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Transcript
The Body’s Response to Infection Topic 6.3 Specification- topic 6 10 Describe the major routes pathogens may take when entering the body and explain the role of barriers in protecting the body from infection, including the roles of skin, stomach acid, gut and skin flora. 12 Describe the non-specific responses of the body to infection, including inflammation, lysozyme action, interferon and phagocytosis. 13 Explain the roles of antigens and antibodies in the body’s immune response including the involvement of plasma cells, macrophages and antigen-presenting cells. 14 Distinguish between the roles of B cells (including B memory and B effector cells) and T cells (T helper, T killer and T memory cells) in the body’s immune response. 15 Explain how individuals may develop immunity (natural, artificial, active, passive). Key terms What is the immune response? What is a pathogen? An organism or something which causes disease What is an antigen? responses of an organism when infected by a pathogen a molecule the body recognises as foreign: this is what activates an immune response What are the 2 types of immune response? non-specific and specific Planning an attack- mission impossible ! Where could our team of intrepid pathogen enter «THE BODY»? What are the weak points? Physical barriers and chemical defences which prevent entry into our body Keratin (protein) of the skin and mucus and cilia in the mucous membranes, physical barrier Lysozyme in tears, saliva, mucous break down bacterial cell walls causing them to burst. Q 6.27 Hydrochloric acid in the stomach kills most bacteria which enter with food Skin and gut flora are harmless bacteria suited to the environment (in gut or on skin in spite of the salty sweat, urea and fatty acids – low pH) which can compete for food and space better than harmful bacteria. The harmless bacterial are better adapted to the conditions. In the gut they may help with digestion and secrete chemicals which harm the pathogens. Lysozyme- more detail Enzyme found in tears, saliva and nasal secretions Breaks down bacterial cell walls Lysozyme hydrolyses peptidoglycan Hydrolysis: Breakdown with the addition of water Examples of hydrolysis reactions: Polypeptide amino acid starch maltose glucose Now the Pathogens are inside !!!! Infection!!!!! The invasion and multiplication of microorganisms within the cells and tissues of the body having evaded the barriers. Damage to tissue causes Inflammation 1. 2. From Latin ‘inflammo’= to set on fire For each of the steps below explain the significance (purpose) Histamine is released by damaged tissues causes: Capillary arterioles to dilate Capillaries become more permeable Increased blood supply= redness and heat More tissue fluid formed= oedema More white blood cells are present in the tissue, these fight off any microbes White blood cells Where Also found in tissues, not just blood Three are they found? types of white cells: lymphocytes, neutrophils and monocytes(macrophages) What are phagocytes? Which of the above are phagocytes? Cells which ingest foreign organisms or chemicals by endocytosis Neutrophils and monocytes Neutrophils 70% of white cells Made in bone marrow Live a few days Non-specific Are attracted by chemicals from damaged cells: chemotaxis Often self destruct during destruction of invaders: can only ingest 5-20 bacteria https://www.youtube.com/watch?v=uNG-jZxvhcg Monocytes /macrophages About 5% of white cells Move into tissues soon after production and become macrophages (big eaters) Some move into infected tissues but some are found permanently in certain tissues: lungs, brain, lymph nodes Longer lived than neutrophils, can ingest up to 100 bacteria Phagocytosis Activity 6.7 Phagocytosis: Watch animation and draw a flow diagram with annotated diagrams Pathogen engulfed by phagocytes Enclosed within a vacuole Lysosome fuses with vacuole Hydrolytic enzymes are released into vacuole= bacteria destroyed Radicals also released into vacuole= damage bacterial DNA and proteins Free radicals: are highly reactive due to having unpaired electrons in the outer shell, important in many processes but are known to cause cell damage Phagocytes then present antigens from bacteria to other immune cells. They do this by placing the antigens in their cell surface membrane - sticking out. Phagocytosis Activity 6.7b, Lymphatic System 1. 2. 3. 4. 5. 