100% CORRECT ANSWERS
Innate immunity - the first line of defence → epithelial barrier (our skin!) and inflammation.
First line of defence in innate immunity - physical and mechanical barriers, biochemical barriers,
normal microbiome
Second line of defence in innate immunity - inflammation
Physical and mechanical barriers - skin and mucous membranes lining the GI, GU, and respiratory
tracts. These cells turnover quickly to "wash" microorganisms off (skin) and vomiting/urinating
(GI/GU). Goblet cells (of the upper respiratory tract) produce mucus that traps microorganisms which
are then removed by cilia which move them upward to expel via coughing or sneezing. Low
temperature and pH of the skin/stomach also inhibit microorganism growth
Biochemical barriers - epithelial surfaces synthesize and secrete substances meant to trap and
destroy microorganisms.
Mucus, sweat, saliva, tears, and earwax trap and kill potential disease-causing microorganisms
Normal microbiome - We are all colonized with a spectrum of microorganisms that is unique. These
do not normally cause disease but are classified as opportunistic, which means they can cause
disease in the integrity of the body surface is compromised (this relationship is commensal- to the
benefit of one organism without affecting the other). These good bacteria compete with pathogens
for nutrients and block attachment to the epithelium.
They also produce chemicals and toxic proteins that inhibit colonization by pathogenic
microorganisms.
Examples of normal microbes - colon is usually sterile at birth but colonization with bacteria begins
quickly and increases during the first year of life.
Prolonged treatment with antibiotics can decrease the activity of the good bacteria and lead to an
overgrowth of opportunistic pathogens such as candida or c. dif. Vagina is colonized with
Lactobacillus
skin is colonized by Pseudomonas
Second line of defense - Inflammation
, inflammation - A rapid initiation and interactive system of humoral (soluble in the blood) and cellular
systems when tissue damage is suspected designed to limit the extent of tissue damage, destroy
contaminating infectious microorganisms, initiating the adaptive immune response, and begin the
healing process
The inflammatory process - Occurs in tissues with blood supply.
Is activated within seconds after damage occurs. Depends on the activity of both cellular and
chemical components.
Is nonspecific, meaning it takes place approximately the same way each time
Cardinal signs of inflammation - Redness (d/t vasodilation and increased blood flow), Heat, Swelling
(d/t exudate (fluid and cells) accumulation), Pain (d/t pressure exerted by exudate accumulations as
well as the presence of prostaglandins and bradykinin), Loss of function (occurs as a result of the
previous 4)
Characteristic changes at the site of injury - Vasodilation → allows slower blood velocity and
increases blood flow to the injured site.
Increased vascular permeability and leakage of fluid out of the vessel which causes swelling.
White blood cells adhere to the inner walls of vessels, and they migrate through enlarged junctions
between the endothelial cells lining the vessels into the surrounding tissue (diapedesis)
Systemic manifestations of acute inflammation - Fever, leukocytosis, plasma protein synthesis,
fever - Induced by cytokines (IL-1) which are released by neutrophils and macrophages.
Fever-causing cytokines are knowns as endogenous pyrogens. They act directly on the hypothalamus
(the portion of the brain that controls the body's thermostat).
Cytokines are released after phagocytosis, after exposure to bacterial endotoxins, or after exposure
to antigen-antibody complexes
Leukocytosis - transient increase in the levels of circulating leukocytes. Increase in the number of
circulating white blood cells. "left-shift"= more immature forms of neutrophils, such as bands, are
present in greater than normal proportions
Plasma protein synthesis - increased levels of circulating plasma proteins. Proteins can either be
proinflammatory or antiinflammatory and are referred to as acute-phase reactants.