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Microbiology: Chapter 16
Terms in this set (30)
Outer layer of skin; tightly packed layers of epithelial cells (keratinocytes)
an epidermal cell that produces keratin (first divide, then migrate up and fill with keratin.. once at outermost layer they are ful of keratin, and now impermeable!)
Inner layer of skin (below the epidermis); made of connective tissue; contains both the sweat glands (produce salty sweat to make skin inhospitable to microbes) and sebaceous glands (produce fatty acid-containing sebum that makes the skin slightly acidic and inhospitable to microbes)
How does the skin serve as a first defense against pathogens?
Difficult for microbes to penetrate (dense keratinocytes in epidermis- physical barrier)
Sweat glands in dermis produce sweat to make skin surface salty (inhospitable to microbes- chemical barrier)
Sebaceous glands in dermis produce sebum to make the skin surface slightly acidic (inhospitable to microbes-chemical barrier)
Staph skin infection
Can grow on/in epidermis, and in sweat glands. Important to keep skin healthy (use natural products to help maintain acidic pH)
Fungal skin infections
Moist skin is more susceptible to infections (athletes foot by tinea pedis)
The epithelial lining of various body cavities, including the nose, ears, and mouth.
How do mucous membranes serve as a first defense against pathogens?
Mucus moistens tracts while trapping and washing off pathogens (ciliary escalator-physical; peristalsis-physical)
Cells in mucous membrane epithelial cells that secrete mucous
microbes trapped in mucus are transported away from the lungs (via synchronous upward beating action of cilia)
the process of wave-like muscle contractions of the intestinal wall that moves food along (for defecation via rectum)
Examples of anti microbial substances
Sebum/cerumen (rich in fatty acids and give environment low pH that is inhospitable)
Stomach Acid (low pH and acidic environments kills 99% of bacteria and toxins- EXCEPT clostridium botulinum toxin)
Lactoferrin (glycoproteins secreted in various fluids that binds iron, which is needed for cellular growth- aka is competitive against pathogenic cells)
AMPs- Defensins (form pores in microbial membranes, causing cytolysis-targets pathogen!!)
AMPs- Lysozyme (made in sweat, tears, saliva, urine; degrades peptidoglycan like a "natural penicillin", can affect bacteria at any life stage)
AMPs= broad spectrum anti microbial peptides produced by our own cells!
How does our normal microbiota serve as a first defense against pathogens?
They prevent overgrowth of harmful microbes either by:
1) Competitive exclusion (covering binding/attachment sites or consuming all the nutrients available; V EFFECTIVE AGAINST SALMONELLA AND SHIGELLA)
2) Production of toxic compounds (fermentation products like acetic and butyric acid can inhibit intestinal pathogens like salmonella; or lactic acid production by lactobacillus that produces low pH and hydrogen peroxide that is effective against chlamydia or Candida albicans)
What does disruption to normal flora often result in?
Infections; examples include oral candidiasis or thrush, vulvovaginal candidiasis or yeast infection (all caused by Candida albicans)
How is Salmonella most commonly killed off by our innate immune system?
1) Stomach acid (low pH kills off)
2) Competitive exclusion (binding/attachment spots blocked, or nutrients taken up by body's normal flora)
3) Fermentation products acetic and butyric acids inhibit intestinal Salmonella growth
How is Candida albicans kept in control? How can this be altered?
Healthy (normal) levels of lactobacillus in our normal flora produce lactic acid and hydrogen peroxide to create a low pH environment, which disfavor/stops/slows Candida albicans. However, any pH alterations (or flora disruption via antibacterial drugs and other compounds) can imbalance the control mechanisms of our body, which predisposes the body to infection! Result is yeast infection/vulvovaginal candidiasis)
Describe the complement system; which part of the immune response is it?
consists of serum plasma proteins (C1-C9) that have an important role in host defence (immunity) and inflammation; can DETECT pathogenic compounds and activate a cascade of events that lead to immune responses!
- can destroy pathogens directly
- can activate or collaborate with every other components of inflammatory response
is part of second-line innate immune response
Describe the actions phagocytosis; which part of immunity is it?
Is the ingestion (via endocytosis) of microbes and pathogens
-often carried out by neutrophils, fixed/free macrophages, and dendritic cells
Part of the second-line innate immune response!
Describe the actions of inflammation; what part of immunity is it?
Is the body's response to tissue damage and/or infection
-helps to contain site of damage, localize bodily response, eliminate the invader (pathogen or object, etc.), and restore tissue function
Included in the second-line innate immune response
Describe the role of fever; what part of immunity is it?
Is an abnormally high body temperature in response to infection
-caused by pyrogens (endogenous vs. exogenous)
Is important part of second-line innate immune response
Bacteria and viruses that elevate body temperature
-can be endogenous (
-can be exogenous (
Is a HOST molecule (antibody or other substance) that binds to foreign microorganisms or cells (aka pathogen)
-makes them more susceptible to phagocytosis (act as a tag/flagger); ENHANCE phagocytosis by activating signals
-several opsonins can bind to the same pathogen, which 'tags' it for phagocytosis
-signals to phagocytes to destroy this pathogen
-MAKES PHAGOCYTOSIS MORE EFFICIENT
What are the 3 pathways of the complement system?
classical, alternative, lectin
C1-C9, plus other factors
Must be activated to mount the complement response
Sometimes are activated by being split (a,b)
What does each pathway of the complement system include?
A detection step
Activation of C3 and C5
All three of outcomes of:
1) Inflammatory Response induced by C3a and C5a
2) Opsonization by C3b (or lectin), causing phagocytosis
3) Cytolysis (lysis of pathogen via MACs formed by C5b, C6, C7, C8 and C9
Where are complement proteins synthesized? What is necessary for them to function?
They are synthesized in the liver, and MUST be activated before they are able to function/produce their effects
What is the role of C3a and C5a?
To induce the inflammatory response of the complement system
What is the role of C3b?
Opsonization for phagocytosis
can also be induced by lectin
What is the role of MACS? Which complement proteins are responsible for MAC formation?
MACs (membrane attack complexes) are responsible for CYTOLYSIS (lysis of foreign cells)
Complement proteins C5b, C6, C7, C8, and C9 are capable of forming these membrane attack complexes
How is C3 activated? What is its role?
Via splitting! (Either by C3 convertase or combination of other complement proteins).
A) C3a (and C5a) induce the inflammatory response via changes that contribute to local vascular permeability in order to attract phagocytes (induce phagocytosis).
*local vascular permeability= blood flow to that area, and opening of
B) C3b can function in 2 ways: 1) by binding to microbial cells and functioning as opsonin (cause Opsonization and subsequent phagocytosis) and 2) by combining with other complement proteins to form C5 convertase (which C5b can then induce cytolysis or C5a can induce the inflammatory response)
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