BIO3 - Chapter 16

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Innate Immunity Nonspecific Defenses of the Host

Last updated 3:15 AM on 4/26/26
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102 Terms

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susceptibility

lack of resistance to a disease

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immunity

ability to ward off disease

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innate immunity

defenses against any pathogen; rapid, present at birth

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adaptive immunity

immunity or resistance to a specific pathogen; slower to respond, has memory component

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what do white blood cell counts measure

leukocytes in the blood

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what do high WBC counts indicate

bacterial infections, autoimmune disease, or side effects of medications

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what do low WBC counts indicate

virla infections, pneumonia, autoimmune diseases, or cancers

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components of the first line of defense

skin, mucous membranes, normal microbiota

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physical factors in first line of defense

barriers to entry or processes that remove microbes from the body’s surface

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chemical factors in the first line of defense

chemicals inhibit or destroy microbial growth

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dermis

part of the skin, inner portion made of connective tissue

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epidermis

part of skin, outer portion made of tightly packed epithelial cells containing keratin

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keratin

a protective protein

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what are mucous membranes

layers that line the gastrointestinal, respiratory, and genitourinary tracts; they secret mucus

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significance of mucus secretion

trap microbes & prevent tracts from drying out

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significance of lacrimal apparatus

tears wash away microbes; washes eyes

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significance of ciliary escalator

microbs trapped in mucus are transported away from the lungs

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significance of earwax

prevents microbes from entering the ear

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saliva significance

washes microbes off

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urine and vaginal secretion method

flows out

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all physical factors of the first line of defense

skin & mucous membranes

lacrimal apparatus

ciliary escalator

earwax

saliva

urine

vaginal secretions

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sebum

produced by oil glands of the skin; oily substance

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what does the skin secrete

fatty acids & lactic acids; low pH

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result of sweat glands

perpiration

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where is lysozyme found

perspiration, tears, saliva, urine

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what do the glands of the stomach produce

gastric juice; low pH

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what type of factor are vaginal secretions

chemical factors

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list of all chemical factors in the first line of defense

sebum

fatty acids & lactic acids

perspiration

kysozyme

gastric juice

vaginal secretions

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normal microbiota

compete w pathogens via microbial antagonism (competitive exclusion)

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how is the normal microbiota helpful in the defense system

competitive advantage for space & nutrients

prod substances harmful to pathogens

alter conditions that affect pathogen survival

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commensalism

one organism benefits while the other is unharmed

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probiotics

live microbial cultures administered to exert a beneficial effect

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components of the second line of defense

phagocytic cells

inflammation

fever

antimicrobial substances

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formed elements in blood

red blood cells, white blood cells, platelets

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types of white blood cells (leukocytes)

granulocytes & agranulocytes

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granulocytes

leukocytes with granules in their cytoplasm that are visible with a light microscope

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types of granulocytes

neutrophils, basophils, eosinophils

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neutrophils

neutral-love, phagocytic; work in early stages of infections, one of the first responders to infections, 60-70% of WBC

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basophils

base-love, 0.5-1% of WBC, prod histamine, work in allergic responses

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eosinophils

acid-loving, 2-4% of WBC, kill parasites

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agranulocytes

leukocytes with granules in their cytoplasm that aren’t visible with a light microscope

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types of agranulocytes

monocytes, dendritic cells, lymphocytes

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monocytes

3-u% of WBC, respond quickly to infection, develop into macrophage, phagocytosis

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dendritic cells

deried from monocytes, phagocytosis, found in the skin, mucous membranes, & thymuc; phagocytic

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lymphocytes

20-50% of WBC, play a role in adaptive immunity

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lymphocytes examples

natural kill cells, t cells, b cells

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natural killer cell function

destroy target cells

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t cell function

cell-mediated immunity

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b cell function

prod antibodies

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phagocytosis

ingestion of microbes or particles by a cell, performed by phagocytes

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first step when an infection occurs

both granulocytes (especially neutrophils) & monocytes migrate to the infected area

