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This 18 page Class Notes was uploaded by Dakotarae Sloniker on Friday August 19, 2016. The Class Notes belongs to 301 at Boise State University taught by E. Meredith in Fall 2016. Since its upload, it has received 6 views. For similar materials see Cell Biology in Biology at Boise State University.
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Date Created: 08/19/16
Microbiology final 2016 Study Guide I. Nonspecific Defenses A. Not specialized to a particular bacteria B. General for any kind of pathogen C. Two levels 1. Barriers a) Skin (1) Sweat glands produce oily acids that inhibit pathogens (2) pH, (3) unsaturated fatty acids, b) Mucous membranes (1) Line the intestines, respiratory system, and genitourinary system (2) Produce saliva, tears, nasal secretions, etc. (a) Lysoso mes are produced in these secretion they digest cell walls of bacteria (b) Produc e toxic oxygen products such as peroxide , nitric oxide, and hydroxyl that help in the breakdown of microorganisms (3) Mucous traps membranes. c) Cilia (1) Small hairs lining respiratory system that beat away from the lungs and move the mucous and trapped particles out of the body d) Gastric Juice (1) Concentrated HCl and protease that destroy pathogens in the stomach 2. Internal defenses a) Leukocytes white blood cells (1) Phagocytes (a) Cell eaters (b) Most important (i) B asophils (ii) E osinophils (iii) N eutrophils (iv) M ast cells (v) M onocytes (vi) M acrophages (a) B ig eaters (b) A moeba (c) M ost famous/not most abundant (2) Lymphocytes (a) Specifi c defense mechanism (3) Natural Killer Cells *NK cells (a) Differe nt from phagocytes (b) Identifi es virus infected cells and some tumor cells (c) Lyses (split open) cells and attacks cell walls 3. Inflammatory Response a) Tissues are injured by bacteria, trauma, toxins, heat, etc. b) Damaged cells produce histamine, bradykinin, and prostaglandins and they cause blood vessels to leak and swell the tissue, isolating foreign particles. c) Chemicals attract white blood cells and they eat the bad stuff in phagocytosis. d) Responds to antigens and destroys the substance e) Complement (1) 30 proteins C1C9 (2) Enhances the abilities of antibodies and phagocytic cells to rid body of pathogens (innate immune system) (3) Liver synthesized by liver, that are normally inactive (4) It amplifies a normal immune response (a) One reaction activates another (i) C lassical Pathway (a) A ntibodies attach to antigens and this body binds to C1 (b) C 1 activates C2 and C4 by splitting them into C2a and C2b and C4a and C4b. (c) C 2a+C4b= C3 (d) C 3 > C3a and C3b, a participates in inflammation and b reacts in cytolysis and opsonization (ii) A lternate Pathway (a) D oes not involve antibodies (b) C 3 is always in the blood combines with compliment protein factors B, D and P on microbe surface. (c) C 3 splits to a and b and triggers inflammation response (b) Opsoni zation enhances phagocytosis of antigens C3b has most important opsonizing activity. 4. AntigenAntibody reaction that initiates immune response. 5. Interferons (glycoproteins produced by virus infected cells): a) alpha (1) Interferes with virus multiplication (2) Host cell specific (3) Trick the host cell into creating antiviral proteins (a) Ogilod enylase synthetase (b) Protein kinase b) Beta (1) Interferes with virus multiplication (2) Host cell (a) Ogilod enylase synthetase (b) Protein kinase c) Gamma interferon activates neutrophils and macrophages among other things. (1) Produced by lymphocytes (2) Induces neutrophils and macrophages (a) Macro phages inhibit ATP production and produce nitric oxide (b) Also increase antigen production d) Species specific (1) Animal cells II. Specific Defenses A. B cells and T cells stem from stem cells in bone marrow B. Blood and lymphoid organs C. Target insides of cells D. Best at fighting viruses E. Epitopes 1. Is