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Immune and lymphatic system > How to fight infection and the body's response > Flashcards

How to fight infection and the body's response Flashcards

1
Q

Describe the barriers the body has to infection

A 
Antimicrobial factors in salive
Mucus and cilia
Skin
pH
Acid
Flushing urinary tract
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2
Q

What is phagocytosis?

A

Cell recognizes and binds to pathogen. This activates the cell to ingest the bacteria (the leading edge and pseudopodium engulf bacterium). Inside the cell, oxidative burst kills it

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3
Q

How does the body respond to bacterial infection?

A
  • Bacteria enter tissue
  • Innate cells have PRRs on surface to bind to PAMPS on bacteria
  • Bacteria phagocytosed
  • At the same time, macrophages release pro-inflammatory cytokines and chemokines
  • Cytokines IL-1 and TNF-alpha and chemokine CXCL-8 are released by macrophage
  • Mast cells have PRRs on surface and can be activated by proteins
  • When activated, mast cells degranulate and release contents into tissue
  • Causes blood vessels to swell and become leaky
  • Tight junctions between endothelial cells separate - allows contents of blood to get into tissue and immune cells to enter site of infection
  • Neutrophils first cell to enter site of infection - engulf and phagocytose bacteria (oxidative bursts and enzymes)
  • Complement and c-reactive protein drawn into wound
  • Proteins enter area to make bacteria clearer for phagocytes
  • Dendrites engulf pathogens and then move to lymph vessel, taking pathogen to lymph node - macrophages can do this too
  • In lymph, t-helper cells are waiting to be activated. Dendritic cell enters and breaks down microbe, presenting a portion of in MHC II
  • Recognized by T-cell receptor on CD4 helper cell
  • In combination with co-signaling process, activates T-helper cell
  • Effector T-helper cell replicates and clonally expands
  • Activates B-cells to produce antibodies
  • IgM enters wound
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4
Q

Which cytokines are released by macrophages?

A

IL-1 and TNF-alpha

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5
Q

Which chemokine are released by macrophages?

A

CXCL-8

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6
Q

What happens to mast cells when they are activated?

A

Degranulate

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7
Q

What do cytokines do?

A

Communication between cells - can be pro/anti inflammatory

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8
Q

What are interleukins?

A

Target leukocytes

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9
Q

What are interferons?

A

Antiviral response

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10
Q

What are chemokine?

A

Mediate chemotaxis

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11
Q

What are the three mechanisms that can activate complement proteins?

A

Alternative, classical and Mannose-binding lectin pathway

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12
Q

What is the alternative pathway to activate complement proteins?

A

Complement protein binds to microbe itself

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13
Q

What is the classical pathway to activate complement proteins?

A

Antibodies bind to bacteria which activates the pathway

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14
Q

What is the MBL pathway to activate complement proteins?

A

MBL binds to microbe initially to initiate pathway

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15
Q

What is the common result of activating complement proteins?

A

C3a is produced to instigate the inflammatory process

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16
Q

What does C3b do?

A

Opsonize and phagocytose microbes

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17
Q

Where are acute phase proteins produced?

A

Liver

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18
Q

Which chemicals signals the liver to produce acute phase proteins?

A

IL-6

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19
Q

What doe acute phase proteins do?

A

Opsonize

Activate complement cascade

20
Q

What do TH2 cells do?

A

Activate B-cells to produce plasma cells to produce antibodies

21
Q

How are B-cells activated?

A
  • Activated when antigen presented to T-helper cell
  • When T-cell activated, B-cell is activated too
  • Co-stimulatory signals and cytokines enables B-cells to become active
  • B-cells clonally expand
  • B-cells can differentiate into plasma cells or memory cells which reside in lymph
22
Q

What is isotope switching?

A

Producing different types of anitbody

23
Q

What is the first antibody to be produced?

A

IgM

24
Q

What is opsonisation?

A

Highlights pathogen to phagocyte
Helps phagocytosis
Important for encapsulated bacteria and viruses

25
Q

How does inflammation occur?

A

Antibodies stimulate mast cells to degranulate

26
Q

What is cytotoxicity?

A

Cytotoxic T-cells and Nk cells bind to antibody

Release enzymes for cytotoxic cell, leads to apoptosis

27
Q

How does the body respond to viral infection?

A
  • Invades epithelial cells
  • Spreads to neighboring cells
  • Cells produce IFN-alpha
  • Stops replication of viruses within tissue
  • Infected cell presents particles on MHC I receptor
  • Mast cells degranulate - break in tight junctions and leaky vessels
  • Neutrophils degranulate
  • Proteins enter area to regulate inflammatory response
  • Pathogenic antigens taken up by dendritic cells - T and B cells are activated
  • Antibodies bind to pathogens
  • NK cells cause apoptosis
28
Q

What are TH1 cells?

A

Part of cell-mediated response

NK cells and cytotoxic T-cells

29
Q

What doe TH1 cells produce

A

B-cells

30
Q

How are CD8 cells activated?

A

MHC I presents antigen to CD8
TH1 activates, which produces IL-2 and IFN-gamma
Helps activate CD8

31
Q

What does CD8 cell do?

A

Travels to site of infection by recognising MHC 1 antigen on pathogen
Can use death signal/releae enzymes

32
Q

How are NK cells activated?

A

TH1 cell produces IFN-gamma and Il-2

33
Q

How are macrophages activated?

A

TH1 cell produces IFN-gamma

34
Q

How is a plasma cell made?

A

TH1 cell produces IFN-gamma which stimulates a B cell to turn into a plasma cell

35
Q

What doe NK cells do?

A

Activate macrophages

Increase cytotoxicity

36
Q

Function of neutrophil

A

Chemotaxis and phagocytosis

37
Q

Function of monocyte

A

Phagocytosis

38
Q

Function of NK cell

A

Opsonization

39
Q

Function of T-cell

A

Mitogen response

40
Q

Function of T-helper cell

A

B-cell activation

41
Q

Function of cytotoxic T-cell?

A

Nk cell activation

42
Q

Why do wounds get hot?

A

Capillary widening

Increased blood flow

43
Q

Why do wounds get red?

A

Increased permeability

Fluid released into tissues

44
Q

Why are wounds tender?

A

Leukocytes attracted

Extravasation of leukocytes to site of injury

45
Q

Characteristics of acute inflammation

A

Duration less than 3 weeks
Not necessarily associated with tissue destruction
Lots of neutrophils
Inflamed

46
Q

Characteristics of chronic inflammation

A

Lasts longer than 6 weeks
Significant tissue destruction
Macrophages, lymphocytes and their derivatives are characteristically dominant

Immune and lymphatic system (27 decks)

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