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what do monocytes develop into

large macrophages

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fixed macrophages

residents in tissues & organs

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wandering macrophages

roam tissues & gather at sites of infection

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steps in phagocytosis

chemotaxis

adherence

ingestion

digestion

discharge

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what are chemotaxis

chemical attraction

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ways microbes evade phagocytosis

inhibit adherence

kill phagocytes

lyse phagocytes

escape phagosome

prevent phagosome-lysosome fusion

survive in phagolysosome

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inflammation

damage to the body’s tissues triggers a local defensive response

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effects of inflammation

redness, pair, heat, swelling, loss of function

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2 types of inflammation

acute inflammation & chronic inflammation

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function of inflammation

destroy the injurious agents

limit the effects on the body

repair or replace tissue damage

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how does inflammation work

inflammation activates acute-phase proteins by the liver that cause vasodilation & increased permeability of blood vessels

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acute-phase proteins

histamine

kinins

prostaglandins

leukotrienes

cytokines

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process of inflammation

vasodilation & increased permeability of blood vessel

phagocyte migration

phagocytosis & tissue repair

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vasodilation

dilation (increase in diameter) of blood vessel

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purpose of vasodilation

increase blood flow to the damaged area

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effects of vasodilation

cause redness & heat associated with inflammation

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significance of increased permeability in inflammation

permits defensive substances normally retained in blood to pass through the walls of the blood vessel & enter the injured area

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what is edema

accumulation of fluid (swelling)

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what is margination

sticking of phagocytes to blood vessels in response to cytokines at the site of inflammation

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diapedesis

phagocytes squeeze between endothelials cells of blood vessels

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what is fever

abnormally high body temp

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hypothalamus significance

body’s “thermostat” located in the brain normally set at 37C, releases prostaglandins that reset the hypothalamus to a high temp

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significance of chills/shivering

sign of body increseing rate of metabolism & temp, skin remains cold, indicates body temp is rising

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body temperature when infection subsides

heat-losing mechanisms (vasodilation & sweating) go into operation: skin becomes warm & person begins to sweat, indicates body temperature falls

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advantage of fever

increase transferrins

increase IL-1 activity

prod interferon

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significance of transferrins

protein that grabs free iron before microbes do

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IL-1 activity significance

help prod T-cells which fight bacteria

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interferon significance

antiviral protein

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disadvantages of fever

tachycardia

acidosis

dehydration

high fevers can be fatal

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what is tachycardia

rapid heart rate

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what is acidosis

too much acid in the body because of chemical production

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list of antimicrobial substances

complement system

interferons

iron-binding proteins (transferrins)

antimicrobial peptides (short protein)

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what is the complement system

defensive system consisting of over 30 proteins produced by the lived & found circulating in the blood serum & within tissues throughout the body

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activation of complement system

serum proteins activated in a cascade

activated by antigen-antibody reaction or proteins C3, B, D, P and a pathogen

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C3b significance

causes opsonization

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C3a + C5a significance

cause inflammation

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C5b + C6 + C7 + C8 + C9 significance

cause cell lysis

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effects of complement activation

opsonization or immune adherence

membrane attack complex

attract phagocytes

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what does opsonization or immune adherence mean

enhanced phagocytosis

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what does membrane attack complex mean

cytolysis

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what are the pathways to complement activation

classical, alternative, & lectin

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classical pathway activation

binding to antigen-antibody complex

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alternative pathway of activation

B,D,P of surface of a microbe

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lectin pathway of activation

lectin binds to an invading cell

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capsule role in evading complement

prevent C activation

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curface lipid-carbohydrates in complement evasion

prevent membrane attack complex (MAC) from forming

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how is C5a impacted in complement evasion

enzymativ digestion of C5a

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what do INF-A & INF-B do

cause cells to prod antivial proteins that inhibit viral replication

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what does gamma IFN do

cause neutrophils & macrophages to phagocytize bacteria