the specific piece the antigen binds to when the antibody binds 2. Determinants determines the antibody that attaches F. B cells (humoral response): 1. viruses 2. bacteria, 3. Toxins cells G. T cells (cellular response): come from Thymus gland 1. Antigenic t cells bind directly to the antigenic peptide of MHC molecules 2. Have receptors 3. T Helper cells coordinate with B cells in producing antigens 4. T cytotoxic cells a) Kill virus infected cells and tumor cells, cause a anergic state that prevents autoimmune disease. b) Are what is behind organ transplant rejection 5. Tlymphocytes 6. Cell mediated immunity 7. Do not bind to antigens but sense the presence of Antigens III. Clonal selection A. Explains the function of cells, lymphocytes, in the immune system B. B cells are pre existing and a specific antigen produces a specific B cell response to produce a specific antibody. C. Explains the diversity in antibody specificity 1. IgG main antibody found in the blood and extracellular fluid a) 80% of antibodies b) Controls infection with tissues c) Binds to viruses, bacteria, and fungi d) Binding to cause immobilization e) Coating pathogen surfaces f) Activates the classical pathway and causes pathogen elimination 2. IgM a) 6% of antibodies b) Stay in blood vessels c) Produced by B cells d) Largest antibody e) In the spleen f) Does Not diffuse well and is found in low quantities g) Found in serum h) Contributes to opsonization i) Causes C3b to bind to an antigen 3. IgA a) 13% of antibodies b) 15 grams secreted from the intestines c) Plays a role in mucous membranes d) Produced in mucous lightings e) Tears, saliva, sweat, colostrum and secretions in the genitourinary tract, and respiratory epithelium 4. IgD a) .02% of antibodes b) In blood, lymph, and the tops of B cells Plasma membranes c) In immature B lymphocytes d) In blood serum e) In species from fish to humans, except birds f) Signals B cells to activate, like IgM cells g) Binds to basophils and mast cells to activate them 5. IgE a) .002% of antibodies b) Allergies and cause an allergic reaction c) In the nose, lungs, and throat d) Asthma, sinusitis, allergic rhinitis e) Chronic urticaria f) Atopic dermatitis g) Anaphylactic drugs, bee stings, antigens in immunotherapy D. T C D8+ bind to MHC class I), 1. Binds to degradation cytosolic proteins 2. Sent into the ER of the cell 3. Shows Tc cells CD8 receptor what molecules to bind to 4. Binds to MHC class 1 E. T H D4+ bind to MHC class II), 1. Occurs by phagocytosis 2. Extracellular proteins are endocytosed and digested in lysosomes and fragments are loaded on MHC class 2 molecules prior to cell surface migration 3. Derived from extracellular proteins (ENDO) F. T REG (TS) 1. 510% of T cell population 2. Sub of CD4+ 3. Combat autoimmunity by suppressing T cells that escape deletion 4. Helps avoid the body reacting against itself 5. Keeps the bacteria needed for digestion from being removed and protects the fetus from rejection G. T H produce activating cellular immunity 1. Produce cytokines and interferon gamma particle 2. Activate cells active in cellular immunity 3. Stimulate production of antibodies 4. Enhances complement and opsonization and inflammation 5. Help fight against bacteria and protozoa 6. and antibody production with respect to complement (opsonization and inflammation)). H. T H 1. Also produce cytokines but the ones associated with production of antibodies 2. IgE 3. Activates eosinophils against infection by parasites I. Antigen presenting cells: 1. macrophages and a) Large white blood cell b) Digests (1) Cellular debris (2) Foreign substances (3) Microbes (4) Cancer cells (5) Anything that does not have a specific protein on its surface (healthy body specific proteins) 2. dendritic cells a) Antigen presenting cells b) Mammalian immune system c) Process antigens material and present it on the surface so the T cells can find it d) Bridge between