Friday, April 11, 2008

Chpt 15 Innate Immunity, etc

Innate Immunity: Nonspecific Defenses of the Host
Nonspecific Immunity
Chapter 16
Functional divisions of immunity:
Nonspecific immunity
Specific immunity

Nonspecific immunity is our first line of defense. It stops most potential pathogens and prevents them from entering the body. It involves various barriers and mechanisms.

I Skin and Mucous Membranes
A. Mechanical factors
1. Skin
a. effective barrier
b. dry, low pH. (stops bacteria, but fungi like low pH)
c. has antimicrobial secretions
d. hard for bacteria to penetrate
e. skin layers
i. dermis
ii. epidermis: contains keratin
2. Mucous membranes: line the body cavities
a. barrier, protects underlying cells
b. traps organisms in mucous. (mucous also keeps the cavities from drying out)
c. offers less protection than skin
d. Eyes
i. lacrimal apparatus: manufactures and drains away tears.
e. Oral cavity:
i. saliva: produced by salivary glands washes microorganisms from the surfaces of the teeth and mucous membranes of the mouth. Prevents colonization.
f. Respiratory tract:
i. Cilia in the respiratory tract move trapped mo’s out
ii. epiglottis cover the larynx during swallowing
iii. Ciliary (mucociliary) elevator: move and propel mo’s trapped in mucous out of the respiratory system
iv. alveolar macrophages
v. coughing and sneezing
h. Digestive tract
1. defecation and vomiting
2. mucous lining
i. urination
1. urinary pH
2. production of urine
3. normal flora

B. Chemical factors
1. sebum: sebaceous oil glands in the skin which form a protective film over the skin surface
2. sweat glands: produce perspiration which flushes mo’s from the skin surface Sweat contains lysozyme which breaks down cell walls of gram + bacteria.
3. Eye: tears contain lysozyme
4. Oral Cavity:
a. saliva: contains lysozyme and salivary enzymes
5. Digestive tract:
a. stomach acid: (gastric juice) Low pH destroys most organisms.
i. Helicobacter can grow in the low pH of the stomach
b. enzymes
c. bile
d. normal flora
C. Normal microbiota (flora) and nonspecific resistance
1. Compete with disease causing organisms (competitive exclusion)
2. inhibit disease causing organisms
3.
II Phagocytosis: the ingestion of solids by eukaryotic cells
A. Formed elements in blood: cells and cell fragments.
1. Plasma: blood fluid
2. Leukocytes: white blood cells.
a. leukocytosis: an increase of white blood cells during infection
b. leucopenia: decreased white blood cells
3. Types of leukocytes:
a. neutrophils (nonspecific): a phagocyte
b. eosinophiles (nonspecific)
c. basophiles (nonspecific)
d. monocytes (become macrophages which are phagocytes)
e. lyphocytes (specific)
i. T cell
ii. B cell
iii. NK cell
B. Actions of phagocytic cells. (did not go over)
C. Mechanism of phagocytosis
1. Chemotaxis: the attraction of mo’s to chemicals
2. Adherence: (attachment) between the cell membrane of the phagocyte and the organism. Facilitated by chemotaxis.
3. Ingestion: the process of a phagocyte folding inward and forming a sac around a mo.
4. Digestion
D. Microbial evasion of phagocytosis (did not go over)


III Inflammation: a host response to tissue damage, characterized by redness, pain, heat, swelling, and perhaps loss of function. A major protective mechanism in response to injury or infection. Activated in multiple ways:
A. Vasodilation: The first stage of inflammation; involving an increase in blood vessel diameter thereby causing more blood flow to the injured area.
1. responsible for the redness, heat, edema and pain of inflammation
B. Permeability: (swelling/edema) allows defense substances in the blood to pass through the walls of the blood vessels.
1. histamine can increase permeability
C. Phagocyte migration and phagocytosis (did not call it that… called it) Leukocyte accumulation/chemotaxis
D. Tissue repair: the final stage of inflammation (connective tissue)
E. Fever
1. Temp can be altered by the ingestion of gram – bacteria by phagocytes.
2. protective mechanism
3. inhibits growth of bacteria and viruses
4. enhances immune response
F. Pus: The last step of inflammation. (according to Sushma) Sign that inflammation has ended.
IV Antimicrobial Substances
A. The complement system
1. Complement: consist of a group of over 20 different proteins found in blood serum. (30 proteins produced by the liver)
a. blood serum: the liquid portion of blood that remains after it is drawn and clotting proteins for a clot with the formed elements.
2. Complements participate in:
a. lysis of foreign cells
b. inflammation
c. phagocytosis
3. Can be activatied by:
a. classical pathway: initiated when antibody molecules bind to the antigen (ex: bacterial cell)
b. alternative pathway: (Does not involve antibodies) Complement proteins, and proteins called factors B, D and P, combine with certain microbial polysaccharides. Especially affected are the lopopolysaccharade cell wall portions (endotoxins) of gram – enteric bacteria.
c. lectin pathway: macrophage stimulate the liver to release lectins which enhance opsonization by binding to cell carbohydrates.
4. Complement proteins act in an ordered sequence, or cascade. (one protein activates another)
a. Designated by “C” numbered 1 through 9
b. Inactive state is denoted by “C”
c. Upon activation they split into Ca; Cb; etc
d. C3 plays a central role in both the classical and alternative pathways.


B. The Result of Complement Activation:
1. Cytolysis: complement protein then binds to 2 adjacent antibodies and initiates a sequence known as the membrane attack complex.
2. transmembrane channels (membrane pores): circular lesions that cause the eventual lysis of the cell to which the antibodies are attached.
3. Inflammation
4. opsonization (immune adherence) promotes attachment of a phagocyte to the microbe.
5. Attract pahgocytes
C. Interferons (IFNs): proteins produced in response to viruses.
1. inhibit viral replication inside cells
2. activates NK cells and macrophages

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Extra Stuff
Definitions:

Immunity: (resistance) Our ability to ward off disease through our defenses.
Susceptibility: Our vulnerability or lack of resistance to disease
Innate (nonspecific) immunity: defenses that tend to protect us from any kind of pathogen.
Adaptive (specific) immunity: is based on antibody production and is a defense against a particular organism.
Immunology: the study of a host’s defense to a pathogen.
Phagocytes: blood cells or derivatives of blood cells that ingest mo’s or a particulate matter.

Immunology is complicated because there are many different enemies out to get you.

3 steps of defense (what I wrote down from lecture, but isn’t inflammation and fever the same thing?)
1. inflammation
2. phagocytosis
3. fever


Ok, the lines of defense: (according to the study guide)
First: skin and mucous membranes
Second: phagocytosis

Signs of inflammation: Pa, He Reads Swell
Pain
Heat
Redness
Swelling


There is a slide from the second handout that discusses ways of preventing phagocytosis. It is not in my study guide:

Inhibit adherence capsules K. ?
Kill phagocytes S. aureus
Escape phagosome Shigella
Prevent phagosome-lysozome fusion HIV and ?

C3 and C5 are major in the complement system

Study pages:
474-484
486-488
Fever 489
Complement system 490-494

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