Innate immunity Flashcards

1
Q

How does Anthrax, a bad bacteria, cause infection?

A

Anthrax is gram-positive, rod-shaped bacteria known as Bacillus anthracis is able to be ingested by macrophages. Inside a macrophage it can multiply causing macrophage death. The macrophage itself would off been travelling to the lymph and upon its death the multiplied anthrax would be liberated. In the lymph it can cause pulmonary blockages, travel to the blood cause blood poisoning and ultimately lead to meningitis and death.

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2
Q

What is our first line defence to infection?

A

Physical barrier: skin, exposed epithelial, cilia, mucus: these are very non-specific and limit the physical entry of bad bacteria.

Biochemical mechanisms: sebaceous glands secretions, containing fatty acids, hydrolytic enzymes and antibacterial. Anything that secretes acts as a biochemical mechanism, preventing any pathogens entering.

Enzymes in saliva, intestinal secretions and pH of the stomach (pit of acid)

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3
Q

What is acute inflammation in a hosts innate immune response?

A

Tumor, calor, rubor, and dolor describe four cardinal signs of inflammation.
This assonant phrase refers to the heat (calor), pain (dolor), redness (rubor), and swelling (tumor) that characterise the clinical symptoms of inflammation

These outcomes are all created by our immune system to promote wound healing in response to recognising foreign bacteria.

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4
Q

How does the immune system recognise foreign bacteria?

A

Sugar coating (pathogen associated molecular patterns) on the surface of bacteria.

We have three receptors on our phagocyte capable of recognising these PAMPs:

  • Toll-like receptors
  • Scavenger receptors
  • Carbohydrate receptors
  • Mannose-binding receptors

Upon binding an intracellular transduction occurs allowing the phagocyte to move and surround the microbe, pinching off the interior forming a phagosome.

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5
Q

What is a phagosome?

A

A phagosome is a vesicle formed around a particle engulfed by a phagocyte via phagocytosis. These vesicles contain lysosome (pockets of digestive enzymes) which fuse with the phagosomes to form a phagolysosome. This is where the bacterium is digested. The components of the microbe that allow recognition are then used to potentiate the immune response.

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6
Q

How does the complement system act as an opsonic fragment?

A

We have a complement protein produced in the liver which is constantly degrading, this process is accelerated in the presence of bacteria. The bacteria will bind to complement 3 component which quickly makes c3a, c3b, c5a, c5b…..

c3b and c4b become opsonic fragments. These fragments of complement will bind to bacteria making them more likely to be phagocytosed. A phagocyte can bind through the complement fragment, promoting the phagocytosis of the bacterium.

The complement acts as an opsonic fragment.

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7
Q

How do complement fragments interact with white blood cells?

A

Complement fragments will bind to white blood cells and cause immune cell activation. They are able to do this through a mechanism of receptor-ligand binding by the complement itself binding to a receptor on white blood cells.

There are complement fragments called anaphylotoxins. Fragments c5a and c3a will bind to receptors on mast cells causing them to degranulate vasoactive things e.g., histamine. These mediators enhance local blood flow causing swelling, heat, pain and redness. The secondary release of cytokines from mast cells cause cellular accumulation.

The complement 5a (c5a) itself acts directly on receptors on monocytes and neutrophils inducing their migration to sites of inflammation and subsequent activation.

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8
Q

What can accentuate the fragmentation of a complement?

A
  • Mannose-binding lectin: if u have a deficiency of this you find your more susceptible to infection.

Mannose-binding lectin is a protein found in the liver and it recognises carbohydrate patterns found on the surfaces of microbes. Binding will result in the activation of the lectin part activating the complement part around c3.

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9
Q

What triggers phagocytosis?

A

We have three receptors on our phagocyte capable of triggering phagocytosis:

  • Toll-like receptors
  • Scavenger receptors
  • Carbohydrate receptors
  • Mannose-binding receptors
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10
Q

How do dendritic cells work?

A

They have the capability to resent anything they’ve eaten on their surface. This antigen-presentation allows phagocytes to bind triggering cytokine release. This promotes dendritic cell maturation.

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11
Q

What is an antigen presenting cell?

A

An ATP is a cell capable of presenting an antigen on its surface. If a phagocyte has broken down microbe protein it then presents it on the external surface. Macrophages and phagocytes all travel in the lymph after they’ve phagocytosed and will interact with B cells and T cells here, activating them. They are activated because B cells and T cells can recognise the ATP and will bind to them.

It is here the innate immune system comes into contact with the adaptive immune system.

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12
Q

What is the mechanism of T cell activation?

A

Activation is through the T cell receptor, these receptors can recognise peptides on the surface of macrophages and phagocytes.

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