IMMUNITY (within host)  Antibodies

Definition of Terms If the first line of defense does not work, the second line will be
activated.
 Resistance – ability to ward off disease
o Non-specific resistance – defenses that If the second line of defense does not work, the third line will
protect against all pathogens be activated.
o Specific resistance – protection against
Non-Specific Host Defense Mechanisms
specific pathogens
 Susceptibility – vulnerability or lack of resistance. If First Line of Defense
susceptible, you are prone to contract disease, getting
infections brought by different pathogens. a. Physical or Mechanical barriers: intact skin and intact
mucous membranes
Host Defense Mechanisms o Skin has layers of epidermis and dermis
- A very effective barrier to most
 Non-specific host defense mechanism
pathogens with few exceptions.
- serve to protect the body from a variety of foreign
- The epidermis is the thin outer layer
substances or pathogens
containing Langerhans cells, dead cells,
- cater to all types of pathogens, they will not
and water proof mechanism provided by
recognize if it is bacteria or virus
the keratinization.
- serves to all substances including toxins
- The dermis is the thicker part of the
- involves two lines of defenses:
skin, containing connective tissue that
- First line of defense – nonspecific
supports the overall skin and its
natural barriers that restrict entry of the
capability, so it is not easily penetrated
pathogen
by pathogens.
 Skin
- Some pathogens can still penetrate
 Mucous membranes
intact skin such as hookworms and fungi
 Secretions of skin and mucous
o Mucous membranes: line gastrointestinal,
membranes
genitourinary and respiratory tracts
- Second line of defense – innate,
- Mucus is the thick secretion that traps
nonspecific defense that provide rapid
many microbes
response against invading pathogens
- Two layers: outer epithelial and inner
once it has breached the first line of
connective layer
defense.
- Epithelial layer secretes mucus which
 Phagocytic WBCs
maintains moist surfaces
(macrophages and neutrophils)
- Although they inhibit microbial entry,
 Antimicrobial proteins against
they offer less protection than skin
different pathogens
- Some pathogens are still capable of
 Inflammatory response
penetrating these membranes like the
 Specific host defense mechanism (immune system)
Trypanoma pallidum, Papilloma virus,
- directed against a very particular foreign
E.coli, and E. histolytica
substance or pathogen that has entered the body
b. Chemical factors - digestive enzymes, acidity of
- Antigen specific immune responses, specifically
stomach (pH 1.5) and alkalinity of the intestine, acidity
targeting and attacking invaders after bypassing
of the vagina, lacrimal apparatus
the two non-specific lines of defenses.
o Sebum
- only has the third line of defense
- Oily substances produced by sebaceous
- Third line of defense mechanism
glands that form a protective layer over
 Lymphocytes
skin.
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 - Contains unsaturated fatty acids which
inhibit growth of certain pathogenic
bacteria and fungi
o pH
- low, skin pH usually between 3-5,
caused by lactic acid and fatty acids
- inhibits growth of pathogenic bateria
o Perspiration
- Produced by sweat glands.
- Contains lysozyme and acids.
o Lysozyme
- Enzyme that breaks down gram-positive
cell walls.
- Found in nasal secretions, saliva, and
tears.
o Gastric juice
Types of Interferon
- Mixture of HCl, enzymes, and mucus
from the parietal cells.
- pH between 1.2-3 kills many microbes
and destroys most toxins.
- Many enteric bacteria are protected by
food particles
 Helicobacter pylori neutralizes
stomach acid and can grow in
the stomach, causing gastritis
and ulcers
c. Normal microbiota
- Microbial antagonism by indigenous microbiota
and overall nutritional status and state of health
- Microbiota are bacteria that are inherently
present in our body, providing protection invading
pathogens, especially bacteria pathogens
- They are part of health and immune system.
Second Line of Defense
a. Transferrin and lactoferrin
 Iron-binding proteins in the blood, preventing
pathogens access to this essential mineral
b. Fever
 Augments host mechanism by stimulating
leukocytes and destroy invaders, reducing
available free plasma iron, and inducing the
production of IL-1, which causes proliferation,
maturation, and activation of lymphocytes in the
immunologic response.
 Elevated body temperature also slow down the
rate of growth of certain pathogens and can
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even kill some especially fastidious pathogens.
The setting will inhibit, kill, or promote growth.
c. Interferons
 small, antiviral proteins that prevent viral
multiplication in virus-infected cells and
serve to limit viral infections
 ar
 Has no effect on infected cells
 Host-specific but not virus-specific
 They interfere with viral infection
 They are unable to see the virus infected
cell and when they do, they attach to the
membranes of the surrounding cells and
prevent viral replication.
 Effective against variety of viruses
 Interferon alpha – produced by B- lymphocytes,
monocytes and macrophages
 Interferon beta – fibroblasts and other virus infected
cells
 Interferon gamma – activated by T- lymphocytes and
NK cells
d. Inflammation
 localizes an infection and prevent the spread
of microbial invaders, neutralizes toxins, and
aid in repair of damaged tissue
 Triggered by tissue damage due to infection,
heat, wound, etc.
 Five cardinal signs:
 Redness (rubor)
 Pain (dolor)
 Heat (calor)
 Swelling (tumor)
 May also observe; loss of function
(function laessa)
Purpose of Inflammation
 Destroy and remove pathogens
 If destruction is not possible, to limit effects
by confining or localizing the pathogen and
its products
 Repair and replace tissue damaged by
pathogen and its products

