8.2 Fighting Back


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UBC Bio 111 - Intro to Biology

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8.2 Fighting Back

  1. 1. 8.2 Fighting back 4. Explain how bacteria and viruses can disrupt regular cellular or body function. 5. Explain how immune systems respond to infections. 2. Specific immunity (specific pathogens are recognized as foreign by lymphocytes and antibodies) Third line of defense: Immune and lymphatic system Lymph moves invaders from the sites of infection into lymph nodes where they are attacked by masses of white blood cells. This is why your lymph nodes ie in your neck can swell up when you are sick Besides macrophages and natural killer cells which are non-specific, lymph contains some lymphocytes called B cells and T cells which provide specific protection. Note: on the importance of cell surface proteins Proteins are found on the surface of virtually all cells and serve very many functions. Receptor proteins are used by cells to sense and respond to incoming signals ie “Grow in this direction” “Ouch!” “Take in more potassium ions” “Work harder” “Turn on gene X” “Beware of invaders” “Die!” A ligand is what binds to a receptor to signal it. Two receptor proteins(R) with bound ligands (L) are shown on the left. Only 1 ligand binds to1 receptor as a rule. They act like lock-and-key. There are many different types of cells in your body with different receptors. As well, cells in different species have different cell surface receptor proteins. There are 1000s of different locks and keys. The way immune system cells and antibodies work is by recognizing foreign substances called antigens. The cells of your immune system recognize the proteins on the surface of your own cells as being “self” and leave them alone. Any shape on an antigen that is recognized as foreign (non-self) is attacked by the immune system. Antigens could be dust, bacteria, viruses, or toxins. Questions: 1. How do prions evade the immune system?
  2. 2. 2. What has gone wrong with the immune system when a person has an auto-immune disease? Three major players in your immune system which detect antigens are: antibodies, B cells and T cells Antibodies are specialized proteins secreted by B cells. Antibodies recognize and bind to antigens. One antibody recognizes one epitope (specific shape). One antigen may be made up of several epitopes (shapes). The specificity of one particular antibody recognizing one antibodies particular epitope is another lock and key relationship. Antibodies can cause foreign bacterial cells to clump together which makes it easier for phagocytes to capture them. Antibodies can also stimulate another feature of the immune system: the complement system (mentioned in the 2nd line of defense) where specific proteins attach to the surface of the foreign cell, punch holes in its plasma membrane causing it to rupture. Both B and T cells are types of lymphocytes or white blood cells initially produced in bone marrow. Both have receptors on their surface to recognize epitopes (specific shapes). One cell only makes one type of receptor that recognizes one epitope. The receptors on their cell surface are basically antibodies that remain attached in their cell membrane. B cells secrete antibodies that, as T cells directly bind and kill to host mentioned, recognize and bind to cells that are cancerous or have been invading cells making the infected by viruses. They can also go pathogenic cells clump together after larger invaders like parasitic before macrophages can attack T cells worms or fungal cells. B cells them. T cells also assist the work of B cells. Because one B cell or T cell also only recognizes and binds to one epitope, at any one time your body is making thousands of B cells, T cells and antibodies to be able to recognize thousands of potential foreign invaders. Question: 3. Why are organ transplants possible, if the body attacks anything it perceives as foreign?is Any B or T cell that recognizes an epitope found on a host (self) cell destroyed before the cells are mature so that the immune system does not attack cells in the host’s own body. During an infection, thousands of copies are http://altered-states.net/barry/newsletter168/antigens4.gif recognize the Figure from: made of the B and/or T cells which specific antigens on the pathogen. Thousands of the correct antibodies are also made to fight the infection. In addition to producing cells actively involved in fighting the infection, extra copies of the specific B and T cells (which recognized the antigen) are made called memory cells. Once the infection lessens the production
  3. 3. of antibodies and white blood cells slows down, however the memory cells persist in the body after the infection is over. These memory cells allow the immune system to respond very quickly if the pathogen is re-encountered. During a second encounter they can divide so quickly and attack the pathogen so fast that you likely will not get sick a second time. When an antigen is first encountered it takes the immune system some time before it produces a significant amount of antibodies and white blood cells to fight the infection. These are the “primary responses” shown on the graph. Antigen X is re-encountered at the time point shown by the arrow is on the graph. Because of the persisting memory cells, antibodies and white blood cells are produced more quickly and at higher concentration than if it was the first time they had been