Microbiology an Introduction

Thirteenth Edition

Chapter 16
Innate Immunity: Nonspecific
Defenses of the Host

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 The Concept of Immunity
 Susceptibility: Lack of resistance to a disease
 Immunity: Ability to ward off disease
 Innate immunity:
 Defenses against any pathogen
 Defenses present at birth
 Does not involve recognition of microbe
 No immunologic memory
 Adaptive immunity:
 Immunity, resistance to a specific pathogen
 Responds once innate defenses are breached
 Slower to respond
 Involves B and T lymphocytes
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 An Overview of the Body’s Defenses

Figure 16.1
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Physical Factors
 Skin
 Epidermis
 consists of tightly
packed cells with
 Keratin,
 a protective protein
 Shedding,
sloughing
 Dryness

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Figure 16.2
Physical Factors
 Mucous membranes
 Mucus: Traps microbes
 Ciliary escalator: Microbes trapped in mucus are
transported away from the lungs

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Factors that can impair ciliary escalator:
 1. smoking
 2. alcohol abuse
 3. infection with influenzavirus
 4. mechanical ventilation

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 Physical Factors
 Lacrimal apparatus: washes eye
 Saliva: washes microbes off
 Ear wax – traps microbes
 Urine: flows out
 Vaginal secretions: flow out
 Peristalsis, vomiting, defecation

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Chemical Factors
 Fungistatic fatty acid in sebum
 Low pH (3–5) of skin
 Lysozyme in perspiration, tears,
saliva, and urine
 Low pH (1.2–3.0) of gastric juice
 Low pH (3–5) of vaginal secretions

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Normal Microbiota and Innate Immunity
 Microbial antagonism/competitive
exclusion: Normal microbiota compete
with pathogens or alter the environment so
that pathogens can’t survive ()
 Commensal microbiota: One organism
(microbe) benefits and the other (host) is
unharmed ()
 May be opportunistic pathogens if
environmental conditions change 
S. aureus, E. coli, S. epidermidis, Enterococcus
faecalis, Pseudomonas aeruginosa
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What about Probiotics and Prebiotics?

 Probiotics

 Prebiotics

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 Leukocytes and Their Precursors.

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 White Blood Cells (Leukocytes)

Neutrophils Phagocytosis
60 – 70%
Basophils Histamine
0.5 – 1% (allergies)
Eosinophils Kill parasites
2–4%

Numbers represent the percentage of each type of white

cell in a sample of 100 white blood cells
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 White Blood Cells (continued)

Phagocytosis, Not a
Monocytes once they wbc wbc
3–8% mature into a
macrophage

Dendritic cells Phagocytosis

Not a wbc, but function similarly to macrophages

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 White blood cells - continued
20 – 25% of circulating wbc’s
T cells Cell-mediated
(lymphocytes) immunity
B cells Produce
(lymphocytes) antibodies
Natural killer Destroy target
cells cells
(lymphocytes)

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 The Lymphatic System
Lymph
Node

ANIMATION Host Defenses: Ov

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 Lymphatic Lymph in lymphatic
capillary

Capillaries Lymphatic capillary

One-way
opening

Interstitial fluid flow

Tissue cells

Lymphatic vessel

Toward lymph node

Lymphatic capillaries and lymphatic vein

Interstitial fluid
(between cells)
Venule
Tissue cell
Lymph in lymphatic Arteriole
capillary
Lymphatic capillary

Blood capillary

Flow of fluid between arteriole, blood capillaries,

lymphatic capillaries, and venule

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 Phagocytosis
 Ingestion of microbes or particles by a cell,
performed by phagocytes
 Neutrophils – primary phagocytic cell type
circulating in blood

 Fixed macrophages
 Wandering macrophages
 Dendritic cells

Descendants of
monocytes

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Phagocytosis

ANIMATION Phagocytosis: Overview

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ANIMATION Phagocytosis: Mechanism
n, Inc.

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n, Inc.

Figure 16.8 The Phases of Phagocytosis

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n, Inc.

Figure 16.8 The Phases of Phagocytosis.

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n, Inc.

Figure 16.8 The Phases of Phagocytosis.

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n, Inc.

Figure 16.8 The Phases of Phagocytosis.

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n, Inc.

Figure 16.8 The Phases of Phagocytosis.

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n, Inc.

Figure 16.8 The Phases of Phagocytosis.