Process of Inflammation
1. Tissue damage
 Chemicals such as histamine, kinins,
prostaglandins, and leukotrienes are
released by damaged cells. It calls out
inflammatory cells to help in the process.
 Blood clot forms
 Abscess starts to form
2. Vasodilation and increased permeability of blood
vessels. Blood vessel diameter is increased,
triggered by the chemicals released earlier.
3. Phagocyte migration and phagocytosis to the site
of injury.
 Margination – phagocytes stick to
endothelium
 Emigration – phagocytes squeeze between
endothelial cells (diapedesis), going to the
surrounding tissue
 Phagocytosis of invading bacteria,
destroying them and removing the damaged
cells.
4. Tissue repair
Acute Inflammation (VIDEO NI MA’M)
 Early, immediate reaction of tissue to injury
 First phase of wound healing
 Complex protective responses to injury that lay
the groundwork to the next stage of the body’s
recovery: immune response and tissue repair
 Triggered by cell or tissue damage, or presence
of dead cells
 Occurs before immune response is established
 Primarily involves removing causative agent and
limiting tissue damage
 Involves two stages:
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o Vascular Stage
 Arterioles and venules constrict
briefly then dilate.
 Dilation promotes congestion,
increasing capillary
permeability leading to
movement of fluid in affected
tissue, resulting to the 5 signs
of inflammation.
 As fluid leaves, the blood
remaining becomes viscous
and flows slowly for clotting to
occur
o Cellular
 Initiated by the WBCs in the
site of injury
 WBCs adhere to the vessel
wall and squeeze through the
wall to move into the inflamed
tissue
 WBCs wander guided by the
signals by chemotaxis
 The WBCs engulfs the bacteria
by phagocytosis
 The products form exudates,
which accumulates serous
fluid, RBCs, fibrinogen, tissue
debris and WBCs breakdown
products, causing swelling and
pain
 Chemical mediators, derived
from the plasma, release
bioactive agents that act to
mediate the inflammatory
response
 Histamine and serotonin – released to
respond to stimuli and causes dilation and
increased capillary permeability
 Plasma derived mediators – present in
plasma in precursor forms that need to be
activated by proteolytic enzymes
 Kinins – increase capillary permeability and
stimulate pain receptors (bradykinin)
 Fibrin strands – part of the clotting system
that traps exudates, microorganisms, and
foreign bodies
  Complement (C3a) – promotes vasodilation,
leukocyte chemotaxis, and phagocytosis
e. Phagocytosis
 Primarily neutrophils and macrophages
 microbe is being engulfed to be contained
 Derived from Greek words that meant “eat
and cell”
 Carried out by WBCs: macrophages,
neutrophils, and occasionally, eosinophils
 During early stages, neutrophils
predominate in infection before
macrophages are involved.
 Wandering macrophages – originate from
monocytes that leave blood and enter
infected tissue, and develop into phagocytic
cells
 Fixed macrophages (histiocytes) – located in
liver, nervous system, lungs, lumph nodes,
bone marrow, and several other tissues
 Phagocytes are ttracted to site of infection
by Chemotaxis
1. Tissue injury, release of chemical signals by
the cells nearby to call out phagocytes to
site of injury.
2. Dilation and increased permeability of
capillary, so the phagocytes can squeeze in
the site of injury.
3. Phagocytosis of pathogens
Process of Phagocytosis
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1. Chemotaxis and adherence of microbe to
phagocyte. It will depend on the virulence
factors of the pathogens.
2. Ingestion of microbe by phagocyte. It creates
an extension to enclose the microbe.
3. Formation of a phagosome, the vesicle that
contains the microbe.
4. Fusion of the phagosome with a lysosome to
form a phagolysosome
5. Digestion of ingested microbe by enzymes
6. Formation of residual body containing
indigestible material
7. Discharge of waste materials (microbial
fragments) out of the cell.
f. Complement system
 involves approximately 30 different blood
proteins that interact in a step-wise manner
known as the complement cascade.
 It is activated directly by pathogens or
indirectly by antigen-antibody reactions
 Generates active components to fight
invading pathogens
 Consequence of activation of the
complement system: initiation and
amplification of inflammation
 Attraction and activation of
leukocytes. They call out help to
rescue from invading pathogens by
means of the activated proteins to
go and be deployed to site of
invasion.
 Cytolysis - lysis of bacteria and
other foreign cells due to the
membrane attack complex (MAC)
which produces lesions in microbial
membranes.
 Increased phagocytosis
by phagocytic cells. They
label pathogens by
opsonization or by coating
them with antibodies.
 Inflammation – complement
components (C3a, C4a, C5a, aka
mast cells) trigger the release of
histamine, which increases
vascular permeability. They also
 attract macrophages and
neutrophils.
 Opsonization – complement properties
(C3b) bind to microbial surface and promote
phagocytosis once the microbe is coated.
The macrophages and neutrophils have
receptors for C3b.
Specific Host Defense Mechanisms
Third Line of Defense
- Actual study of immunity
- Immunology - scientific study of the immune
