Ch 16 Notes - Innate Immunity PDF
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2013
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This document details chapter 16 of a textbook on innate immunity. It covers topics such as resistance against diseases, the concept of immunity, and body defenses against infections, including nonspecific and specific defenses. It also touches on microbial evasion and recognition, inflammation, and fever responses to infection.
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Chapter 16 Innate Immunity: Nonspecific Defenses of the Insert Fig CO 16 Host © 2013 Pearson Education, Inc. Resistance against disease ▪ Resistance can be defined as the ability of the body to ward off disease ▪ Resistance factors include skin, stomach acid, and...
Chapter 16 Innate Immunity: Nonspecific Defenses of the Insert Fig CO 16 Host © 2013 Pearson Education, Inc. Resistance against disease ▪ Resistance can be defined as the ability of the body to ward off disease ▪ Resistance factors include skin, stomach acid, and antimicrobial chemicals that protect the body from infections ▪ The disease-producing properties of a pathogenic microbial species and the host’s resistance are important factors in determining whether a person will contract a disease. © 2013 Pearson Education, Inc. The Concept of Immunity ▪ Susceptibility: lack of resistance and vulnerability to a disease ▪ Immunity (resistance): ability to ward off disease ▪ Innate ▪ Adaptive © 2013 Pearson Education, Inc. ✶ Body Defenses Against Infection A. Disease-causing agents, also called pathogens, can produce infections within the body. B. The body has 3 lines of defense that work together to protect the body against infection: 1) Nonspecific defenses that guard against many types of pathogens (1st and 2nd line). 2) Specific defenses (adaptive immunity) that mount a response against a very specific target (3rd line). - Specific defenses are carried out by specialized lymphocytes that recognize a specific invader. 4 © 2013 Pearson Education, Inc. An overview of the body’s defenses. First line of defense Second line of defense Third line of defense Intact skin Phagocytes, such as neutrophils, Specialized lymphocytes: Mucous membranes eosinophils, dendritic cells, and T cells and B cells and their secretions macrophages Antibodies Normal microbiota Inflammation Fever Antimicrobial substances © 2013 Pearson Education, Inc. Microbial Evasion of Phagocytosis Inhibit adherence: Streptococcus pyogenes, S. pneumoniae M protein, capsules Kill phagocytes: Leukocidins Staphylococcus aureus Lyse phagocytes: Listeria monocytogenes Membrane attack complex Escape phagosome Shigella, Rickettsia Prevent phagosome–lysosome HIV, Mycobacterium tuberculosis fusion Survive in phagolysosome Coxiella burnettii © 2013 Pearson Education, Inc. Recognition of pathogens by immune cells in innate immunity ▪ Toll-like receptors (TLRs) and Pattern-recognition receptors (PRRs) ▪ protein receptors on plasma membranes of defensive host cells (such as neutrophils, macrophages and dendritic cells) ▪ attach to various components found on pathogenic microbes that are not associated with mammalian cells, called pathogen-associated molecular patterns (PAMPs) − PAMPs can include lipopolysaccharide of outer membrane, flagellin in a flagella, peptidoglycan, bacterial DNA, viral DNA and RNA, components of fungi and parasites, etc. http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit5/innate/induced%20innate_PRRs.html and http:// faculty.ccbcmd.edu/courses/bio141/lecguide/unit5/innate/prrecep.html © 2013 Pearson Education, Inc. TLRs and PAMPs © 2013 Pearson Education, Inc. Example of a Differential White Cell Count ▪ Normal “healthy” percentage of each type of white cell in a sample of white blood cells Neutrophils (phagocytosis) 60–70% Basophils (release histamine) 0.5–1% Eosinophils (produce toxins to 2–4% kill parasites) Monocytes (precursors of 3–8% macrophages) Lymphocytes (Natural killer 20–25% cells, B and T cells) ▪ An increase = leukocytosis ▪ A decrease = leukopenia ▪ Changes occur depending on