CHEMICAL FACTORS

 Sebum contains unsaturated fatty acids

CHAPTER 7
which inhibit the growth of pathogenic
Host Defenses to bacteria
Microorganism  Perspiration washes MO off the skin
 Lysozymes is found in tears, saliva, nasal
secretions and perspiration
 Non-Specific Defenses  Gastric juice destroys bacteria and most
 Skin and Mucous Membrane bacterial toxins
o Mechanical and Chemical factors  Vaginal secretions are also slightly acidic
o Normal microbiota which discourages bacterial growth
 Phagocytes
 Inflammation
 Fever MICROBIOTA

 Specific Defenses  Microbial Antagonism

─ Microbiota compete with pathogens for
 Lymphocytes nutrients
 Antibodies ─ Microbiota produces toxins that are
harmful to pathogens
Resistance - Ability to ward-off disease
(pathogenic) through defenses.
PHAGOCYTOSIS
Susceptibility - Vulnerability or lack of
resistance to pathogens.  Ingestion of MO or other particles like debris
 Phagocytes or Phagocytic cell – cell that
NON-SPECIFIC DEFENSES
perform phagocytosis
Defenses against any pathogen, regardless of
the species. MECHANISM OF PHAGOCYTOSIS
Chemical attraction of
 Skin and Mucous Membrane CHEMOTAXIS
phagocytes to MO
 Mechanical Factors Attachment of phagocyte’s
 Chemical Factors ADHERENCE plasma membrane to the
 Microbiota surface of the MO
 Phagocytosis The plasma membrane of the
 Neutrophils/ PMNs phagocyte extends
INGESTION
 Macrophages projections that engulf the
 Reticuloendothelial system MO
 Inflammation Lysosomes digests the engulf
DIGESTION
 Fever MO or foreign material