encountered. We call this acquired immunity. The host likely does even develop any symptoms of illness because of the faster response. Viral infections: Viruses can only bind to cells where their surface proteins can bind to receptors on a cell’s surface. This is what tends to make viruses have such specific host ranges. Egs. the HIV virus  bind and infect helper T cells in your immune system. Cauliflower mosaic virus  bind and infect leaf cells of plants in the Broccoli family (which includes cauliflower) Adenoviruses  cells of our respiratory tract (and often only part of the tract which is why different viruses give us different varieties of cold symptoms) Example of how a virus uses its receptors to infect a cell: The influenza virus has specialized proteins on its surface like hemagglutinin which binds to a specific type of sugar molecule (sialic acid) found on glycoproteins of some cells. Once the virus binds to this sugar this stimulates the host cell to engulf the virus by endocytosis. The cell attempts to digest the virus by turning the vesicle into a lysosome (low pH, many enzymes to breakdown whatever is inside). The hemagglutinin protein refolds into a new shape in the low pH environment and reacts with the lysosomal membrane to allowing the viral genome to exit into the cytoplasm unharmed. Why do we keep getting colds and flus? Mutations can change what proteins viruses have on their surface  these new proteins are no longer recognized by a person’s immune system. Cold and flu virus genomes are made of RNA rather than DNA. RNA mutates much more frequently than DNA  This means that cold and flu viruses are changing from year to year.
  4. 4. Regular flu shots contains fragmented viruses from last year’s flu viruses. If this year’s flu strains have changed too much compared to last year’s you may still catch the flu. The H1N1 flu shot contains fragmented (dead) pieces of the H1N1 virus. Questions: 4. What part of the deactivated flu viruses are in the flu shot –the genetic material or the capsule? Why was this part chosen? 5. A vaccine against any cellular pathogen uses dead fragmented cell walls and membranes. If the process of fragmenting the cells is too destructive the vaccine may not be effective. Why not? Bacterial and protist infections Bacterial and protist cells, like viruses, are recognized as foreign by the presence of epitopes on their cell surface. As explained earlier antibodies (and possibly T cells) work together with macrophages and complement proteins to kill foreign cellular pathogens. Do bacteria and protists recognize specific cells like viruses do? More commonly they release toxins which make us sick, and they obtain energy and multiply in one particular part of the body (site of infection or environment they can tolerate). Fighting Infections with Antibiotics: These are drugs which can kill cellular (not viral) pathogens. Antibiotics target cellular components or processes which are different from the host. The first antibiotic discovered was a chemical (penicillin) made by a fungus to kill a bacterium which was competing for the same food source. Penicillin binds to the sugar peptidoglycan in the cell walls of gram-positive bacteria. This weakens the cell walls causing the cells to burst. Fungi produce a number of natural antibiotics against bacteria. In every case the antibiotic targets some structure or process in the bacterial cell that is not shared by fungi. If you want to become an antibiotic designer you need to be a good cell biologist and study what is different between the host cells and pathogen cells! Figure from: http://www.socialfiction.org/img/penicillin_1.jpg Some common targets of bacterial antibiotics are: –their cell walls or enzymes used to synthesize their cell walls causing the cells to stop dividing or to burst (as with penicillin) –unique bacterial components of their ribosomes shutting down their ability to make proteins  causing their cells to shut down and die Questions: 6.Bacteria have an enzyme that allows them to synthesize folic acid from scratch. Folic acid is used in all cells to make nucleotides, the building blocks of DNA and RNA. We lack the enzyme that bacteria have to make folic acid, so instead we must get folic acid from the food we eat. Could we make an antibiotic that inhibits the folic acid synthesizing enzyme in bacteria or would it harm us? Sulfa – antibiotics (lots of people get sick when they take sulfa. May be do to shape and foreign stuffs. Eukariotic cell)
  5. 5. a. Yes we could make and then use such an antibiotic because we lack this enzyme b. No because we lack the enzyme we would make antibodies to both the unknown enzyme and the antibiotic against it causing an allergic reaction. 7. Although there are some antibiotics against protists like Giardia lamblia and Trichomonas vaginalis, it is generally harder to find antibiotics against protists and there is often a greater chance that some of these antibiotics may make people sick. Considering what you know about protist cells why might this be? Giardia lamblia Trichomonas vaginalis http://www.biotech-weblog.com/ http://www.uthscsa.edu/mission/ 50226711/giardia_lamblia_genom spring00/std.htm e_sequenced.php A fungus Epidermophyton floccosum which causes athletes foot is shown at left. 8. If you were going to try to develop an antibiotic to treat a fungal infection, what might you target? Hint: how do fungal cells different from animal cells? http://en.wikipedia.org/wiki/Image:Epiderm ophyton_floccosum_01.jpg