6. Tissue fluid Blood in under pressure and the high hydostatic pressure forces some of the plasma out of the thin, permeable capillary walls. Small molecules can also cross the capillary wall. Some water re-enters the capillary due to osmosis at the venule end of the capillaries. Lymphocytes and macrophages, they destroy microbes Through the right lymphatic duct and thoracic duct, which enter into the subclavian vein. Due to the production of more white blood cells to destroy the pathogen and fight the infection. Septic shock/blood poisoning- pathogens spread around the body via blood. Antimicrobial proteinsInterferon What Protein produced by virus infected cells What does it do? Protein diffuses to nearby cells Prevents viral protein synthesis and therefore formation of new viral particles AND prevents viruses from attaching to the host cell and therefore prevents the entry of DNA/RNA into host cell How is it? can it be produced as a drug? Can be produced by using GM bacteria Why is it not widely used? Fever- explained Discuss in pairs: what do you think? Why do we get a fever when we have an infection? What is the significance of this fever? Caused by pyrogens, chemicals released by some white blood cells Raises the thermostat- the temperature our body is set to remain at a higher temperature than 37 degrees Centigrade Inhibits growth of some microbes Speeds up reactions, may speed up repair of tissues Can facilitate phagocytosis https://www.youtube.com/watch?v=GIJK3dwCWCw Checkpoint 6.4 Complete the flow diagram about the sequence of events that occur in the nonspecific response at the site of a cut Specific Immune System https://www.youtube.com/watch?v=CkTKZTCxrtc In what way if the specific immune system specific? How is this possible? Explain using your knowledge of the tertiary structure of proteins. Review: What is an antigen. 1. 2. Lymphocytes have receptors that bind to specific non-self antigens on pathogens. Usually a protein molecule expressed on cell surface membrane or virus exterior. Our immune system recognises it as foreign when it comes from another organism. Two main types of cells involved in the specific immune system? Describe the function of each one. B cells – secrete antibodies: memory cells and plasma cells T cells – aid B cell division(T helper cells), and destroy virus- infected cells (T killer): memory cells, helper cells and killer cells Antibody: Class of protein called immunoglobulin Antibodies What is the function of an antibody? Bind to non-self antigens and label the cell for destruction by phagocytes See figure 6.38 Each B cell produces one type of antibody and has receptors on its surface including trans-membrane versions of the antibody Activation of T helper cells Initiated by professional antigen presenting cells. Ie. Macrophages and B lymphocytes Function? Present «non-self» antigens on the surface of their cells Bind to complementary CD4 receptors on T helper cells to activate them Significance? T helper cells can activate specific B cells (the ones which produce antibodies complementary to the antigen) by clonal selection Activation of T Killer cells Infected cells present «non-self» antigens on the surface of their cells Bind to complementary CD8 receptors on T killer cells to activate them Significance? T killer cells kill any cells infected with viruses containing this specific antigen Primary and secondary immune response Primary: occurs after first exposure to an antigen Secondary: If infected by same antigen again Response is much faster, involves the memory cells http://highered.mcgrawhill.com/sites/0072507470/student_view0/chapter22/animation__the_immune_response.html Activity 6.8d 1. What happens during the primary immune response? Macrophages engulf and present antigen of pathogen which activates T-helper cells and produce memory cells T-helper cells bind with B-cells specific for the antigen, release cytokines which stimulate B-cell division to produce plasma cells which will produce antibodies specific to antigen – labelling them for easier destruction by macrophages. T-helper cells also release cytokines that stimulate T-killer cells to divide and destroy infected body cells. B and T-cell memory cells are made for a secondary exposure to same antigen. Activity 6.8d How long did it take for the antibody number to reach a maximum after the first exposure to antigen A? Why does the antibody number remain higher than the original value? Some of the antibodies remain in the blood How long did it take for the antibody number to reach a maximum after the second exposure to antigen A? 2 weeks Less than 2 weeks Describe the differences between the responses to the two antigens after exposure to both. Antibody production occurs sooner (happens immediately – not really a big difference in graph), faster (Second exposure line is steeper) and more antibody is produced (peak is higher). Activity 6.8d Explain these differences. Why are people often unaware of infections during the secondary immune response? Secondary immune response involves memory cells that detect the antigen faster and can respond to it faster meaning that antibody production occurs