Immune Defense against Bacterial Pathogens: Innate Immunity (page 2)
(This chapter has 6 pages)
© Kenneth Todar, PhD
Innate Immunity
Innate Immunity is a form of
non specific host defense against invading
bacteria. It is natural or "innate" to the host, depending, in part, on
genetics. Innate defense mechanisms are contitutive to the host,
meaning they are
continually
ready to respond to invasion and do not require a period of time
for induction. The most important components of innate immunity are
anatomical barriers,
intact normal flora, tissue bactericides including complement, and
ability to undergo inflammatory and phagocytic responses.
Innate immunity provides the
first line of defense against invading bacteria. The skin and mucous
membranes provide physical and chemical barriers to infection.
The normal bacterial flora antagonize colonization of body surfaces by
nonindigenous bacteria. The internal tissues invariably contain
bactericidal
substances. The most noteworthy antibacterial substance is the
enzyme lysozyme, which is
present in mucus and all bodily tissues and secretions. If these
barriers are
penetrated, the body contains cells that respond rapidly to the
presence of the invader. These cells include macrophages and
neutrophils that engulf foreign organisms and kill them. Bacterial
invasion is also challenged by the activation of complement in blood
and tissues and the incitement of an inflammatory process which has the
tendency to focus both the innate and adaptive immune defenses on the
site of invasion.
Categories of
Innate or Nonspecific Immunity
The first four categories are generally considered non cellular
defenses.
Inflammation and Phagocytosis are forms of cellular defense.
1. Differences in
susceptibility to certain pathogens
2. Anatomical defense
3. Tissue bactericides, including complement
4. Microbial antagonism
5. Inflammation (ability to undergo an inflammatory response)
6. Phagocytosis
Differences in Susceptibility of Animal Hosts
to
Microbial Pathogens (Natural Immunity)
Natural immunity or resistance is based on the genetics of the host.
There are two aspects: (1)
resistance
among all members of a species, called species resistance and
(2) resistance within members of the same animal species, called
individual resistance.
Species resistance
Certain animals are naturally resistant or non susceptible to
certain
pathogens. Certain pathogens infect only humans, not lower animals,
e.g.
syphilis, gonorrhea, measles, poliomyelitis. On the other hand, certain
pathogens (e.g. canine distemper virus) do not infect humans. Shigella
infects humans and baboons but not chimpanzees. Little information is
available
to explain these absolute differences in susceptibility to a pathogen
but
it could be due to:
Absence of specific tissue or cellular receptors for attachment
(colonization)
by the pathogen. For example, different strains of enterotoxigenic
E.
coli, defined by different fimbrial antigens, colonize human
infants,
calves and piglets by recognizing species-specific carbohydrate
receptors
on enterocytes in the gastrointestinal tract.
Temperature of the host and ability of pathogen to grow. For
example, birds do not normally become infected with mammalian strains
of
Mycobacterium
tuberculosis because these strains cannot grow at the high body
temperature
of birds. The anthrax bacillus (Bacillus anthracis) will not
grow
in the cold-blooded frog (unless the frog is maintained at 37o).
Lack of the exact nutritional requirements to support the growth
of the pathogen. Naturally-requiring purine-dependent strains of Salmonella
typhi grow only in hosts supplying purines. Mice and rats lack this
growth factor in blood and pur-
strains are avirulent. By injecting purines into
these animals, such that the growth factor requirement for the
bacterium
is satisfied, the organisms prove virulent.
Lack of a target site for a microbial toxin. Most toxins
produced
by bacterial cells exert their toxic activity only after binding to
susceptible
cells or tissues in an animal. Certain animals may lack an appropriate
target cell or specific type of cell receptor for the toxin to bind to
and may therefore be nonsusceptible to the activity of the toxin. For
example,
injection of diphtheria toxin fails to kill the rat. The unchanged
toxin
is excreted in the urine. If a sample of the rat urine (or pure
diphtheria
toxin) is injected into the guinea pig, it dies of typical lesions
caused by
diphtheria
toxin.
Individual resistance
There are many reasons why individuals of the same animal species
may
exhibit greater or lesser susceptibility to the same ineffective agent.
Age. Usually this relates to the development and status of
the
immunological system which varies with age. It may also be associated
with
changes
in normal flora coincidental to developmental changes in the animal.
Sex. Usually this is linked to the presence and/or
development of the
sex organs. For example, mastitis and infectious diseases leading to
abortion
will obviously occur only in the female; orchitis would occur only in
males. It could also be due to anatomical structure related to sex
(bladder
infections
are 14-times more common in females than males), and possibly the
effects
of sex hormones on infections.
Stress. Stress is a complex of different factors that
apparently
has a real influence on health. Undue exertion, shock, change in
environment,
climatic change, nervous or muscular fatigue, etc. are factors known to
contribute to increases in susceptibility to infection. The best
explanation
is that in time of stress the output of cortisone from the adrenal
cortex
is increased. This suppresses the inflammatory processes of the host
and
the overall effect may be harmful. There are also a number of
relationships
between stress-related hormones and the functioning of the immune
defenses.
Diet, malnutrition. Infections may be linked with vitamin and
protein deficiencies, and this might explain partly why many infectious
diseases are more prevalent and infant mortality rates are highest in
parts
of the world where malnourishment is a problem. Also, overfed and obese
animals are more susceptible to infection. Diets high in sucrose
predispose
individuals to dental caries.
Intercurrent disease or trauma. The normal defenses of an
animal
are impaired by organic diseases such as leukemia, Hodgkin's disease,
diabetes,
AIDS, etc. Frequently, inflammatory or immune responses are delayed or
suppressed. Colds or influenza may predispose an individual to
pneumonia.
Smoking tobacco predisposes to infections of the respiratory tract.
Burned
tissue is readily infected by Pseudomonas aeruginosa.
Therapy against other diseases. Modern therapeutic procedures
used in some diseases can render an individual more susceptible to
infection.
Under these conditions not only pathogens, but organisms of the normal
flora and nonpathogens in the host's environment, may be able to
initiate
infection. Examples of therapeutic procedures that reduce the
efficiency
of the host's defenses are treatment with corticosteroids, cytotoxic
drugs,
antibiotics, or irradiation.
Anatomical Defenses
The structural integrity of the body surfaces, i.e., the skin and
mucous
membranes, forms an effective barrier to initial lodgment or
penetration
by microorganisms. The skin is a very effective barrier to bacterium,
so
that no bacterium by itself is known to be able to penetrate unbroken
skin.
Of course, a puncture, cut or scrape in the skin could introduce
infectious
bacteria. The mucous membranes are more vulnerable to penetration by
infectious
bacteria but still pose a formidable barrier of mucus and antimicrobial
substances.
The anatomical defenses are associated with all other aspects of
noncellular immunity, including individual resistance, mechanical
resistance, chemical resistance and resistance established by the
normal flora (Figure 3)
Figure 3. Anatomical defenses
associated with tissue surfaces
chapter continued
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