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Nonspecific Defenses Against Microorganisms

I). Nonspecific Defenses

II). First Line Of Defense: Surface Barriers-

A). Skin

1). Barrier because of keratin

2). Acidity of skin secretions

B). Mucous Membranes

Cover all body cavities with exterior openings.

1). Sticky mucus

2). Stomach:  HCl and protein-digesting enzymes.

3). Saliva & lacrimal fluids:   bacteria destroying enzymes.

4). Nasal hairs

5). Cilia

6). Acidity of the vagina

7). Acidity of urine

III). Second Line of Defense: Nonspecific Cellular and Chemical Defenses

A). Phagocytic Cells

1). Types

i). Macrophages

monocytes become macrophages:

ii). Neutrophils

 

iii). Eosinophils

iv). Mast Cells

 

2). Mechanisms of phagocytic cells

i). The phagocyte adheres to the microbe by recognizing the carbohydrates on the membrane.

ii). Cytoplamsic arms surround it.

iii). Lysomes kill & digest it.

(Free radicals are highly reactive chemicals with unpaired electrons that can scramble the structure of proteins, lipids, and nucleic acids)

B). Natural Killer Cells

Can lyse and kill cancer and virus infected body cells

They do not phagocytize the cells but inject chemicals called perforins that open up channels and disintegrate the nucleus.

IV). Inflammation Response

A). Is triggered whenever body tissues are injured it:

1). Prevents the spread of damaging agents

2). Disposes of cell debris

3). Sets the stage for tissue repai

B). Signs of Inflammation

 

C). Steps

There are 2 main steps to inflammation response.

1). Release of chemical mediators

• histamine
• prostaglandins
• kinines
• complement
• cytokines

 

 

Mediators function to:

i). Increase blood flow by vasodilatation -->redness and heat

--->increases the metabolic rate

ii). Increase permeability of local capillaries --->swelling (thus pain from pressure)

    -----> pressure causes pain

---> but  brings in oxygen & nutrients and clotting proteins

iii). Aid in phagocyte mobilization.

2). Phagocyte mobilization

i).  Tissue Injury

ii).  Leukocytosis inducing factor

iii). Neutrophils cling to capillaries in the injured areas.

iv).  Neutrophils squeeze through the capillary walls.

v).  Inflammatory chemicals attract more neutrophils

vi). Monocytes  become macrophages,

Pus is a mixture of dead neutrophils, broken down tissue cells and dead pathogens.

V). Antimicrobial Proteins

A). Interferon

1). The synthesis of a protein (PKR) which blocks protein synthesis at the ribosomes

2). Macrophages

3). Natural killer cells

Types of interferons:

Gamma (g )

Alpha (a )

Beta (b )

 

B). Complement

1). 2 pathways can activate them:

i). Classical Pathway depends on the binding of antibodies.

ii). Alternative Pathway triggered by the interaction of several protein factors .

2). Activation results in a cascade affect where one protein activates the next.

3). The results will be

i).  inflammation response

ii). coats the microorganism and provides receptors for the macrophages.

VI). Fever

Pyrogens:

Advantages:

• Inhibits microbial multiplication
• Increase the metabolic rate

Disadvantage

•  Inactivates enzymes