system and immune responses
- The immune system is the third line of defense
against pathogens
Types of Acquired Immunity
 Active acquired immunity – body has something to do
to make it, obtained from the body’s activity and
reaction towards the material injected or the pathogen
itself, stimulating immunity.
o Natural active acquired immunity
- acquired in response to the entry of
a live pathogen into the body (e.g.
in response to an actual infection)
- it has long duration
o Artificial active acquired immunity
- Immunity that is acquired in
response to vaccines.
- Its duration is for many years but
must be reinforced by boosters
 Passive acquired immunity – the body does not do
anything, just simply receives immunity from the
material.
o Natural passive acquired immunity
- Immunity acquired by a fetus when
it receives maternal antibodies in
utero or by an infant when it
receives maternal antibodies
contained in colostrum from breast
milk.
- Its duration is from 6mos-1yr.
o Artificial passive acquired immunity
- Immunity that is acquired when a
person receives antibodies
contained in anti-sera or gamma
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globulin. Its duration is from 2-3
weeks
Types of Immunity
 Humoral immunity: Antibodies and antigens play a
major role in the cell-mediated immunity (antibody
mediated immunity)
- Mostly extracellular
- An antibody is a protein produced in response to
foreign substance (antigen) that will react
specifically with that substance. The reaction
between the antibody and the antigen will lead to
destroy the antigen or the pathogen that carry the
antigen or inhibit it, if not kill.
- Found in blood, lymph, saliva, colostrum
- The type produced depends on the antigen,
stimulus, and exposure time.
- Antibodies are glycoproteins produced by the B
lymphocytes, transformed by plasma cells, and
binds to the specific antigen in the antigenic part
(antigenic determinant), and once it binds, they
can destroy or inhibit it.
- Antibodies are produced by WBCs (plasma cells)
and may present in the blood and the body fluids
or attached to surfaces of cells. They are also
called immunoglobulins (Ig).
- Antibodies are very specific.
- Antigens are substances that stimulate the
animal body to produce antibodies that will
specifically react with the antigens
- Antigens are antibody generating molecules,
antigenic, or immunogenic.
- The best antigens are the foreign proteins
because of its complexity.
o Bacteria cell is a mosaic of antigen
determinants called the epitopes
(antigenic sites)
- Antigens can also be small molecules (haptens)
that act as antigens only if they are coupled with
large carrier molecules such as protein but they
are less immunogenic.
- Antigen is always complex macromolecules
(mostly glycoproteins)
Classes of Immunoglobulins
 IgG – greatest percentage of the antibody molecules
in the blood, these globulins combine to small
 antigen, and combine and neutralize toxins Typical CMI response
(antitoxins); long lived and crosses the placenta.
 IgM – a pentamer, has 10 antigen binding sites, first 1. A macrophage engulfs and partially digests a
antibodies formed in primary response to antigens; pathogen. Fragments (antigenic determinants) of
does not cross the placenta because they are big. the pathogen are then displayed on the surface
 IgA – secretory antibodies; found in breast milk, of the macrophage.
respiratory and intestinal mucin, saliva, tears, and 2. A T-helper cell binds to one of the antigenic
vaginal secretions protect these parts of the body determinants being displayed on the
from infectious agents. Total serum immunoglobulin is macrophage surface. The T-helper cell produces
IgA. lymphokines which reach an effector cell of the
 IgD – found on the surfaces of the B- lymphocytes immune system.
where it acts as specific antigen receptor. 3. The effector cell binds to a target cell.
 IgE – activities involved in both the resistance to 4. Vesicular contents of the effector cell are
parasites infections and hypersensitivity (allergy). discharged.
5. Toxins produced by the effector cells enter the
Cell-Mediated Immunity (CMI) target cell, causing disruption of DNA and
organelles. The target cell dies.
- Does not involve production of antibodies
because they might be useless at this point.
- Controls intracellular pathogens
- Cells that participate are macrophages, T- helper
cells, cytotoxic T-cells, NK cells, Killer cells and
granulocytes.
- Big players are the B and T cells.
- Cells with intracellular pathogens, NK and Killer
cells are subpopulation of lymphocytes that
destroy infected cells where pathogens reside in
- Once the cells are destroyed, the pathogens are
also destroyed.

Lymphocytes – key players in CMI

a. B-lymphocytes
- 10-15% of lymphocytes in peripheral blood
- B cells migrate to lymphoid tissues where they
produce antibodies that circulate through lymph
and blood
- They live about 1-2 weeks

b. T-lymphocytes

- T cells are phagocytotic cells, it engulfs the

antigen or the pathogen that carries that antigen,
it destroys the infected body cells, and it rejects
the foreign tissue
- About 70-80% in the peripheral blood
- Several types: T-helper, cytotoxic T-toxic, etc.

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