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Threats and Defence > L14 inflammation & acute inflammatory response > Flashcards

L14 inflammation & acute inflammatory response Flashcards

1
Q

What cytokines do macrophages release?

A

IL-1β, IL-6, TNFα and IL-8

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2
Q

What cytokines do mast cell release?

A

histamine, prostaglandins and leukotrienes

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3
Q

What IL attracts neutrophils?

A

IL-8

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4
Q

What activates mast cells in AIR?

A

C3a and C5a

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5
Q

What cytokines attract NK to site of infection released by what cell?

A

By macrophages, TNFα

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6
Q

What do neutrophils chemotax towards?

A

C3a, C5a and IL-8

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7
Q

What receptors do mast cells have?

A

Apart from ofc PRRs, they have complement receptors.

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8
Q

What receptors do neutrophils have?

A

PRRs, complement and Fc/ab

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9
Q

What is the acute inflammatory response?

A

Coordinated response by the cells and mediators of the innate immune system in response to tissue damage or pathogen entry. It brings phagocytic cells in from blood to clear cellular debris, and repair tissue or kill pathogen.

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10
Q

What are the key characteristics clinically of inflammation?

A

Pain, swelling, redness, heat.

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11
Q

What are the causes of the inflammatory response?

A

burns, trauma, irradiation and sunlight, smoking, alcohol, drugs, poisons and toxins, invasion by viruses, bacteria, protozoa, funghi and worms. Breaching of the epithelial carrier activates the innate immune response.

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12
Q

What happens when PRRs are activated? (specifically on macrophages)

A

Release of cytokines and chemokines that alert host immune response to threat of infection. Main acute phase cytokines are TNFα, IL-1β and IL-6. These propagate immune response by upregulating acute phase proteins in the liver such as CRP. CRP can opsonise and activate complement. Cytokines have other effects like increasing body temp by stimulating hypothalamus, neutrophil mobilisation an increased activation of DCs.

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13
Q

Which are the acute phase main cytokines?

A

IL1β, TNFα and IL-6

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14
Q

What are the two first things to happen when a pathogen breaches a barrier?

A

PRRs recognise and complement activation

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15
Q

In terms of compliment activation what happens immediately after pathogen entry?

A

Opsonisation with C3b and iC3b to target pathogen for phagocytosis by macrophages and neutrophils. Opsonin receptors include CR1 for C3b and CR3/4 for iC3b.
C3a and C5a release activates mast cell degranulation and neutrophil chemotaxis via a conc gradient.

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16
Q

What is inflammation caused by?

A

The acute phase response

17
Q

Which cell is key in innate recognition?

A

Mast cells

18
Q

Which innate cell initiates the acute phase?

A

Mast cells

19
Q

What are the main mediators of inflammation?

A

Histamine, eicosanoids - PGs and leukotrienes

20
Q

Why do we feel systemically unwell when we have local inflammation?

A

Acute phase cytokines partially responsible (TNFα, IL-1 and IL-6) e.g. chest infection and feeling unwell systemically

21
Q

What happens in septic shock?

A

Overproduction of TNFα and IL-1 from e.g. endotoxin LPS by gram neg bacteria like E. Coli. This lead to massive macrophages activation in liver and spleen –> overproduction of these cytokines –> dilation of bv, leakage of fluids, disseminated intravascular coagulation, multiple organ failure

22
Q

What are the outcomes of inflammation?

A

Complete restitution, healing with scar, granulomas, chronic inflammation, abscess formation

23
Q

Where are mast cells found?

A

Long lived cells present in most tissues, surround b and nerves and prominent under the skin and mucosal surfaces of the body.

24
Q

What do mast cells release?

A

histmamine, PG and leukotrienes

25
Q

What happens in chronic inflammation?

A

acute phase can’t be resolved in:
persistent injury or infection
prolonged toxic agent exposure
autoimmune disease

26
Q

What are the mechanisms of chronic inflammation?

A

cellular infiltration, tissue destruction by inflamm cells and attempts at repair with fibrosis and angiogenesis

27
Q

How does acute inflammation terminate?

A

Eradication of an offending agent should lead to discontinuation of inflamm response. Most mediators short lived and degraded immediately. Anti-inflamm agents like IL-10 and TGFβ inhibit production of pro-inflamm cytokines

28
Q

What will happen to ESR in infection/inflamm/injury?

A

ESR will go up as acute phase reactants presence leads to erythrocyte aggregate due to loss of their negative charge resulting increased sedimentation.

29
Q

What is leukocytosis

A

leukocyte increase in blood, direct effect of IL-1 and IL-6

Threats and Defence (12 decks)

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