immunity to bacteria Flashcards

1
Q

are bacteria intracellular or extracellular ?

A

can be both

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2
Q

when dealing with a bacteria what must the immune response deal with ?

A

the bacteria , the infected cells and the viral toxins

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3
Q

how does the innate response recognise the pathogen ?

A

through the PAMP’s

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4
Q

how does the acquired recognise the pathogen ?

A

through the B or T cell recognising the specific antigen

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5
Q

how can phagocytic cells remove bacteria ?

A

using phagocytosis or produce toxic products e.g. tumour necrosis alpha, superoxide, nitric oxide

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6
Q

what are the most numerous cell in the body ?

A

neutrophils

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7
Q

what occurs if the bacteria goes systemic ?

A

it is very difficult to control and treat

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8
Q

how would the body deal with a local gram negative infection of bacteria ?

A

the macrophages are activated to secrete TNF alpha a cytokine causes apoptosis and this increases the plasma proteins into the tissue. This in turn increases phagocytosis

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9
Q

how does the body deal with a systemic infection of gram negative bacteria?

A

the macrophages are activated in the liver and spleen to secrete TNF alpha into the blood stream. This causes swelling and a decreased blood volume.

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10
Q

why is it important to have lot’s of PRR’s ?

A

so if the pathogen blocks one then the cell can still recognise it

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11
Q

what are NET’S ?

A

neutrophil extracellular traps

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12
Q

what do the NET’s do ?

A

they immobilize the bacteria at the site of infection. Also special cell death program occurs , it is a specialised type of apoptosis called ‘NETosis

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13
Q

what is MPO ?

A

myeloperoxidase it is only produced from neutrophils and has a bleach like effect.

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14
Q

what can the bacteria cause the macrophages to release ?

A

IL-6 which is a proinflammatory cytokine acts on the hepatocytes to induce the synthesis of acute phase proteins in response to the damage and they are used to control the infection as the innate system.

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15
Q

what does the C reactive protein bind to on the bacterial surface to opsonise it ?

A

the phosphocholine which also activates complement

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16
Q

the bacteria can also produce super antigens , what are these ?

A

class of proteins that can activate a large population of T cells. They work by activating the T cell but not through the receptor. This can lead to toxic shock.

17
Q

when is bacteria more easily phagocytosed ?

A

when it is clumped together

18
Q

how is apoptosis induced by innate cells ?

A

when TNF alpha is produced by macrophages and neutrophils

19
Q

what is staphylococcus aureus ?

A

This is a gram-positive bacterium that is extracellular . It causes both community and hospital-acquired infections

20
Q

what is important in the innate when controlling ?

A

neutrophils are important

21
Q

when is phagocytosis more efficient ?

A

if complement or antibody - IgG coats the bacteria

22
Q

how do the neutrophils cause killing ?

A

superoxide, hydrogen peroxide, kill the bacteria in phagosome.
granules present – toxic products – e.g. defensins, lysozyme and bacterial permeability increasing protein and this kills the bacterium in phagosome.
They are also phagocytic

23
Q

how can the S.aureus evade the detection ?

A

They can produce and secrete and surface-bound molecules that inhibit neutrophils activity. This also inhibits the neutrophil recruitment. As well as,
• Inhibit bacterial binding to neutrophils
• Inhibit phagocytosis by neutrophils
• Inhibit toxic products produced by neutrophils

24
Q

what does the mycobacterium tuberculosis cause ?

A

a lung disease TB

25
Q

where does the bacteria live ?

A

inside the macrophage

26
Q

how do you kill the TB ?

A

stimulate the macrophages to kill by IFN gamma. The nitric oxide and reactive nitrogen intermediates are important. Apoptosis of infected macrophage – NK/Tc release TNF alpha can induce apoptosis. A granuloma can form an multicellular structures that limits growth of Mt.

27
Q

the infected macrophage secreates more IL -10 , why ?

A

– IL-10 down regulates activity of macrophages – less NO, reactive oxygen intermediates etc and this switches off macrophage killing mechanisms
– IL-10 induces the release of TNFR-2 – and soluble TNFR-2 forms a complex with TNF-α and downregulates the TNF-α induced apoptosis of macrophages – causing survival of Mtb infected macrophages