Download Non-Specific Defenses

Non-Specific
Defenses
The first line against disease
Nonspecific Defenses of the
Host

Susceptibility

Resistance

Nonspecific resistance

Specific resistance
Lack of resistance to a
disease
Ability to ward off
disease
Defenses against any
pathogen
Immunity, resistance
to a specific pathogen
Host Defenses
Figure 16.1
Mechanical Factors

Skin


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Mucous membranes
Ciliary escalator


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Epidermis consists of tightly packed cells with Keratin, a
protective protein
Microbes trapped in mucus are transported away from the
lungs
Lacrimal apparatus

Washes eye

Washes microbes off

Flows out

Flow out
Saliva
Urine
Vaginal secretions
Chemical Factors

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Fungistatic fatty acid in sebum
Low pH (3-5) of skin
Lysozyme in perspiration, tears, saliva,
and tissue fluids
Low pH (1.2-3.0) of gastric juice
Transferrins in blood find iron
NO inhibits ATP production
Normal Microbiota

Microbial antagonism/competitive
exclusion

Normal microbiota compete with
pathogens.
Formed Elements In Blood
Table 16.1
Differential White Cell
Count

Percentage of each type of white cell in a
sample of 100 white blood cells
Neutrophils
Basophils
60-70%
0.5-1%
Eosinophils
2-4%
Monocytes
3-8%
Lymphocytes
20-25%
White Blood Cells



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Neutrophils: Phagocytic
Basophils: Produce histamine
Eosinophils: Toxic to parasites, some
phagocytosis
Monocytes: Phagocytic as mature macrophages
Fixed macrophages in lungs, liver, bronchi
Wandering macrophages roam tissues
Lymphocytes: Involved in specific immunity
Phagocytosis
Figure 16.8a
Microbial Evasion of
Phagocytosis
• Inhibit adherence: M
protein, capsules
Streptococcus pyogenes, S.
pneumoniae
• Kill phagocytes:
Leukocidins
Staphylococcus aureus
• Lyse phagocytes:
Membrane attack
complex
Listeriamonocytogenes
• Escape phagosome
Shigella
• Prevent phagosomelysosome fusion
HIV
• Survive in
phagolysosome
Coxiella burnetti
Inflammation








Redness
Pain
Heat
Swelling (edema)
Acute-phase proteins activated
(complement, cytokine, kinins)
Vasodilation (histamine, kinins,
prostaglandins, leukotrienes)
Margination and emigration of WBCs
Tissue repair
Chemicals Released by
Damaged Cells
• Histamine
Vasodilation, increased
permeability of blood vessels
• Kinins
Vasodilation, increased
permeability of blood vessels
• Prostaglandins
Intensity histamine and kinin
effect
• Leukotrienes
Increased permeability of blood
vessels, phagocytic attachment
Inflammation
Figure 16.9a, b
Inflammation
Figure 16.9c, d
Fever: Abnormally High
Body Temperature





Hypothalamus normally set at 37°C
Gram-negative endotoxin cause
phagocytes to release interleukin 1
Hypothalamus releases prostaglandins
that reset the hypothalamus to a high
temperature
Body increases rate of metabolism and
shivering to raise temperature
When IL-1 is eliminated, body
temperature falls. (Crisis)
The Complement System

Serum
proteins
activated in
a cascade.
Figure 16.10
Effects of Complement
Activation



Opsonization or
immune adherence:
enhanced
phagocytosis
Membrane attack
complex: cytolysis
Attract phagocytes
Figure 16.11
Effects of Complement
Activation
Figure 16.12
Classical Pathway
Figure 16.13
Alternative Pathway
Figure 16.14
Lectin Pathway
Figure 16.15
Some bacteria evade
complement



Capsules prevent C activation
Surface lipid-carbohydrates prevent
MAC formation
Enzymatic digestion of C5a
Interferons (IFNs)

Alpha IFN & Beta IFN


Cause cells to produce antiviral proteins
that inhibit viral replication
Gamma IFN

Causes neutrophils and macrophages to
phagocytize bacteria
Interferons (IFNs)
2 The infecting
virus replicates
into new
viruses.
5 New viruses released
by the virus-infected
host cell infect
neighboring host
cells.
6 AVPs degrade viral
m-RNA and inhibit
protein synthesis and
thus interfere with
viral replication.
1 Viral RNA from an
infecting virus
enters the cell.
3 The infecting virus also
induces the host cell to
produce interferon on
RNA (IFN-mRNA), which
is translated into alpha
and beta interferons.
4 Interferons released by the virus-infected host cell bind to plasma
membrane or nuclear membrane receptors on uninfected neighboring
host cells, inducing them to synthesize antiviral proteins (AVPs). These
include oligoadenylate synthetase, and protein kinase.
Figure 16.16