulate matter regularly, e.g. fossil fuel from vehicle exhausts, fossil fuel stoves
  • The surprise is that the lung is not permanently inflamed
  • Crucial role for the respiratory epithelium in suppressing alveolar macrophage activation in health, which is lost in disease
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2
Q

What is an acute inflammation?

A
  • Vasodilation leads to plasma (including antibodies) to escape blood vessels
  • This activates biochemical cascades e.g. coagulation cascades
  • This means leukocytes move into the tissues (mainly neutrophils but also some monocytes) because of an increase in blood flow
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3
Q

What is acute inflammation traditionally characterised by?

A
  • Calor (hot)
  • Rubor (red)
  • Dolor (painful)
  • Tumor (Swollen)
  • Functio laesa (loss of function, Galen)
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4
Q

Why is inflammation good and bad?

A

Inflammation is our defence against infection and a hostile environment
BUT
Many of us will die of diseases caused by inflammatory processes

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5
Q

How many people are affected by pneumonia per year in the UK?

A

250,000 adults

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6
Q

What is an example of Inflammation-mediated tissue damage in the lung?

A

COPD (chronic obstructive pulmonary diseases)
- Repeated inflammation of the lungs
- Normally due to smoking

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7
Q

What is ARDS?

A

Acute Respiratory Distress Syndrome
- Respiratory failure
- Water and neutrophils fill the alveoli
- Leads to a multi-system failure
- Normally comes from trauma, lung infection, sepsis, surgery…

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8
Q

What physiologically happens when someone has ARDS?

A
  • Endothelial leak: leading to extravasation of protein and fluid
  • Lungs: reduced compliance, increased shunting (blood not flowing through the normal pathway)
  • Heart: pulmonary hypertension, reduced cardiac output
  • Hypoxia
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9
Q

Where is acute inflammation initiated?

A

In the tissues, by epithelial production of hydrogen peroxide and release of cellular contents

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10
Q

What is acute inflammation amplified by?

A
  • Kupffer cells (liver)
  • Alveolar macrophages (lung)
  • Histiocytes (skin, bone)
  • Dendritic cells
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11
Q

How does acute inflammation respond to pathogens?

A

Respond to pathogens or to tissue injury by recognising:
- PAMPs (pathogen-associated molecular patterns)
- DAMPs (damage-associated molecular patterns)

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12
Q

What are Pattern recognition receptors (PRRs)?

A

Signalling Toll-like receptors (TLRs)
Nod-like receptors (NLRs)

Endocytic Mannose receptors
Glucan receptors
Scavenger receptors

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13
Q

What is an innate immune response?

A

Recognises things as foreign that the body has never seen before

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14
Q

What is an adaptive immune response?

A

Specific to a certain foreign pathogen. Has seen it before and knows how to target it (memory)

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15
Q

What are Toll-like receptors?

A
  • Recognise conserved molecular patterns in pathogens
    E.g. TLR4 recognises lipopolysaccharide (LPS)
    TLR2 recognises lipotechoic acid (LTA)
  • Also recognise endogenous mediators of inflammation
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16
Q

What is the alveolar macrophage?

A
  • Alveolar macrophages are phagocytes that play a critical role in homeostasis, host defence, and tissue remodelling
  • Comprises of 93% of pulmonary macrophages
    -Functionally, cytochemically and morphologically similar to mature tissue macrophages.
  • Long-lived and arise from monocytes.
17
Q

What is macrophage plasticity?

A

Macrophages can polarise towards foreign cells, which activates an immune response.
This plasticity allows them to effectively adapt to the changing environments associated with infection and wound healing and facilitate the return to immune homeostasis.

18
Q

What is a neutrophil?

A
  • 70% of all white blood cells
  • 80 million made each min
  • Turnover 100 million a day
  • Related to monocytes and macrophages
  • Contain granules:
    Primary (e.g. elastase) and Secondary (e.g. receptors, lysosome)
19
Q

How does the neutrophil help when we have a cut?

A
  • Break in skin/ wall
  • Neutrophil adhere to wall of blood vessel and then squeeze out
  • Fix break
  • Then taken up by macrophages and disposed of
20
Q

What are the functions of neutrophils?

A
  1. Identify the threat – receptors
  2. Activation
  3. Adhesion
  4. Migration/chemotaxis
  5. Phagocytosis
  6. Bacterial killing
  7. Apoptosis – programmed cell death
21
Q

How do neutrophils act as receptors?

A

Bacterial structures – cell walls, lipids, peptides

  • Host mediators – cytokines, complement, lipids
  • Host opsonins (- Stick onto bacteria and flag them as foreign so neutrophils/ phagocytes can break them down )
    E.g. FcR (immunoglobulin) + CR3 (complement)
  • Host adhesion molecules
22
Q

How do neutrophils become activated?

A

By signal transduction pathways involving:
- calcium
- protein kinases
- phospholipase
- G Proteins

23
Q

How do neutrophils adhere?

A

Margination – Selectins (stuck on cell wall and slow the neutrophils down)
Adhesion – Integrins (Then a firm interaction occurs which adheres them)

Require changes in endothelium and in neutrophil

24
Q

How do neutrophils migrate?

A
  • Ability to detect a concentration gradient and move along it by moving receptors to the leading edge
25
Q

How do neutrophils get involved with phagocytosis?

A

Membrane invagination (folding inwards) and pinching (phagosome)
Fusion with granules (phagolysosome)

26
Q

How are neutrophils involved with bacterial killing?

A

On encountering bacteria, neutrophils engulf these microbes into a phagosome, which fuses with intracellular granules to form a phagolysosome. In the phagolysosome the bacteria are killed after exposure to enzymes, antimicrobial peptides and reactive oxygen species (ROS)

27
Q

How are neutrophils involved with apoptosis (destroying harmful cells)?

A
  • Neutrophil signal to pathogens letting them know they contain harmful bacteria in them
  • So granules are released to destroy the bacteria
  • And are then engulfed

CVR Lectures (28 decks)

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