innate and adaptive immunity e) In tissues that come in contact with external environment f) Inner lining of the lungs,nose, stomach and intestines g) Interact with T and B cells in lymphs J. NK cells 1. Natural killer cells are cytotoxic lymphocytes 2. Innate immune system 3. Rapid response to viral infection 3 days and respond to tumor formation 4. Detect MHC on infected cell that triggers cytokine release and apoptosis or lysis of the infected cell then occurs 5. Analogous to cytotoxic T Cells K. Cytokines: 1. IL1, a) 11 cytokines that regulate immune and inflammatory response to infection b) Induces a complex proinflammatory cytokines c) Discovered first and have a strong proinflammatory response 2. IL2 a) Signaling molecules regulate white blood cells b) Responsible for immunity c) And is responsible for bodies natural response to microbial infection d) Discriminates between self and nonself proteins 3. IL12 a) Close with natural killer cells b) Enhances cytotoxic activities c) Produced by dendritic cells, macrophages and neutrophils and human Blymphoblastoid cells d) Response to antigenic stimulation e) Differentiated T cells f) Stimulates growth and function in T cells g) Stimulates gamma interferon production from NK cells and reduces IL4 suppression of interferon gamma 4. others Cytokine Cytokine Cytokine Cytokine Cytokine Cytokine Receptor Source Targets Main Function Disease Association IL1α; IL1RI and Macropha Macropha Inflammatory; ↑ = IL1b IL1RAcP ges, many ges, promotes inflammatory others thymocyt activation, bone es, CNS, costimulation, and resorption; others secretion of gout; promotes cytokines and Th17 response other acutephase proteins; pyrogenic IL1ra Soluble IL1ra and the (antagonis decoyrece soluble decoy t) ptor:IL1R receptor complex II and inhibit IL1 IL1RAcP mediated inflammatory responses IL2 IL2Rα, T cells T, B, NK Proliferation; ↓ = IL2Rb, cells, andenhancement of lymphoprolifer and macropha cytotoxicity, IFNγ ative disease IL2Rγ ges secretion, and and antibody susceptibility production to autoimmune disease; reduced Treg development. ↑ = reduced Th17 development. IL3 IL3Rα T cells, Hematopo Differentiation and and mast ietic survival of IL3Rb cells, progenitor lymphoid and eosinophil s, macro myeloid s phages, compartment mast cells IL4 IL4Rα T cells, T cells, B Proliferation; ↓ = and mast cells cells, differentiation ofusceptibility IL2Rγ or macropha Th2; promotes IgG to IL4Rα ges, and IgE extracellular and monocyte production; pathogens and IL13Ra1,I s inhibits cell L13Ra2 mediated decreased immunity and response to Th17 development allergens. ↑ = allergic asthma. IL5 IL5Rα Th2 cells Eosinophi Proliferation and ↓ = and ls, B cells activation; eosinophil and IL3Rb hallmark of Th2B-1 cell effector cells deficiency. ↑ = allergic asthma. IL6 IL6Rα Macropha Wide Inflammatory and ↓ = deficient and ges, T variety of costimulatory innate gp130 cells, cells: B action; induces immunity and fibroblast cells, T proliferation and acute- phase s, and cells, differentiation; responses, others thymocyt synergizes with lymphopenia es, TGFb to drive myeloid Th17 cells, osteoclast s IL7 IL7Rα Thymic B cells, T Homeostasis, ↓ = severe and stromal cells, differentia tion,combined IL2Rγ cells, thymocyt and survival immune bone es deficiency marrow, (SCID) and spleen IL9 IL9R and T cells T cells, Proliferation; IL2Rγ (Th2) mast promotes Th2 cells, cytokine secretion neutrophil s, epithelial cells IL10 IL10R1 Differenti Macropha Immune ↓ = immune and ated T ges, T suppression; pathology due IL10R2 helper cells, decreases antigen to uncon- cells, dendritic presentation and trolled Tregs, B cells, B MHC class II inflammation. ↑ = inhibits cells, cells expression of dendritic dendritic cells; sterile cells, down regulates immunity to others pathogenic Th1, some Th2, and Th17 pathogens. responses IL11 IL11Rα Stromal Hematopo Proliferation ↑ = and cells ietic