SKIN AND MUCOUS MEMBRANE NEUTROPHILS / PMNS

MECHANICAL FACTORS  Derived from hematopoietic cell from bone
marrow
 Structure of the skin and the waterproof
 Migrate to the site of inflammation by
keratin provide resistance to microbial
chemotaxis and exert phagocytic action
invasion
 Mucous membrane provides less protection MECHANISM OF PHAGOCYTIC ACTION
against microbial invasion Activation of lysozymes
 Lacrimal apparatus protects the eyes from NONOXIDATIVE
and hydrolytic enzymes in
irritating substances and microorganisms MECHANISM
specific granules
 Saliva washes microorganisms from teeth OXIDATIVE Production of superoxide
and gums MECHANISM radical, H2O2 and NO
 Mucus traps many MO that enter the
respiratory and GIT
─ In lower respiratory tract the mucociliary MACROPHAGES
apparatus helps in the removal of
 Derived from monocyte stem cells in bone
bacteria
marrow have longer life span and active at
 MO are also prevented from entering the
lower respiratory tract by small lid of low pH
cartilage called epiglottis MECHANISM OF PHAGOCYTIC ACTION
 Flow of urine moves the MO out of the NONOXIDATIVE Activation of lysosomes
urinary tract MECHANISM and release of interleukin-1
─ Same as vaginal secretions OXIDATIVE Production of superoxide
MECHANISM radical, H2O2 and NO
RETICULOENDOTHELIAL SYSTEM
 A system that involves mononuclear
phagocytic cells of the lymphatic organs
and other organs
MOA: Filtration of MO from the bloodstream
INFLAMMATION
 Vascular reaction that involves the delivery
of fluids, dissolved blood and cells from the
circulatory system to the affected area
 Causes:
─ Microbial Infection
─ Physical Agents
─ Chemical Agents
 Cardinal signs:
─ Redness
─ Pain
─ Heat
─ Swelling
─ Loss of function
 Functions:
─ Destroy the injurious agent, if present,
and to remove its by products from the
body
─ If destruction is not possible, confining or
walling off the injurious agent and its by-
products
─ Repair or replace the tissue damaged
by the injurious agent and its by-
products
 Inflammatory Process
1. Vasodilation and Increased
Permeability of Blood Vessels
2. Phagocyte Migration and
Phagocytosis
3. Tissue Repair
FEVER
 Systemic response to injury
 Most common manifestation of the
inflammatory response and a cardinal
symptom of infectious disease
 Mechanism of Fever Production
1. Hypothalamus – “body’s thermostat”
2. Pyrogens
o Endotoxin – LPS of Gram (-) bacteria
o Interleukin-1 – “endogenous
pyrogen”
 Beneficial Effects of Fever
─ Defense against disease
─ Increase T-cell proliferation and
antibody production
─ Speeds up the body’s reactions thereby
helping body tissues to repair
themselves more quickly
IMMUNITY
 Body’s defense against a particular disease
 Innate – inborn, natural immunity,
nonspecific, different barrier in the body
 Acquired or Adaptive – specific, need to
have a disease
─ Naturally acquired active immunity –
certain person contracted a disease will
produce an antigen
─ Naturally acquired passive immunity –
natural transfer of antibodies (mother to
baby through the colostrum or trans-
placental transfer)
─ Artificial acquired active immunity –
through vaccination (immunization)
─ Artificial acquired passive immunity –
introduction of antibodies directly to a
person from another person or animal
IMMUNE RESPONSE
Classes:
 Antibody-Mediated (Humoral)
─ Involves B-cells producing antibodies
─ Responds to extracellular antigens
 Cell-Mediated (Cellular)
─ Involves T-cells
─ Responds to intracellular antigens
Properties:
─ Self-recognition
─ Memory
─ Specificity
ANTIGEN
 or “immunogen” is a chemical substance
that can induce a detectable immune
response
 As a rule, antigens are foreign substances
 Most are CHON and are components of
invading MO
 May be nonmicrobial source
 ‘Antigenic determinants’ or ‘epitopes’ are
essential in provoking immune response
 HAPTEN - substance that is not immunogenic
by itself but can act as antigen if combined
with a carrier
ANTIBODIES
 or “immunoglobulin” is a protein produces
by B-cells in response to the presence of
antigen
 An antibody has at least two “antigen-
binding” site – monomer
 Antibodies are highly specific
Structure:
 Contains 4 CHON chains: 2 L-chains and 2-H
chains linked by disulfide bonds giving a
characteristic Y-shape
 Each chain contains variable region and a
constant region
 It consists of a Fac fragment (tip) and Fab
fragment (base)
IMMUNOGLOBULIN CLASSES
 IgG
─ A monomer, 80% in serum
─ Most predominant in the blood
─ Only immunoglobulin that can cross the
placenta
 IgM
─ A pentamer, -10% in serum
─ Predominantly involved in response to
the ABO blood group antigen
─ First antibody to appear in response to
initial infection
─ Bactericidal to gram negative bacteria
 IgA
─ A dimer with secretory components, 10-
15% in serum
─ Most abundant in the body
─ Antibosy present in colostrum
─ Saliva, tears, colostrum,seminal fluid,
mucous secretions of nose and lungs,
GIT
 IgD
─ A monomer, 0.2% in serum
─ Antigen receptor in B-cells
─ Surface of b cells
 IgE
─ A monomer, 0.002% in serum
─ Involve in allergic reactions
─ P-K body(Prausnitz and Kustner.
Produced in response to allergen found
in surface of basophils and mastcells
(tissues)
B-CELLS AND HUMORAL ACTIVITY
ORIGIN OF B-CELLS
 Derived from stem cells in bone marrow of
adults and in the liver of fetus
 Stay and mature in bone marrow
 Migrate to lymphoid organs
 Nonspecific to antigen
ANTIBODY-MEDIATED IMMUNE RESPONSE
 Exposure to extracellular antigens
 Binding of B-cells with antigen
 Clonal selection
 Primary responses
 Secondary responses
MECHANISMS OF HUMORAL IMMUNE RESPONSE
CAUSING CELL DESTRUCTION
 Neutralization
 Agglutination
 Precipitation
 Activation of complement system
COMPLEMENT SYSTEM
 Defensive mechanism consisting of serum
proteins that participates in cell lysis,
inflammation and phagocytosis
 Can be activated by:
─ An immune reaction in the classical
pathway
─ Direct interaction with a bacterium in
alternative pathway
MAJOR BIOLOGICAL EFFECTS
Enhance phagocytosis
OPSONITIZATION
ANAPHYLATAXINS Causing allergic reaction
Attachment to
CHEMOTAXIS
chemicals
CYTOLYSIS Cell lysis
T-CELLS AND CELLULAR IMMUNITY
ORIGIN OF T-CELLS
 Derived from stem cells in bone marrow of
adults and in the liver of fetus
 Move to ‘thymus’ and undergo maturation
 Migrate to lymphoid organs
TYPES OF T-CELLS
 Helper T-cells
─ Stimulate other cells of the immunesystem
─ Help B-cells respond to antigen
 Cytotoxic T-cells
─ Destroys target cells in contact
 Delayed Hypersensitivity T-cells
─ Protection from infectious agent
─ Causes inflammation associated with
allergic reactions and tissue transplants
 Suppressor T-cells
─ Regulates immune response
─ Help maintain self-tolerance
CELL-MEDIATED IMMUNE RESPONSE attracting leukocytes and leading to
tissue damage from leukocyte products
 Exposure of antigens to APC’s
 Arthus reaction, serum sickness, various
 Positioning of the antigen fragments on
forms of glomerulonephritis
APC’s surface and bonding with MHC-
molecule Type IV – Delayed Reactions
 Associative recognition
 34-48 hours
 Binding of T-cells and MHC-antigen
 No antibodies involved: reaction of T
complex
cells with antigen lead to cytokine
 Clonal selection
release, direct cytotoxicity and
 Cell-mediated cytotoxicity by perforins
recruitment of reactive cells

