Chapter 16: Nonspecific Defenses Flashcards

(68 cards)

1
Q

Nonspecific (innate) defenses

A

-Defenses against any potential pathogens; does not involve specific recognition of a microbe
-Present at birth
-Provide a rapid response against any pathogen
-Does not involve specific recognition or memory
-Activated by toll-like receptors (TLR)- on neutrophils or macrophages

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2
Q

Toll-like receptors (TLRs)

A

Transmembrane protein of immune cells that recognizes pathogens and activates an immune response directed against those pathogens

-Phagocyte on membrane
-Pathogen associated molecular pattern (PAMP)
-Ex. peptidoglycan in cell wall
-Phagocyte triggers release of cytokines which then send messages (initiate innate defenses)

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3
Q

Body’s defenses

A

-Pathogens (viruses, bacteria, fungi)
-(innate defense) 1st line of defenses: skin, mucous membranes,
-(innate defense) 2nd line antimicrobial substances, inflammation, fever, phagocytes (macrophages, neutrophils, and some eosinophils_
-(specific defenses) 3rd line of defense:Humoral (B cells) and cell immunity (T cells)
-adaptive immunity

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4
Q

Physical (mechanical) factors

A

-Intact skin
-Mucous membranes and mucus

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5
Q

Lacrimal apparatus

A

-Produces tears- wash away microbes from the eye
-Chronic dry eyes
-More susceptible to eye infections

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6
Q

Mechanical factors: saliva

A

-Washes microbes off
-Chronic dry mouth
-More susceptible to oral infections

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7
Q

Ciliary escalator

A

Microbes are trapped in mucus and propel up and out of respiratory tract

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8
Q

Physical factors

A

-Urine: flows out
-Vaginal secretions: flows out
-Peristalsis, defecation, vomiting

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9
Q

Chemical factors

A

-Unsaturated fatty acids in sebum inhibits growth
-Low pH (3-5) of skin
-Perspiration rem’s microbes from skin and contains lysozyme enzyme (breaks down peptidoglycan- cell wall)
-Lysozyme in perspiration, nasal secretion, tears, saliva, and tissue fluids
-Gastric juice (pH 1.2-3..0) acidity destroys bacteria and most toxins
-Botulism exotoxin and enterotoxin of S. aureus an exception

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10
Q

Microbiome shaping the innate immunity

A

-Altering conditions that affect survival of pathogens
-Lactobacillus- pH more acidic
-Producing substance that are harmful to pathogens
-Bacteriocins (peptides)
-Microbial antagonism

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11
Q

Defense components of blood

A

-Plasma contains complement antibodies
-Formed elements
-WBC’s
-Serum= plasma- clotting factors

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12
Q

Neutrophil

A

-Function: phagocytosis
-2-5 lobes
-Wright stain: nuclei stay purple
-Most abundant- 60%
-First to arrive at sight of infection
-Polymorphonuclear leukocyte

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13
Q

Basophils

A

-Function: histamine production
-Wright stain: purple granules

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14
Q

Mast cells

A

-Function: release chemicals to activate inflammation
-Wright stain: blue granules

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15
Q

Eosinophils

A

-Function: production of toxic proteins against certain parasites; some phagocytosis
-Wright stain: orange/red granules

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16
Q

WBC functions: monocytes

A

Function: leave the bloodstream mature into resting or wandering phagocytes (when they mature into macrophages)

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17
Q

WBC functions: Dendritic cells

A

Function: antigen processing and presentation to T cells; phagocytosis and initiation of adaptive immune responses by presenting antigens

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18
Q

WBC: lymphocytes: natural killer cells

A

-Function: destroy target (cancer or virus infected cells) by cytolysis and apoptosis
-Nonspecific

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19
Q

WBCs: lymphocytes: T cells

A

-Function: cell-mediated (cellular) immunity
-Response to intracellular antigens

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20
Q

WBCs: lymphocytes: B cells

A

-humoral immunity
-Function: develop into plasmocytes that produce antibodies
-Respond to extracellular antigens

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21
Q

Leukocytes: Granulocytes

A

Basophils, neutrophils, eosinophils

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22
Q

Leukocytes: Phagocytes

A

Neutrophils, eosinophils, monocytes, macrophages

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23
Q

Leukocytes

A

Basophil, neutrophil, eosinophils, monocytes, macrophage, lymphocyte (T cell and B cell)