sooner, faster and more antibody is produced. Pathogen is destroyed before body has any symptoms of the disease Define ‘immune’. Already have antibodies and or memory cells present in body for that specific antigen/pathogen. Avoiding attack to one’s own immune system Some membrane proteins on our cells label us as self. B and T cell mature in bone marrow and thymus -any lymphocytes for self membrane proteins are destroyed by apoptosis Sometimes cells may change so that they appear foreign to body Auto immune diseases Insulin dependent diabetes Rheumatoid arthritis Multiple sclerosis Becoming actively immune Active natural immunity – you are exposed to the pathogen and this causes an specific immune response. You now have B and T memory cells to this antigen Active Artificial immunity – you are vaccinated with an antigen and this causes an immune response. You now have B and T memory cells to this antigen Passive immunity Passive natural – you received antibodies across the placenta and in breast milk when you were a foetus and newborn. You were able to fight any antigen you came in contact with at the time but this immunity only lasts for a few months You had no immune response, therefore no memory cells made. Passive artificial immunity You are given an injection of antibodies if you know you have been exposed to a pathogen but have not previously been vaccinated against it. The disease is known to be very fast acting and deadly. eg tetanus, rabies This fights the pathogen immediately but does not give you long lasting immunity. Q 6.38 Vaccinations Attenuated pathogen eg. measles, BCG, polio Killed pathogen eg. whooping cough bacteria Harmless form of toxin eg, tetanus Antigen bearing fragment eg hepatitis B, meningitis C Challenges for vaccinations Poor immune response eg. due to malnutrition Antigenic changes Due to mutations eg. flu Due to different stages in a life cycle eg. malaria Antigenic concealment In cells In intestine eg. cholera Boosters required for some vaccinations Herd immunity • When enough people are immunised the pathogen is less likely to be transferred. • Therefore there is less disease in the community. • Anyone who cannot have a vaccination for medical reasons is also protected. • Eg. for measles 95% of the population needs to be immunised for herd immunity. Successful vaccination programme – smallpox https://www.youtube.com/watch?v=jJwGNPRmyTI Edward Jenner noted that cowpox sufferers never developed smallpox In 1796 he inoculated a healthy boy with cowpox then injected him later with smallpox The boy do not develop smallpox Smallpox vaccination was developed and made compulsory in UK in 1853 Successful vaccination programme - smallpox WHO aimed to eradicate smallpox The disease was devastating and deadly The vaccination was safe, effective and easy to administer The pathogen was stable and did not mutate Sufferers were easy to spot and isolate Last case was in Somalia in 1977 A stalled vaccination programme - measles Deadly and debilitating in developing countries – leading cause of blindness, 2.6 million deaths per year prior to vaccination. Targeted by WHO for eradication. Effective, safe vaccine. 95% vaccination needed for herd immunity. A stalled vaccination programme - measles However the uptake of the vaccine in developed countries has declined significantly. Measles seen as a “minor” illness. Vaccination fraudulently linked to several diseases eg. autism, bowel disease. Serious outbreaks of measles in central Europe eg 2008 Switzerland Vaccinations for TB? Were you vaccinated against TB? Vaccine introduced to UK in 1950s Vaccine gave immunity to 80% of TB strains Initially very effective TB cases declined Vaccine not given to all children in UK now. Why? Vaccination for TB TB now limited to very specific groups - London or major cities Born abroad in certain countries Regular visitors (or close family members)to certain countries No longer as effective Vaccine for HIV? Not yet Would you vaccinate your children? Side effects? Specification- topic 6 10 Describe the major routes pathogens may take when entering the body and explain the role of barriers in protecting the body from infection, including the roles of skin, stomach acid, gut and skin flora. 12 Describe the non-specific responses of the body to infection, including inflammation, lysozyme action, interferon and phagocytosis. 13 Explain the roles of antigens and antibodies in the body’s immune response including the involvement of plasma cells, macrophages and antigen-presenting cells. 14 Distinguish between the roles of B cells (including B memory and B effector cells) and T cells (T helper, T killer and T memory cells) in the body’s immune response. 15 Explain how individuals may develop immunity (natural, artificial, active, passive).