Ch 12 Host Defenses I: Nonspecific Defenses Copyright

Ch 12 Host Defenses I: Nonspecific Defenses Copyright

Ch 12 Host Defenses I: Nonspecific Defenses Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings SLOs Differentiate between innate and adaptive immunity. Define and explain PRRs and PAMPs Differentiate physical from chemical factors, and list examples of each. Describe the role of normal microbiota in innate resistance.

Classify phagocytic cells, and describe the roles of granulocytes and monocytes. Define and explain phagocyte and phagocytosis. Explain the different stages of inflammation. Describe the cause and effects of fever. Describe the activativation of complement and describe the 3 outcomes. Explain the antiviral action of interferons Describe the role of transferrins and antimicrobial peptides in innate immunity. Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 12.1 Defense Mechanisms of the Host

Immunity: Ability to ______________________. Susceptibility: Lack of ________________to a disease. Innate immunity: ________________Specific or not? Acquired immunity: __________________________ Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Fig. 12.1 First Line of Defense: Physical Factors

Skin & Mucous Membranes Epidermis Mucus of mucous membranes (Muco)-ciliary escalator Nose hairs Lacrimal apparatus Saliva

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Fig 16.3 Ciliary Defense ninth edition TORTORA FUNKE CASE MICROBIOLOGY an introduction

PowerPoint Lecture Slide Presentation prepared by Christine Case Fig.L.12.3 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings First Line of Defense: Nonspecific Chemical Factors Fungistatic fatty acids in sebum Skin pH and osmolarity Lysozyme in ______________________ pH of gastric juice

Transferrins in blood Also important: Antagonism and competitive exclusion of normal microbiota Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Concept Check For each of the barriers below, state whether it is a physical, chemical, or genetic barrier. A. Hydrochloric acid of the stomach B. Sloughing of skin C. Lysozyme in saliva and tears D. Mutation in the gene for complement

proteins E. Ciliary escalator Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 12.2 SECOND AND THIRD LINES OF DEFENSE: AN OVERVIEW Kick in if 1st level of defense breached System of protective cells and fluids Includes inflammation and phagocytosis Rapid action at local and systemic levels Immune system responsible for: Body surveillance

Recognition of foreign and abnormal material Destruction of these entities Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings The Bodys Defensive Cells Can you name them? Host has PRRs (Pattern Recognition Receptors), e.g.: Toll-like receptors (TLRs). These attach to Pathogen-associated molecular patterns (PAMPs) Binding to PRRs induces release of cytokines that regulate the intensity and duration of immune

responses Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings PRRs =? PAMP recognition Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements of Blood Red Blood Cells

Transport O2 and CO2 White Blood Cells: Phagocytosis Histamine Kill parasites. Involved in allergies Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements in Blood White Blood Cells cont:

Phagocytosis Phagocytosis Natural killer cells Destroy target cells Cell-mediated immunity Produce antibodies Blood clotting Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings ninth edition

TORTORA FUNKE CASE MICROBIOLOGY an introduction Fig. 12.7 PowerPoint Lecture Slide Presentation prepared by Christine L. Case Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings ninth edition

TORTORA FUNKE CASE M I C R O B I Review OLOGY Communicating an introduction Body Compartments on your own if necessary MPS Lymphatic system (Thymus, LNs,

Spleen) Blood PowerPoint Lecture Slide Presentation Fig. 12.4 prepared by Christine L. Case Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 12.3 The Second Line of Defense Generalized and nonspecific defenses that support and interact with specific immune responses: - Phagocytosis - Inflammation

- Fever - Antimicrobial proteins Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Phagocytosis: Cornerstone of Inflammation and Specific Immunity Neutrophils (part of PMNs): General purpose phagocytes Early inflammatory response to bacteria and other foreign materials and to damaged tissue

Primary component of pus Monocytes and Macrophages Stationary Macrophages, e.g.: Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Fig. 12.8 Process/Phases of Phagocytosis Phagocytes engulf and kill microorganisms 1. Chemotaxis 2. Adherence: Recognition and attachment 3. Ingestion: Engulfment and creation of

phagosome 4. Digestion: a. Fusion of phagosome with lysosome b. Destruction and digestion c.

Residual body Exocytosis Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Phagocytosis Various Mechanisms of Microbial Evasion of Phagocytosis!! Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Compare to Table 12.1

Inflammation Tissue damage leads to inflammatory response Purpose: Destroy pathogen limit spread of infection pave way for tissue repair Powerful defense mechanism but has potential to CAUSE disease. CVD due to chronic inflammation? Aging? Easily identifiable by 4 (5) cardinal signs: Rubor, Calor, Tumor, Dolor, and loss of function

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings The 3 Stages of Inflammation 1. Vascular Reaction: Vasodilation and increased vessel permeability due to histamine, chemokines, prostaglandins, and other cytokines 2. Pus Formation: Phagocyte migration and phagocytosis Margination and diapedesis (emigration) Chemotaxis(due to various cytokines and components of complement system) 3. Resulution: Tissue repair and scar formation. Depends on type of tissue

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings TORTORA FUNKE CASE ninth edition MICROBIOLOGY an introduction Diapedesis Margination

PowerPoint Lecture Slide Presentation prepared by Christine Case Fig.L.12.10 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Inflammation review Treatment of abscess? Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Fever: An Adjunct to Inflammation Abnormally High Body Temperature. ______________acts as bodys thermostat.

Normally set at? Exogenous vs. Endogenous pyrogens Endotoxin causes phagocytes to release interleukin1 (IL1). IL-1 acts on hypothalamus Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Fever cont. Thermostat set to higher temp. Body reacts how? What happens when no more IL1?

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Beneficial effects of moderate fever: Inhibited pathogen growth Increased cellular metabolism e.g.: Increased transferrin production Increased T cell production Faster repair mechanisms Problematic effects of high fever: > 40.7C (> 105F) can be dangerous (Tachycardia, acidosis, dehydration, seizures) Death when > 44 - 46C

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Antimicrobial Proteins 1. Interferons 2. Complement system 3. Antimicrobial peptides 4. Iron-binding proteins: _____________ Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Interferons (IFNs) Family of small glycoproteins

Not virus-specific -IFN and -IFN: Produced by virus infected cells. Mode of action is to induce uninfected cells to produce antiviral proteins (AVPs) that inhibit viral replication. -IFN: Produced by T- lymphocytes. Causes neutrophils and macrophages to phagocytize bacteria. Also involved in tumor immunology. Recombinant interferons have been produced. However short-acting and many side-effects. No effect on already infected cells.

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Interferons (IFNs) Compare to Fig 12.11 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Complement System Summary Series of >30 plasma (serum) proteins, activated in a cascade 3 outcomes of complement system: 1. Enhances inflammatory response, e.g.: attracts phagocytes

2. Increases phagocytosis through opsonization or immune adherence 3. Creates Membrane Attack Complexes (MACs) Cytolysis Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings The Complement System Compare to Fig 12.12 Complement System Overview

MAC Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Opsonins (complement proteins or antibodies) coat bacteria and promote attachment of micro-organism to phagocyte Process is called ______________ Some bacteria evade complement system!! Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Antimicrobial Peptides Produced by MM and phagocytes 15 20 amino acids Cause bacterial cell lysis by inserting themselves into prokaryotic membranes Research looks for ways to turn them into therapeutic drugs the end

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Fig 12.13

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