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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– HIV, Mycobacterium tuberculosis

lysosome fusion
Survive in phagolysosome Coxiella burnettii

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Inflammation

 Redness
 Swelling (edema)
 Pain
 Heat
 Immobility

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Functions of Inflammation

 Destroy the agent causing injury

 Limit the effects of the agent on the rest

of the body

 Repair or replace damaged tissue

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Chemicals Released by Damaged Cells

Histamine Vasodilation, increased permeability

of blood vessels
Kinins Vasodilation, increased permeability
of blood vessels, attract neutrophils
Prostaglandins Intensify histamine and kinin effect
Leukotrienes Increased permeability of blood vessels,
phagocytic attachment

Vasodilation ( facilitated by
histamine, kinins,
prostaglandins, and
leukotrienes)
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Figure 16.8a-b 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).

(b) Vasodilation and increased

permeability of blood vessels
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Figure 16.8c The process of inflammation.
Blood vessel
endothelium
Monocyte
4
Margination—
phagocytes stick
to endothelium.

5
Diapedesis— Insert Fig 16.8c
phagocytes
squeeze between
endothelial cells.

6
Phagocytosis of
invading bacteria
occurs. Red
Macrophage blood
cell
(c) Phagocyte migration
and phagocytosis Bacterium Neutrophil
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Figure 16.8d The process of inflammation.

Scab

Blood clot
Regenerated
epidermis
(parenchyma)
Insert Fig 16.8d
Regenerated
dermis
(stroma)

(d) Tissue repair

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Fever

 Abnormally high body temperature

 Systemic response
 Hypothalamus is normally set at 37°C
 Gram-negative endotoxins cause phagocytes to
release interleukin-1 (IL-1)
 Fever can also be caused by gram positive bacteria
and viruses – but mechanism is less clear
 Hypothalamus releases prostaglandins that reset
the hypothalamus to a high temperature

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Fever

 Advantages  Disadvantages
 Increases transferrins  Tachycardia
 Increases IL-1 activity  Acidosis
 Intensifies effects of  Dehydration
interferon  44–46 C fatal

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 The Complement System

 System of over 30 serum proteins activated

in a cascade
 Activated by
 Antigen-antibody reaction (classical
pathway)
 Bacterial surfaces (alternative and lectin
pathways)

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Effects of Complement Activation
 Opsonization
 Attract phagocytes Phagocytosis
 Inflammation
 Lysis: through formation of Membrane attack
complex by complement proteins
 O–I–L

Figure 16.10
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 The Complement System

Figure 16.9
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 Figure 16.12 Outcomes of Complement Activation

outcomes of complement activation

C3

Splits into activated C3a and C3b

cytolysis opsonization inflammation

C3a C3b C3a C3b C3a C3b

C5 C5

C5a C5b C5a C5b

C6 Histamine

C7 C8 C3a C5a
Microbe

C3a C5a
C9 receptor Mast cell receptor

Channel C3b protein Microbes Phagocytesa

C6
C7 C5b
C8
C9
Phagocyte

Microbes burst as extracellular Coating microbes with C3b Blood vessels become more
fluid flows in through transmembrane channel enhances phagocytosis. permeable, and chemotactic agents
formed by membrane attack complex. attract phagocytes to area.

KEY CONCEPTS

The complement system is another way the body fights infection and destroys pathogens. This component of innate immunity
“complements” other immune reactions.
Complement is a group of over 30 proteins circulating in serum that are activated in a cascade: one complement protein triggers
the next.
The cascade can be activated by a pathogen directly or by an antibody–antigen reaction.
Together these proteins destroy microbes by (1) cytolysis, (2) enhanced phagocytosis, and (3) inflammation.

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Some Bacteria Evade Complement

 Capsules prevent C activation

 Enzymatic digestion of C5a (by bacterial
enzymes)

Complement and Disease

 Lack of complement proteins causes increased
susceptibility to infections

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Interferons (IFNs)

 IFN- and IFN-:

 Produced by cells in response to viral
infections
 Cause neighboring cells to produce
antiviral proteins (AVPs) that inhibit viral
replication
 IFN-:
 causes neutrophils and macrophages
to phagocytize and kill bacteria
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 Action of Interferons

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 Action of Interferons
(continued)
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 Iron-Binding Proteins
 Transferrin: found in blood and tissue fluids
 Lactoferrin: found in milk, saliva, and mucus
 Ferritin: found in the liver, spleen, and red bone
marrow
 Hemoglobin: located in red blood cells
 Bacteria produce siderophores to compete with iron-
binding proteins

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Antimicrobial Chemicals

 Antimicrobial peptides (AMPs)

 Over 600 have been discovered, in all plants and animals
 Broad spectrum antimicrobial activity(antibacterial, antifungal, antiviral
antiparasitic)
 May inhibit cell wall synthesis, disrupt membranmes, destroy DNA or RNA
 Lyse bacterial cells
 Dermcidin: sweat glands
 Defensins: white blood cells

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