Innate Immunity

Front 1

What is the innate immune response?

Back 1

A non-specific, non-memory-generating response which is the body's first line of defence against infection.

At best, it eradicates the infection.
Otherwise, it will suppress the infection while the adaptive immune response is raised.

Front 2

Key Features of the Innate Immune Response

Back 2

No memory (Key, distinguishing feature!)
Non-specific.
Cellular and soluble components.
Physical Barriers.

Front 3

Why does the innate immune response show the same severity each time?

Back 3

It generates no memory cells, so there is no secondary response.

Front 4

Cellular Components & Actions

Back 4

Monocyte/Macrophage System - Intracellular Pathogens.
Neutrophils - Kill rapidly dividing bacteria.
Eosinophils - responsible for parasitic infection control.
Natural Killer Cells - A lymphocyte which targets virally infected cells.
Mast Cells - trigger inflammatory response.
Dendritic Cells - activate the adaptive immune response.

Front 5

Soluble Components

Back 5

Complement
Acute Phase Proteins
Interferon

Front 6

Complement

Back 6

Complex group of proteins (20 in total)
Key role in innate immunity is opsonisation of pathogens by C3b to make them more recognisable to phagocytotic cells.

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Acute-Phase Proteins

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During the 'acute phase' of an infection, protein synthesis in the liver is diverted to production of specialised proteins (C reactive Protein, Mannose Binding Lectin) which are secreted into the plasma and act in a similar way to complement.

Front 8

Interferon

Back 8

Molecules which stimulate cells to produce anti-viral proteins.

Front 9

Physical Barriers to Infection

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- Skin
- G.I Tract
- Respiratory Tract
- Urinary Tract
- Vaginal Mucosa
- Conjunctiva

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Skin as a Barrier

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Physical:
Dead, keratinised, anuclear layer of squamous cells.

Chemical:
- Lack of Water
- Lysozyme (=Peptidoglycan target)
- Lactic Acid
- Alcohol

Subaceous Glands - Waxy skin, Free fatty acids.

Commensals - normal flora and fauna better adapted to survival on host so out-compete pathogens for resources.

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Urinary Tract as a Barrier

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FLUSHING is the main method of protection (although E.coli attaches and swims up the urinary tract using its flagella)

- Specialised epithelium (transitional)

- Chemical/microbial defences

- Urine has low pH.

Front 12

This condition develops during urinary stasis caused by a blockage of some form in the urinary tract.

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Cystitis

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Vaginal Mucosa as a Barrier

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- Chemical/microbial defences
- epithelium
- low pH during menstrual years
- Oestrogen stimulates the production of glycogen by uterine glands for commensals

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Bacterial Infections

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Controlled by Macrophages and mainly neutrophils

Front 15

Monocyte/macrophage system

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- Monocytes have short half-life (around 1 day).
- Differentiate into macrophages when they enter the tissues.
- Macrophages exist in reticuloendothelial complexes.
- They are mono-nucleate and are able to recycle their granules.
- 6 -16 days is typical life span.

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Neutrophils

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- Polymorphonucleated Cells
- Multi-lobed nucleus
- Shorter life span (7-8 hours)
- Principle 'killers' of rapidly dividing bacterial.
- raised counts are indicative of bacterial infections.

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Destruction of Rapidly Dividing Bacteria by Neutrophils

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- Circulating antibodies will coat the pathogens/they will be recognised by their opsonins (i.e. LPS on bacteria)
- Complement C3b also opsonises the pathogens.
- Chemoattractants cause chemotaxis of neutrophils to the pathogen.
- Pathogen recognises opsonins through its receptors and binds
- Phagocytosis takes place

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Example of a Bacterial Infection

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Cellulitis

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What must bacteria overcome prior to infection?

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Barriers
- navigation through tight junctions of epithelial layers.
- or some form of transport

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Bacteraemia

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= When bacteria enter the blood. Potentially lethal.

Front 21

Parasitic Infection by Larvae.

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Same mechanism as bacterial infection - but controlled by Eosinophils.

Front 22

Two forms of 'Killing' by phagocytosis.

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Oxygen Dependent
Oxygen Independent

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Lactoferrin as an antibacterial agent.

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Contains oxidised iron.
Oxidises the bacterial cells such that they produce ROS via formation of peroxides.
Leads to destruction of the cell wall and lysis.
Particularly important in providing an innate immune system in infants

Front 24

Interferon

Back 24

- The body's own anti-viral
- Virus infects cell.
- dsRNA produced.
- dsRNA binds to receptors which trigger transcription of IFNA/IFNB.
- These cause the cell to enter an anti-viralstate where they do not divide and hence propogate the virus.
- Also secreted to nearby cells where interferon binds to receptors.
- This induces the same state in the nearby cells.
- Very important for suppressing the bacterial infection.

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What is the key difference between IFNA/B and IFN Gamma?

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IFN Gamma is secreted by T lymphocytes and activates macrophages in chronic inflammatory responses.

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Natural Killer Cells

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- Target Virally Infected Cells.
- Recognise Viral Proteins on the Surface of infected cells.
- Then bind to these cells and secrete granules containing perforin (which forms the hole in the membrane) and of granzyme (induces apoptosis).

* Mechanism is more intricate than this *

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Role of Dendritic Cells

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Capable of engulfing pathogens and presenting portions of the pathogen peptides on their surface (through MHC molecules)
Then migrate to the lymph nodes where they acivate the adaptive immune response.