C.3.2 - Defence against disease

Pathogens + types

Small organisms that cause disease:

• Viruses

• Bacteria

• Protozoa

• Fungi

Defence mechanisms aagainst pathogens

Physical barriers: skin, mucous membranes, blood clotting

Chemical response: innate and adaptive immune systems

Innate immune system

Phagocytes recognise foreign pathogens and engulf & digest them by endocytosis

Adaptive immune system

Antigens on pathogens are chemically recognised, b-lymphocytes produce antibodies to destroy them, long-lived lymphocytes remember how to produce the antigen, provides “true” immunity

Skin layers

1. Epidermis: main protective layer (cosists of dead skin cells, difficult to penetrate by living organisms)

2. Dermis

3. Hypodermis

Mucous membrane functions 

Secrete mucous to trap pathogens and prevent further entry

Blood clotting

• Collagen exposure at ruptured blood vessel stimulates platelets to attach to open wound, eventually forming a platelet “plug”

• Plug slows bleeding, platelets and damaged tissue release clotting factors

• Clotting factors convert prothrombin into enzyme thrombin

• Thrombin converts insoluble fibrinogen into soluble fibrin

• Fibrin stabilises the platelet plug by forming a mesh-like net

• More cellular debris is attracted, stopping bleeding and pathogen entry

Fibrinogen to fibrin mechanism

Exposure to chemicals outside the blood vessel turns polar fibrinogen into non-polar fibrin, so fibrinogen within the blood vessel doesn’t randomly clot. 

Phagocytes

White blood cells capable of ameboid movement (plasma membrane extension) and phagocytosis

Receptors and ligands

Integral membrane proteins and the structures that attach to their surface, changing cell functions (e.g. glycoproteins)

Antigens

Molecules that make up pathogens, allow endocytosis (the virus is englufed by a cell and can change the function), typically glycoproteins

Why do viruses need to be internalised 

In order to take over the function of the cell to produce more viruses 

Antibodies

Y-shaped proteins that bind to specific antigens - can collect them in a large cluster to make it easier for phagocytes to locate and engulf them.

Phagocytosis

Phagocytes engulf pathogenic cells, which are then hydrolised by lysosomes. Phagocytes recognise the Fc- regions on antibodies (genetic, varies between each person), which initiates phagocytosis

Antigen-antibody binding

Antigens and antibodies fit the lock-and-key model, so they can bind to specific sites

Antibody production not triggered by pathogens

RBC have antigens on the surface:

A, B, AB, none (O)

Plasma therefore contains corresponding antibodies that respond to foreign blood type transfusions:

Anti-B, anti-A, none (AB), both (O)

Autoimmune disease exp.

Type I diabetes

Lymphocytes in adaptive immunity

• Phagocytes engulf viruses and pass antigens to the T-lymphocyte,

• T-lymphocyte finds the B-lymphocyte with a matching antibody. (Can take several days)

• The T-lymphocyte binds to the B-lymphocyte, releasing cytokines that activate the B-lymphocyte,

• B-lymphocyte encounters the pathogen in the body, triggers cell division  

• New cells: plasma cells that produce antibodies in the bloodstream, specialised long-lived memory cells provide long-term immunity

Why can one pathogen trigger the activation of multiple B-lymphocytes?

Pathogens have multiple types of antigen on their surface

HIV transfection

Glycoprotein on HIV cell attaches to the T lymphocyte cell’s CD-4 receptor and is then internalised into the cell due to conformation changes to other membrane proteins and glycoproteins

HIV effect

Destroys ability of T-lymphocytes to help the B-lymphocyte, this way antibodies cannot be produced, results in development of AIDS

HIV treatment

3 types of inhibitors:

• Attachment (bind to CD4 receptor so HIV can’t)

• Reverse transcriptase (block RT enzymes which allow viruses to enter their RNA to host DNA for copying)

• Assembly & building (disrupts assembly process of virus)

Antibiotic effects

• Selectively block biochemical pathways needed by bacteria, e.g. inhibition of cell wall or protein synthesis, which doesn’t affect eukaryotes.

• No effect on viruses because they have no metabolism

Bacterial resistance to antibiotics

• Mutations occur spontaneously during DNA replication stage of binary fission

• The higher the rate of DNA replication, the higher the risk of a consequential mutation occurring

• One such mutation = resistance to antibiotics (protection from certain biochemical action)

• All bacteria descended from this cell will have the same mutation

• This mutated bacteria could also infect other people

Antibiotic-resistant bacterial strain

MRSA (S. aureus), causes staphylococcal infections that are difficult to treat (swollen, painful red bumps)

Outline how the body defends itself against pathogens

• Skin + mucous membranes act as physical barriers

• Skin and stomach acid prevents the growth of many pathogens

• Lysozymes in mucus can kill bacteria

• Pathogens get caught in mucus and removed from the body

• Inflammatory response (fever, swelling, etc.) can inhibit pathogens

• Phagocytes identify foreign pathogens and ingest them

• T-helper cells recognise specific antigens

• B-lymphocytes produce antibodies + divide to reproduce

• Antigen - antibody complex formed which stimulates destruction of antigens

Zoonotic diseases

Pathogens that can “cross the species barrier”

Zoonotic diseases exp.

• Rabies (viral, transmitted by dog bite)

• Tuberculosis (bacterial, airborne)

• Japanese Encephalitis (viral, transmitted by mosquitoes)

• COVID-19 (viral)

Traditional vaccine

Inactive pathogen is injected to serve as the first exposure, activating B-lymphocytes against it in case of secondary exposure

RNA vaccine

DNA or RNA coding for a specific protein antigen is injected, exposing the body to the antigen for primary exposure (creates memory cells) rather than the pathogen

Herd immunity

• Before immunity, everyone in a population is equally susceptible to infection

• The more people are immune, the less often the suscpetible come into contact with contagion

• Thus, the spread of contagion is contained

• Achieved through vaccination

Cells with lots of rER

Plasma cells - for producing antibodies