Upload
rosemary-burke
View
227
Download
3
Tags:
Embed Size (px)
Citation preview
16Innate
Immunity: Nonspecific Defenses of the Host
Student Learning Outcomes
Differentiate between innate and adaptive immunity.Define toll-like receptors.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 two of the three pathways of activating complement and
describe the 3 outcomes. Compare and contrast the actions of -IFN and -IFN with -IFN.Describe the role of transferrins and antimicrobial peptides in innate
immunity.
The Concept of Immunity
Immunity: Ability to ______________________.
Susceptibility: Lack of ________________to a disease.
Innate immunity: ________________Specific or not?
Adaptive immunity: __________________________
Fig 16.1
The Body’s Defensive Cells
Can you name them?
Host Toll-like receptors (TLRs) attach to
Pathogen-associated molecular patterns (PAMPs)
Binding to TLRs induces release of cytokines that regulate the intensity and duration of immune responses
TLRs = ?
PAMPs recognition
Horseshoe structure of TLR3, showing attached sugars (spheres) and internal structures
Fig. 16.7
First Line of Defense: Skin & Mucous Membranes
Fig 16.3
Physical Factors Epidermis
Mucus of mucous membranes (Muco)-ciliary escalator Nose hairs Lacrimal apparatus Saliva
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
1st Line Defense in
Human
Mastering: Host Defenses – The Big Picture
Red Blood Cells Transport O2 and CO2
White Blood Cells:Phagocytosis
Histamine
Kill parasites. Involved in allergies
Formed Elements in Blood
Compare to Table 16.1
Formed Elements in BloodWhite Blood Cells cont:
Phagocytosis
Phagocytosis
Natural killer cellsDestroy target cells
Cell-mediated immunity
Produce antibodies
Blood clotting
Second Line of Defense: Formed Elements in Blood
20-25%
3-8%
0.5-1%%
2-4%60-70%
Process of Phagocytosis
Phagocytes engulf and kill microorganisms
Steps of phagocytosis:
1. Chemotaxis
2. Adherence: Recognition and attachment
3. Ingestion: Engulfment and creation of phagosome
4. Digestion:
1. Fusion of phagosome with lysosome
2. Destruction and digestion
3. Residual body ExocytosisFig 16.7
Inhibit adherence: capsules, M protein S. pyogenes, S. pneumoniae
Kill phagocytes: Leukocidins S. aureus
Lyse phagocytes: Membrane attack complex
L. monocytogenes
Escape phagosome Shigella
Prevent phagosome-lysosome fusion HIV
Survive in phagolysosome Coxiella burnetti
Microbial Evasion of Phagocytosis
Phagocytosis and Evasion of Phagocytosis
Phagocytosis: Microbes That Evade It
Virulence Factors: Inactivating Host Defenses
Virulence Factors: Hiding From Host Defenses
Review the Following MasteringAnimations
Phagocytosis: Mechanism
Phagocytosis: Overview
InflammationTissue damage leads to
inflammatory responsePurpose:
Destroy pathogen limit spread of infection pave way for tissue repair
Acute-phase proteins activated (such as TNF-, kinins, and other cytokines) quickly leads to 1st stage of inflammation (?)
4 (5) cardinal signs:?
The 3 Stages of Inflammation
1. Vasodilation and increased vessel permeability due to histamine, kinins, prostaglandins, and other cytokines
2. Phagocyte migration and phagocytosis Margination and diapedesis (emigration) Chemotaxis(due to various cytokines and
components of complement system) Pus formation
3. Tissue repair and regeneration depends on type of tissue
Inflammatory Process
DiapedesisMargination
Fig 16.8
Treatment of abscess?
Inflammation review
Fever: Abnormally High Body Temperature
Hypothalamus releases prostaglandins that reset the thermostat
Body reacts to raise the temperature. How?
When no more IL–1, body temperature falls (crisis).
Hypothalamus acts as body’s thermostat. Normally set at?
Endotoxin causes phagocytes to release interleukin–1 (IL–1). IL-1= endogenous pyrogen
Beneficial effects of moderate fever:
Inhibited pathogen growth
Increased cellular metabolism e.g.: Increased transferrin production Increased IL–1 activity T cell production Faster repair mechanisms
Problematic effects of high fever:
> 40.7C (105F) can be dangerous (Tachycardia, acidosis, dehydration)
Death at temp. > 44 - 46C
Antimicrobial Substances
1. Complement system
2. Interferons
3. Transferrins: _________________
4. Antimicrobial peptides: cause bacterial cell lysis. Produced by mucous membrane cells and phagocytes.
Complement System Summary
Series of 30 plasma (serum) proteins, activated in a cascade
3 effects 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
The Complement System FoundationFig 16.9
MAC
Complement System Overview
Opsonins (complement proteins or antibodies) coat bacteria and promote attachment of micro-organism to phagocyte Process is called ______________
Fig 16.12
Classical Pathway
Alternative Pathway
Fig 16.13
Does not require a specific antibody to get started
Some Bacteria Evade Complement
Capsules prevent Complement activation
Surface lipid-carbohydrates of some Gram-negatives prevent MAC formation
Enzymatic digestion of C5a by Gram-positives
Mastering Animations: Complement System1. Overview2. Activation3. Results
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 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.
Interferons (IFNs)
Fig 16.15
Review Questions: 1 – 4 and 9 Multiple Choice Questions: 1 – 3, 5, 6, and 8
– 9 Critical Thinking Questions: 1 and 2Clinical Application Questions: 2 and 3