CHAPTER

Non-Specific Host Defense Mechanism 10

INTRODUCTION
Pathogenic microorganisms are endowed with special proper es that enable them to
cause disease if given the right opportunity. If microorganisms never encountered resistance
from the host, we would constantly be ill and would eventually die of various diseases. In
most cases, however, our body's defenses prevent this from happening. Some of these
defenses are designed to keep out microorganisms altogether, other defenses remove the
microorganisms if they do get in, and s ll others combat them if they remain inside. Our
ability to ward o disease caused by microbes or their products and to protect against
environmental agents such as pollen, drugs, foods, chemicals, and animal dander is called
immunity or resistance. Vulnerability or lack of immunity is referred to as suscep bility. We
have two lines of defense against pathogens. The rst line of defense is our skin and mucous
membranes. The second line of defense consists of various defensive cells, in amma on,
fever, and an microbial substances produced by the body.

LEARNING OUTCOMES
At the end of the chapter, students must have:
1. Explained the role of rst line and second line defenses in innate immunity;and
2. Applied concepts from non-speci c host defense mechanism on given case studies.

WARM-UP ACTIVITY
How do you deal with stress and anxiety?

CENTRAL ACTIVITIES
Learning Input 1 (Lecture)
Non-Speci c Host Defense
• General and serve to protect the body against many harmful substances.
• The body a empts to destroy all types of substances that are foreign to it,
including pathogens.
1. First Line of Defense
a. Skin and Mucous Membranes as Physical Barriers
• Serve as a physical or me- chanical barrier to pathogens.
• Very few pathogens are able to penetrate intact skin.
• Certain helminth infec ons (e.g., hookworm infec on,
schistosomiasis) are acquired by penetra on of the skin by
parasites, it is unlikely that many, if any, bacteria are capable of
penetra ng intact skin.
• In most cases, it is only when the skin is cut, abraded (scratched), or
burned that pathogens gain entrance or when they are injected
through the skin (e.g., by arthropods or the sharing of needles by
intravenous drug abusers). Even the niest of cuts (a paper cut, for
example) can serve as a portal of entry for pathogens.

Angelica May DC. Mendoza, RPh, MS Page 1 of 5

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 •
The s cky mucus that is produced by goblet cells within the mucous
membranes serves to entrap invaders; thus, it is considered part of
the rst line of defense.
b. Cellular and Chemical Factors
• These are addi onal factors that account for the skin’s ability to
resist pathogens.
‣ The dryness, acidity, and temperature of the skin inhibit
coloniza on and growth of pathogens; perspira on ushes
them away.
‣ S cky mucous serves as a nonspeci c host defense
mechanism by trapping pathogens. It also contains toxic
substances, such as lysozyme, lactoferrin, and lactoperoxidase.
‣ The mucociliary covering on epithelial cells in the respiratory
tract move trapped dust and microbes upward toward the
throat, where they are swallowed or expelled.
‣ Pathogens entering the GI tract are o en killed by diges ve
enzymes or the acidity or alkalinity of di erent anatomical
regions.
‣ Peristalsis and urina on serve to remove pathogens from the
GI tract and urinary tract, respec vely.
‣ The acidity of vaginal uid usually inhibits coloniza on of the
vagina by pathogens.
c. Microbial Antagonism
• When indigenous micro ora prevent the establishment of arriving
pathogens.
• A decrease in the number of indigenous micro ora at a par cular
anatomical site can lead to an overgrowth of pathogens or
opportunis c pathogens present at the site; this is referred to as a
superinfec on.
• Some bacteria produce proteins that kill other bacteria;
collec vely, these an bacterial substances are known as
bacteriocins.
• Example is colicin,which is produced by certainstrains of Escherichia
coli. Similar an bacterial substances are produced by some strains of
Pseudomonas and Bacillus species as well as by certain other
bacteria. Bacteriocins have a narrower range of ac vity than do
an bio cs, but they are more potent than an bio cs.
2. Second Line of Defense
• Pathogens able to penetrate the rst line of defense areusually destroyed
by nonspeci c cellular and chemical responses, collec vely referred to as
the second line of defense.
a. Transferrin
• Serves as a host defense mechanism by depriving pathogens
of iron.

