Bio- Unit 4 AOS1- Pathogens

Antigen

A molecule that promotes an immune response

MHC Markers (Major Histocompatibility Complex)

Proteins on the surface of all nucleated cells in the body (not RBC). Each protein contains a peptide that was bound to it inside the cell. The protein is then moved to the plasma membrane and presents its peptide on the outer surface. If the peptide is part of one of the cell’s own proteins, it will be ignored by leucocytes. However, if the peptide is a degraded protein from a non-self biological entity, leucocytes will destroy the cell.

Pathogen

the causative agent of an infectious disease

Pathogenic bacteria

Unicellular, prokaryotic organisms that usually produce endotoxins or exotoxins. These toxins affect functioning of cells or cause their death. They typically reproduce asexually through binary fission.

Fungi

Eukaryotic organisms that can be unicellular or multicellular. They contain long, branching filaments called hyphae. They reproduce via asexual reproduction and sexual reproduction called spore formation.

Worms

Multicellular, invertebrate parasites. Development includes egg, larval, and adult stages. They reproduce sexually.

Protozoa

Single-celled eukaryotes that can be free-living or parasitic. They have many different mechanisms of action. They reproduce through both sexual and asexual reproduction

Viruses

Non-living infectious agents composed of genetic material inside a protein capsid. They cannot reproduce independently, instead, they insert their genetic material into a host’s cell and use the cell’s machinery to replicate.

Prions

Abnormally folded proteins that can only effect neural structures in mammals. They are the only known infectious agents that don’t contain nucleic acids. They induce misfolding in nearby proteins, therefore spreading throughout a tissue.

First line of defence

a component of the innate immune system, providing physical barriers, chemical barriers, and microbiological barriers to prevent pathogenic invasioun

Physical barriers in plants

bark, waxy cuticles, cellulose cell walls

chemical barriers in plants

chemicals (e.g. toxins) which are harmful to the pathogen and/or enzymes that affect the functioning or development of the pathogen. Some chemicals can also act to repel insects or animals that may damage the plant. E.g- phenols, glucanases

Physical barriers in animals

intact skin, mucous membranes

mechanical barriers in anmials

sneezing/coughing, diarrhea, vomiting, tears

chemical barriers in animals

stomach acid, lysozyme in tears

microbiota barriers in animals

the human gut contains microbes which exist in a mutualistic relationship with the person. They prevent the growth of colonies of other species of bacteria by outcompeting them for nutrients and adhesion sites, and secreting antimicrobial chemicals that prevent the growth of pathogenic bacteria

Second line of defence

a component of the innate immune system, composed of a variety of cells and molecules that destroy pathogens which have entered the body, preventing the spread of infection

mast cells

Leucocytes that embed themselves in connective tissues. When they detect damage to surrounding cells, they release histamines that have 3 effects, which are referred to as the inflammatory response- vasodilation, increased permeability of blood vessels, and attraction of phagocytes.

phagocytes

Cells that engage in phagocytosis, a process where they consume and destroy foreign or dead material present in the body by engulfing it through endocytosis. Once engulfed, lysosomes containing antimicrobial enzymes called lysozyme present in the cell destroy  the foreign or dead material by fusing with the vesicles containing the engulfed material. The important phagocytes are neutrophils, macrophages, and dendritic cells.

Natural killer (NK) cells

Large, granular, lymphocytes. They are instrumental in destroying self-cells that have been infected by a virus, or which have become cancerous. NK cells, on finding a self-cell displaying non-self antigens on its surface, release a death ligand, which is a signalling molecule that stimulates the cell to die by apoptosis

Eosinophils

Large, granulated cells which contain various toxic chemical mediators such as DNases, RNases, and proteases, which help destroy pathogens. They typically target pathogens which are too large to be phagocytosed by degranulating on contact with them and releasing chemical mediators contained with their granules.

Interferons (INF)

Signalling molecules (cytokines) released from virus-infected host cells. They cause nearby cells to heighten their antivirus defences. Cells stimulated by INF’s produce various enzymes that inhibit protein synthesis. Interferons also cause cells to upregulate the production of MHC I markers.

Complement system

A suite of small proteins called complement proteins that are synthesised by the liver, and circulate in the blood in an inactivated state. When activated they achieve 3 primary outcomes; oponisation, chemotaxis, and lysis.

Oponisation

Complement proteins stick on the outside surface of pathogens and make it easier for cells of the immune system, such as phagocytes, to recognize them as foreign

Chemotaxis

Complement proteins gather near a pathogen and attract phagocytes to it, making it more likely to be destroyed.

Lysis

Complement proteins can join together on the surface of pathogens, forming a membrane attack complex (MAC), which creates pores in their membrane. This destroys the pathogen by causing lysis via the sudden influx of fluid into the pathogen, causing it to burst.

Fever

A temporary increase in body temperature. A complex series of responses can raise the set temperature point of the body during a fever, meaning the body will initiate a number of countermeasures to increase core body temp to reach this new setpoint. This is an innate response to potential infection, as many pathogens cannot survive at the elevated temperatures created by a fever. Prolonged fevers can be detrimental to the body due to the additional stress placed on our cells.

Steps in the inflammatory response

Initiation, vasodilation, migration

Initiation in the inflammatory response

When pathogens break through the first line of defence, macrophages situated in the tissue where the pathogens were introduced become activated and along with damaged cells, release cytokines. Mast cells will also degranulate, releasing histamine.

Vasodilation in the inflammatory response

the histamines released from the mast cells travel to nearby blood vessels and bind to specific receptors, causing vasodilation. This causes blood vessels to widen, increasing blood flow to the injury site, causing swelling, redness, and warmth associated with inflammation. Additionally, the formation of gaps in the vessel wall increases it’s permeability to cells of the immune system.

Migration in the inflammatory response

Vasodilation and the increased leakiness of blood vessels allow for a number of innate immune system components to leave the bloodstream and enter the site of injury. These components include: phagocytes, which are guided by the cytokines to the site of injury. they then phagocytose pathogens and digest them using enzymes such as lysozymes. There’s also complement proteins, which are attracted to pathogens and make it easier for phagocytes to destroy them. The response continues until the site has been cleared of pathogens and debris, and the site of the injury has been healed and will eventually return to normal.

Third line of defence

it is designed to destroy pathogens that have passed the first line of defence. It has 2 unique features: specificity (the immune system responds to each distinct pathogen in a unique manner), and immunological memory (the adaptive immune system results in the production of memory cells to respond to future re-infections quickly)

Antigen presentation

Antigen-presenting cells engulf pathogens via phagocytosis, displaying pathogenic antigens on their MHC Class II markers. They then travel to the lymph nodes to present foreign antigens on their surface using MHC Class II proteins. Then, they interact with the complementary T cell receptors on the surface of T helper cells, activating the T helper cell. The selected T helper cell can then help initiate the adaptive immune response through the humoral or cell-mediated immune response.

Cell-mediated immune response

Involves the destruction of infected or abnormal cells through the clonal selection of a cytotoxic T cell.

1. While T helper cells are being selected, antigen-presenting cells find a naïve T cell with a matching T cell receptor, initiating clonal selection. Cytokines from the T helper cell activate the naïve T cell to multiply and differentiate.

2. The clones of the selected T cell differentiate into 2 types of T cells. T memory cells are copies of the originally selected T cell that reside in the body for extended periods of time and help form immunological memory. Most T cells differentiate into cytotoxic T cells, which leave the lymph node and travel throughout the body, eventually reaching the site of infection.