Immune Deficiency

CHAPTER 8  Absence of sufficient immune response

Immune System Disorders  Types:
─ Congenital Immune Deficiency
─ Acquired Immune Deficiency

Disorders
Congenital Immune Deficiency
 Hypersensitivity
 Immune Deficiency  Inborn with a defective immune system
 Autoimmunity  DiGeorge syndrome
─ Lacks thymus gland; lacks cell-mediated
Hypersensitivity immunity
 “Allergy”
 Condition in which an immune response
results in exaggerated or inappropriate Acquired Immune Deficiency
reactions that are harmful to the host  Can be caused by drugs, cancers or
 Usually occurs after the second contact
infectious agents
of the specific antigen
 Hodgkin’s disease
─ Lowers the cell-mediated response
 Removal of spleen decreases humoral
immunity

Autoimmune Disease

 Action of the immune system in response to

Type I – Anaphylactic Reactions
 <30 minutes
 Antigen reacts with antibody (IgE)
bound to mast cells: results in mediator
release and mediator effects
 Asthma, Hay fever, Scratch test,
Anaphylaxis
self-antigens and causes damage to one’s
own organs
 Loss of ‘self-tolerance’
─ Immune system’s ability to discriminate
self from nonself
 Leads to the production of antibodies or a
response by T cells against a person’s own
tissue antigens

Type II – Cytotoxic Reactions

 5-12 hours
 Circulating IgG and IgM writers with
antigen on cell surface
 Leads to complement activation, cell
lysis or phagocytosis of target cell,
antibody mediated cytotoxicity
 Immune hemolytic anemia, transfusion
reaction, Rh incompatibilities

Type III – Immune Complex Reactions

 3-8 hours
 Union of antigen and IgG forms immune
complexes that activates complement,