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 b. Fever
• A body temperature greater than 37.8°C (100°F) is
generally considered to be a fever.
• Substances that s mulate the produc on of fever are called
pyrogens or pyrogenic substances.
• Elevated body temperatures also slow down the rate of
growth of certain pathogens and can even kill some especially
fas dious pathogens.
• There are, of course, detrimental aspects of fever— especially
prolonged high fevers. These include increased heart rate,
increased metabolic rate, increased caloric demand, and mild
to severe dehydra on.
c. Interferons
• Small, an viral proteins produced by virus-infected cells.
• They are called interferons because they “interfere” with viral
replica on.
• Cause the nonspeci c ulike symptoms (malaise, myalgia,
chills, fever) that are associated with many viral infec ons.
• Three types:
i. Alpha - produced by B lymphocytes (B cells), monocytes,
and macrophages
ii. Beta - by broblasts and other virus-infected cells
iii. Gamma - by ac vated T lym- phocytes (T cells) and
natural killer cells (NK cells)
d. The Complement System
• A group ofapproximately 30 di erent proteins (including nine
proteins designated as C1 through C9) that are found in
normal blood plasma.
• The ac on is complementary to the immune system.
e. Acute-Phase Proteins
• Increase rapidly in response to infec on, in- amma on, and
ssue injury.
• They serve as host defense mechanisms by enhancing
resistance to infec on and promo ng the repair of damaged
ssue.
• Acute-phase proteins include C-reac ve protein (which is used
as a laboratory marker for, or indica on of, in amma on),
serum amyloid A protein, protease inhibitors, and coagula on
proteins.
f. Cytokines
• Chemical mediators that are released from many di erent
types of cells in the human body.
• They enable cells to communicate with each other.
• They act as chemical messengers both within the immune
system and between the immune system and other systems of
the body.

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 g. In amma on
• The body normally responds to any local injury, irrita on,
microbial invasion, or bacterial toxin by a complex series of
events.
• Three major events:
a. Vasodila on
b. Increased permeability of the capillaries
c. Escape of leukocytes from the capillaries
• Primary purposes:
a. Localize an infec on
b. Prevent the spread of microbial invader
c. Neutralize any toxins being produced at the site
d. Aid in the repair of damaged ssue
• Four cardinal or main signas and symptoms:
a. Redness
b. Heat
c. Swelling (edema)
d. Pain
h. Phagocytosis
• Phagocy c white blood cells are called phagocytes, and the
process by which phagocytes surround and engulf (ingest)
foreign material is called phagocytosis.
i. Macrophages
• Serve as a “clean- up crew” to rid the body of
unwanted and o en harmful substances, such as
dead cells, unused cellular secre ons, debris, and
microorganisms.
• Develop from a type of leukocyte called
monocytes during the in ammatory response to
infec ons.
ii. Phagocy c Granulocytes
• Neutrophils and Eosinophils
‣ Neutrophils are much more e cient at
phagocytosis than eosinophils.
‣ An abnormally high number of eosinophils in
the peripheral bloodstream is known as
eosinophilia.

Ac vity 1
You are expected to par cipate in the online lecture on November 24, 2020
(Tuesday; 8am-8:30am for Level IIA and 9am-9:30am for Level IIB).

Angelica May DC. Mendoza, RPh, MS Page 4 of 5

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 Learning Input 2 (Laboratory)

In amma on is a nonspeci c, defensive response of the body to ssue damage.
Among the condi ons that may produce in- amma on are pathogens, abrasions, chemical
irrita ons, dis- tor on or disturbances of cells, and extreme temperatures. The four
characteris c signs and symptoms of in amma on are redness, pain, heat, and swelling.
In amma on can also cause a loss of func on in the injured area (for example, the inability
to detect sensa- ons), depending on the site and extent of the injury. In amma on is an
a empt to dispose of microbes, toxins, or foreign material at the site of injury, to prevent
their spread to other ssues, and to prepare the site for ssue repair in an a empt to
restore ssue homeostasis. Because in amma on is one of the body’s nonspeci c defense
mechanisms, the response of a ssue to a cut is similar to the re- sponse to damage caused
by burns, radia on, or bacterial or viral invasion. In each case, the in ammatory response
has three basic stages: (1) vasodila on and increased permeability of blood vessels, (2)
emigra on (movement) of phagocytes from the blood into inters al uid, and, ul mately,
(3) ssue repair.

Ac vity 2
You are expected to par cipate in the online lecture on November 24, 2020
(Tuesday; 8:30am-9:00am for Level IIA and 9:30am-10:00am for Level IIB).

WRAP-UP ACTIVITY
Summarize what you have learned or how your new learnings has changed your
thoughts on the topic.

POST-ASSESSMENT

Worksheet 10 (Lecture)
You are required to accomplish the Worksheet 10. The ac vity will be posted on
November 23, 2020 (Monday) in the mVLE course page. Make sure to complete and submit
your output on or before 11:59 pm November 29, 2020 (Sunday).

Worksheet 10 (Laboratory)
You are required to accomplish the Worksheet 10. The ac vity will be posted on
November 23, 2020 (Monday) in the mVLE course page. Make sure to complete and submit
your output on or before 11:59 pm November 29, 2020 (Sunday).

Quiz 10
You are required to take the Quiz 10. The quiz will be posted on November 24, 2020
(Tuesday) a er the Discussion Forum 10 in the mVLE course page. Make sure to complete
and submit your output on or before 11:59 pm November 24, 2020 (Tuesday).

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