type of infection © 2013 Pearson Education, Inc. Inflammation 1. Inflammation, a tissue response to a pathogen, is characterized by redness, swelling (edema), heat, and pain. 2. Major actions that occur during an inflammatory response include: - vasodilation of blood vessels which increases permeability of blood vessels and thus increase blood flow and volume in affected areas (swelling occurs) - invasion of white blood cells into the affected area - certain cells that produce tissue fibers enclose the infected area and help prevent the spread of pathogens © 2013 Pearson Education, Inc. Chemicals Released by Damaged Cells KNOW THIS ONE Histamine Vasodilation, increased permeability of blood vessels Kinins Vasodilation, increased permeability of blood vessels Prostaglandins Intensify histamine and kinin effect Leukotrienes Increased permeability of blood vessels, phagocytic attachment © 2013 Pearson Education, Inc. KNOW THESE STEPS: the process of inflammation. Bacteria entering on knife Bacteria Epidermis Blood vessel Dermis Nerve Subcutaneous tissue (a) Tissue damage Chemicals such as histamine, 1 kinins, prostaglandins, leukotrienes, and cytokines (represented as blue dots) are released by damaged cells. 2 Blood clot forms. 3 Abscess starts to form (orange area). © 2013 Pearson Education, Inc. (b) Vasodilation and increased KNOW THESE STEPS: the process of inflammation. Bacteria entering on knife Bacteria Epidermis Blood vessel Dermis Nerve Subcutaneous tissue (a) Tissue damage 1 Chemicals such as histamine, kinins, prostaglandins, leukotrienes, and cytokines (represented as blue dots) are released by damaged cells. 2 Blood clot forms. 3 Abscess starts to form (orange area). © 2013 Pearson Education, Inc. (b) Vasodilation and increased KNOW THESE STEPS: Blood vessel (c) Phagocyte migration The process of and phagocytosis endothelium inflammation. Monocyte 4 Margination— phagocytes stick to endothelium. 5 Diapedesis— phagocytes Insert Fig 16.8c squeeze between endothelial cells and into tissue area. 6 Phagocytosis of invading bacteria occurs. Red Macrophage blood cell Bacterium Neutrophil © 2013 Pearson Education, Inc. The process of inflammation. Scab Blood clot Regenerated epidermis (parenchyma) Insert Fig 16.8d Regenerated dermis (stroma) (d) Tissue repair © 2013 Pearson Education, Inc. Fever ▪ Abnormally higher body temperature ▪ Hypothalamus, the body’s thermostat, is part of the brain and is normally set at 37°C (98.6°F) ▪ Gram-negative endotoxins cause phagocytes to release cytokines, which cause the… ▪ Hypothalamus to release “prostaglandins” that reset the hypothalamus to a higher temperature = fever ▪ Vasoconstriction (blood vessels constrict, holding in heat), an increase in rate of metabolism, and shivering all raise body temperature ▪ When infection subsides, vasodilation and sweating occurs: body temperature falls (phase called “crisis”) © 2013 Pearson Education, Inc. Endotoxins and the pyrogenic response (the response that produces fever). (KNOW THIS INFO) Endotoxin Macrophage Nucleus Endotoxin Cytokines Hypothalamus of brain Prostaglandin Fever Blood vessel Pituitary Vacuole gland Bacterium 1 A macrophage 2 The bacterium is 3 The cytokines 4 The cytokines ingests degraded in a are released into induce the a gram-negative vacuole, releasing the bloodstream hypothalamus to bacterium. endotoxins by the produce that induce the macrophages, prostaglandins, macrophage to through which which reset the produce cytokines they travel to the body’s IL-1 and TNF-α. hypothalamus of “thermostat” to a the brain. higher temperature, producing fever, in an effort to slow the multiplication © 2013 Pearson Education, Inc. of the pathogen. Fever Fever offers powerful protection against infection by interfering with the proper conditions that promote bacterial and fungal growth. a. During fever, the amount of iron in the blood is reduced; this slows growth and reproduction of pathogens that require more iron at higher temps. b. Also, phagocytic white blood cells attack with greater vigor when the body temperature rises. © 2013 Pearson Education, Inc.