stem exacerbates gp130 cells, B airway cells, diseases megakary ocytes IL12 IL12Rb1 Macropha T cells, Differentiation and ↓ = impaired (p35 + andIL12R ges, NK cells proliferation; Th1 responses p40) b2 dendritic promotes Th1 and and increased cells, B cytotoxicity susceptibility to intracellular cells, neutrophil pathogens s IL13 IL13Ra1,I T cells B cells, Goblet cell ↓ = impaired Th2 responses L13Ra2 macro activation in lung and phages, and gut; to extracel- IL4Rα others proliferation and lular promotion of IgE pathogens production; and allergens. ↑ = regulation of cell exacerbates mediated immunity airway diseases. IL14 Not T cells B cells Promotion of B defined cell growth IL15 IL15Rα, Broad T cells, Proliferation and ↓ = IL2Rb, expressio NK cells, survival; cytokinedeficiency in and n in epithelial production NK cells and IL2Rγ hematopo cells, defective ietic cells others generation of memory T cells IL16 Not T cells, CD4+ T Recruitment of defined eosinophil cells CD4+ T cells s, mast cells IL17A IL17RA Th17 Mucosal Proinflammatory; ↓ = or cells and tissues, protective susceptibility IL17RC others epithelial immunity in lung; to and tight junction extracellular endothelia integrity; promotes pathogens ↑ = exacerbates l cells mobilization of neutrophils and organ- specific cytokine autoimmune production by inflammation epithelial cells; promotes angiogenesis IL17B Intestine and pancreas IL 17C thymus and spleen IL17D T cells, smooth muscle cells, epithelial cells IL17F IL17RA Th17 Mucosal Similar function as Not well or cells tissues, IL17A but with 2 defined. ↑ = IL17RC epithelial logs lower receptor increases neutrophil and affinity endothelia recruit- ment l cells at high concentration. IL18 IL18R Macropha Th1 cells, Proinflammatory; ↓ = impairs and IL18 ges, NK cells, induction of IFNγ Th1 responses RAcP others B cells IL19 IL20R1 Monocyte Keratinoc Proinflammatory ↑ = psoriasis and s, others ytes, other IL20R2 tissues IL20 IL20R1 Monocyte Keratinoc Proinflammatory ↑ = psoriasis or s, others ytes, other IL22R1 tissues and IL20R2 IL21 IL21R Differenti T cells, B Proliferation of T and ated T cells, NK cells; promotes IL2Rγ helper cells, differentia tion of cells (Th2 dendritic B cells and NK and Th17 cells cytotoxicity subsets) IL22 IL22R1 Th1 and Fibroblast Inflammatory, ↑ = psoriasis and Th17 s, antimicrobial IL10R2;I cells, NK epithelial L22BP cells cells IL23 IL23R Macropha T cells Inflammatory; ↓ = (p19 + and ges and promotes susceptibility p40) IL12Rb1 dendritic proliferation of to extracellular cells Th17 cells pathogens. ↑ = exacerbates organ- specific autoimmune inflammation. IL24 IL20R1, Monocyte Keratinoc ↑ = antitumor IL22R1, s, CD4+ ytes effects IL20R2 T cells IL25 (IL IL17RB Th2 cells, Non-B, Promotes Th2 ↓ = impairs 17E) mast cells non-T, differentiation and Th2 responses cKit+, proliferation to FcεR− extracellular cells pathogens such as worms IL26 IL22R1 Activated and T cells IL10R2 IL27 WSX1 Activated T cells, Induction of early ↓ = immune (p28 + and dendritic others Th1 differentiation pathology due to EBI3) gp130 cells by stimulating expression of thencontrolled Tbet transcrip tioninflamma- factor; Inhibitiontory response of effector Th17 cel responses by inducing STAT1 dependent blockade of IL17 production IL IL28R1 Activated May promote 28A/B/IL and subsets of antiviral responses 29 (IFNλ IL10R2 dendritic family) cells? IL30 (p28 subunit ofIL27) IL31 IL31Rα Activated Myeloid Proinflammatory ↑ = atopic and T cells progenitor dermatitis; OSMRβ s, lung allergic epithelial asthma cells, keratinoc ytes IL32 Induces proinflammatory cytokine production IL33 ST2 and Macropha Mast Costimulation, ↑ = atopic IL1RAcP ges, cells, Th2 promotes Th2 dermatitis, dendritic cells cytokine allergic asthma cells production IL35 Tregs Effector T Immune (p35 + cells suppression EBI3) L. Monoclonal antibodies (how are they produced?) 