Ch. 20 - Part 1 Flashcards
immune system
provides resistance to disease
immune system two intrinsic systems
innate (nonspecific) & adaptive (specific)
first line of defense
external body membranes (skin and mucosae)
second line of defense
antimicrobial proteins, phagocytes, and other cells (inhibit spread of invaders; inflammation most important mechanism)
third line of defense
attack particular foreign substances (takes longer to react than innate)
pathogens
disease-causing microorganisms
surface barriers are skin and mucous membranes, along with their secretions
physical barrier to most microorganisms; keratin is resistant to weak acids and bases, bacterial enzymes, and toxins; mucosae provide similar mechanical barriers
protective chemicals of the skin and mucous membranes
acid, enzymes
acid mantle
acidity of skin and some mucous secretions inhibits growth
enzymes
lysozyme of saliva, respiratory mucus, and lacrimal fluid kills many microorganism; enzymes in stomach kill many microorganisms
mucin
sticky mucus that lines digestive and respiratory tract traps microorganisms
defensins
antimicrobial peptides that inhibit microbial growth
other chemicals
lipids in sebum and dermcidin in sweat are toxic to some bacteria
respiratory system also has modifications to stop pathogens
mucus-coated hairs in nose trap inhaled particles; cilia of upper respiratory tract sweep dust-and bacteria –> laden mucus toward mouth
innate system necessary if microorganisms invade deeper tissues; includes:
phagocytes, natural killer (NK) cells, inflammatory response, antimicrobial proteins, fever
pattern recognition receptors
found in second-line cells; recognize and bind tightly to structures on microbes, disarming them before they do harm
Toll-like receptors (TLRs)
plays central role in triggering immune responses; human have 11 different ones and each recognizes a particular class of attaching microbe
phagocytes
white blood cells that ingest and digest (eat) foreign invaders
neutrophils
most abundant phagocytes, but die fighting; become phagocytic on exposure on infectious material
macropahges
develop from monocytes and are chief phagocytic cells
free macrophages
wander through tissue spaces; ex –> alveolar macrophages
fixed macrophages
permanent residents of some organs; ex –> stellate macrophages (liver) and microglia (brain)
opsonization
immune system uses antibodies or complement proteins as opsonins that coat pathogen
Phagocytosis
(1) phagocyte recognizes and adheres to pathogen’s carb “signature”; (2) cytoplasmic extensions (pseudopods) bond to and engulf particle in vesicle called phagosome; (3) phagosome fuses with lysosome, forming phagolysosome; (4) phagolysosome is acidified, and lysosomal enzymes digest particles; (5) indigestible and residual waste is exocytosed from phagocyte
respiratory burst
kills pathogens resistant to lysosomal enzymes by: releasing cell-killing free radicals, producing oxidizing chemicals, increasing pH and osmolarity of phagolysosome
Benefits of inflammation
prevents spread of damaging agents, disposes of cell debris and pathogens, alerts adaptive immune system, sets the stage for repair
Four cardinal signs of acute inflammation
redness, heat, swelling, pain
Stages of inflammation
inflammatory chemical release, vasodilation and increased vascular permeability, phagocyte mobilization
inflammatory chemical release
chemicals are released into ECF by injured tissues or immune cells
inflammatory chemical release example
histamine released by mast cells
other inflammatory mediators besides histamine
kinins, prostaglandins (PGs), cytokines, complement (if pathogens are involved)
What do inflammatory mediators do?
cause vasodilation of local arteries, make capillaries leaky, attract phagocytes to the area
Vasodilation causes..
hyperemia - congestion with blood which leads to redness and heat
increased capillary permeability causes
exudate - fluid containing clotting factors and antibodies to leak into tissue
Benefits of edema
surge of fluid in tissue sweeps foreign material into lymphatic vessels for processing in lymph nodes; delivers clotting proteins and complement to area
phagocyte mobilization
neutrophils flood area first, macrophages follow; if inflammation is due to pathogens, complement is activated, adaptive immunity elements arrive
Steps for phagocyte mobilization:
(1) Leukocytosis, (2) Margination, (3) Deapedesis, (4) Chemotaxis
Leukocytosis
release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells
Margination
endothelial cells of capillaries in inflamed area project cell adhesion molecules (CAMs) into vessel lumen that grab onto passing neutrophils, causing them to slow and roll along, clinging to vessel wall
Deapedesis
neutrophils flatten and squeeze between endothelial cells, moving into interstitial spaces
Chemotaxis
inflammatory chemicals act as chemotactic agents that promote positive chemotaxis of neutrophils toward injured area
___ hours after leaving the bloodstream, chemotactic agens are transformed into ____
12; macrophages
Pus
creamy yellow mixture of dead neutrophils, tissue/cells, and living/dead pathogens
Abscess
collagen fibers are laid down, walling off sac of pus; may need to be surgically drained
granulomas
area of infected macrophages surrounded by uninfected macrophages and outer capsule
antimicrobial proteins enhance innate defense by
attacking microorganisms directly or hindering their ability to reproduce
Most important antimicrobial proteins
interferons, complement proteins
interferons (IFN)
family of immune-modulating proteins
complement system
consists of ~20 blood proteins that circulate in blood in inactive form
complement
activation enhances inflammation and directly destroys bacteria; enhances both innate and adaptive defenses
Complement system can be activated by three different pathways
classical, lectin, alternative
Classical pathway
antibodies first bind to invading organisms and then bind to complement components, activating them; once ignition complement proteins are activated, an activation cascade is triggered
Lectin pathway
lectins are produced by innate system to recognize foreign invaders; when it’s bound to specific sugars on foreign invaders, it can also bind and activate complement
Alternative pathway
complement cascade is activated spontaneously when certain complement factors bind directly to foreign invader; lack of inhibitors on microorganism’s surface allows process to proceed
Cell lysis begins when
C3b binds to target cell, triggering insertion of complement proteins called membrane attack complex (MAC) into cell’s membrane; MAC forms and stabilizes hole in membrane of microbe, causing influx of water and lysis of microbe
pyrogens
act on body’s thermostat in hypothalamus, raising body temp
Benefits of moderate fever
causes liver and spleen to sequester iron and zinc (needed by microorganisms); increases metabolic rate, which increases rate of repair
Natural killer (NK) cells
promote apoptosis by directly attacking virus-infected or cancerous body cells; recognize general abnormalities rather than specific antigens
inflammatory response
prevents injurious agents from spreading to adjacent tissues, disposes of pathogens and dead tissue cells, and promotes tissue repair; released inflammatory chemicals attract phagocytes to the area