1. Made by identical immune cells 2. Clones of parent cells M. Immunological memory: 1. The ability of the body to remember a certain antigen and the pieces that 2. Allows more rapid response 3. protect it 4. primary response, a) Is the adaptive immune response to initial exposure of an antigen b) Also known as priming, generates immunological memory 5. secondary response a) Memory response b) It can go to secondary, tertiary and so on depending how many times you are exposed to that antigen N. Active vs passive immunity etc., antiserum 1. Active a) Produced when it comes in contact with antigen b) Not immediate c) Long lived d) Antibodies are produced 2. Passive a) Antibodies are obtained outside b) Develops immediately c) Few days lived d) Introduction of antiserum called serum sickness, allergic reaction to a serum typically because of medications with certain proteins , the liquid part of the blood that produces antibodies helps prevent from poisonous substances O. Serology: ELISA (direct and indirect), 1. Enzymelinked immunosorbent assay 2. Fluorescent antibody a) Introduction of fluorescence helps count the presence quality of antigen in wells 3. Agglutination a) Ultrasensitive solution phase that detects antibodies b) Antibodies bind to agglutinate and synthetic antigenDNA conjugates 4. complement fixation a) Immunological test that detects the presence of specific antibody or specific antigen in a patient's serum b) Diagnose infections IV. Hypersensitivity A. Type I anaphylaxis (local, systemic) 1. Immediate 2. Allergic reaction to a specific type of antigen referred to as an allergen 3. Exposure can be ingestion, inhalation or injection 4. B cells are stimulated by CD4+TH2 cells to make IgE, which make it a hypersensitivity reaction. 5. Minutes after exposure a) Localized (1) Includes allergic rhinitis, itchy watery eyes congestion coughing sneezing short breath hives skin rash food allergies b) Systemic (1) Counters epinephrine injection B. Type II (cytotoxic) thrombocytopenic purpura 1. Antibodies in immune system bind to antigens on cell surfaces 2. These can be intrinsicself antigens or extrinsic absorbed during exposure 3. Cells are recognized by macrophages or dendritic cells and causes B cell response to form antibodies 4. Grave’s disease a) Autoimmune disease that affects the thyroid b) Hyperthyroidism and enlarged thyroid c) Overactive production of thyroid hormones d) Thyroid autoantibodies that activate the thyroid stimulation hormone receptor stimulating synthesis 5. myasthenia gravis a) Neuromuscular disease that leads to muscle weakness, circulating antibodies block acetylcholine receptors that inhibits secretion and causes muscle weakness C. Type III (immune complex) glomerulonephritis 1. Accumulation Of immune complexes that have not adequately cleared and it causes a rise in inflammatory response and attraction of leukocytes 2. Progresses to a point of disease 3. Soluble antibodies unlike in type 2 4. lupus, 5. rheumatoid arthritis D. Type IV (celluar=delayed hypersensivity) contact dermatitis, 1. MS, Hashimoto’s thyroiditis, 2. Addison’s disease E. Many of the above are autoimmune diseases V. Vaccines A. Inactivated virus – 1. polio, 2. rabies, 3. influenza B. Attenuated virus – 1. Mumps, 2. measles, 3. rubella, 4. chickenpox, 5. Sabin (polio), 6. vaccinia C. Toxoid – 1. diphtheria, 2. tetanus D. Inactivated whole cells – 1. pertussis , 2. typhoid E. Others: attenuated influenza, acellular fragments of Bordetella pertussis F. Conjugated vaccine: Hib (polysaccharide from Hemophilus influenzae G. Conjugated with protein). Also, meningitis vaccine H. HepB (antigenic fragments produced by recombinant technology) Pneumococcal vaccine: polysaccharide from multiple strains of Streptococcus pneumoniae. I. DNA vaccines. VI. Ch 25 know tables on page 728 (Bacteria) and 740 (Protozoa) VII. Ch 26 know table on page 767
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