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24
Q

Leukocytosis

A

-Increase in leukocyte count
-Causes leukocytosis- leukemia, acute infection

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25
Leukopenia
-Decrease in leukocyte count -Causes leukopenia- cancer, immunosuppressant drugs
26
Phagocytosis
Ingestion of microbes or particles by a (eukaryotic) cell, performed by phagocytes Phagocytes are types of WBCs or derivative or WBCs
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Fixed macrophages
-Remain in certain tissues -Langerhans cells: skin- epidermis -Kupffer cells: liver -Alveolar macrophage: lungs -Microglial cells: Nervous system
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Stages of Phagocytosis
1) Chemotaxis 2) Adherence 3) Ingestion -Formation of phagosome- phagocytic vesicle 4) Digestion -Formation of phagolysosome -Anything digestible will be discharge by exocytosis
29
Microbial inhibition of adherence
-Capsules- TLR cannot attach to PAMP -M protein -S. pyogenes -Opsonization (immune adherence) is the coating of the microorganism w/ serum proteins -Enhancement of phagocytosis by coating w/ C3b (complement) -Ex. opsonins, complement C3b, antibodies
30
Microbial evasion of phagocytes
-Inhibit adherence (capsules, M protein) -Killing phagocytes (leukocidins) -S. aureus, S. pyogenes -Exoenzyme -Membrane attack complexes -Listeria -Pore-forming protein -Escaping phagosome -Listeria, Shigella -Not ingested -Preventing phagolysosome formation -HIV, M. tuberculosis -Pathogen not ingested -Biofilms -Pseudomonas, S. epidermidis, Legionella
31
Inflammation
-Local response of the body to injury characterized by -Redness, swelling (edema), pain, warmth (heat) -Sometimes loss of function -Can be acute or chronic (hepatitis, TB, chlamydia- pelvic inflammatory disease) -Functions of inflammation: destroy injurious agent, confine or wall off the injurious agent, repair or replace tissue damage
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Inflammation stages
1) chemicals such as histamine, prostaglandins, kinins, leukotrienes, and cytokines are released by damaged cells 2) blood clot forms 3) Abscess starts to form -Collection bacteria, fluid and pus 4) Margination- phagocytes stick to endothelium 5) Diapedesis (emigration)- phagocytes squeeze between endothelial cells 6) phagocytosis invading bacteria
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Stages of inflammation
1) tissue damage 2) Vasodilation and increased permeability 3) Phagocyte migration and phagocytosis 4) tissue repair- leukocyte infiltration
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Fever
-A systemic, or overall response -An abnormal high temp produced in responded to a bacteria (and their toxins- endotoxin- gram-(-) bacteria) or viruses (Flu, RSV)
35
Benefits of fever
-Viral infection- intensifies interferons -Increases production of transferrin (iron-binding proteins) -Inhibits microbial growth -Helps body to repair tissue
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Sticking of phagocytes to the epithelium is called:
Margination
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Complement system
-A defensive system containing over 30 proteins that participate in destroying foreign cells, inflammation, and opsonization -C3 - enzymatic cleave (C3 cleaved by enzyme into C3a and C3b) -Over 30 proteins designated by uppercase letter “C” and number “C1” through “C9” -Complement proteins become inactive until they are split into products which are designated by lower case “a” and “b" -Serum proteins activated in cascade -C3 plays a central role in classical and alternative pathway
38
Outcomes of complement activation
-Cytolysis- microbes burst as extracellular fluid flows in through transmembrane channel formed by membrane attack complex -Opsonization- coating microbes w/ C3b enhances phagocytosis -Inflammation- blood vessels become more permeable, and chemotactic agents attract phagocytes to area
39
Classical Pathway
1) C1 is activated by binding to antigen-antibody complex Includes foreign cell and antibody (defense protein- 2 IgG) 2) Activated C1 splits C2 into C2a and C2b and C4 into C4a and C4b 3) C2a and C4b combing and activates C3, splitting into C3a and C3b -Result: opsonization, cytolysis inflammation
40
Alternative Pathway: immunocompromised
1) C3 combing w. Factors B, D, and P (properdin- stabilizes reaction) on the surface of the microbe 2) this causes C3 to split into fragments C3a and C3b -Activated by contact between complement proteins and pathogens -Result: opsonization, cytolysis, inflammation
41
Lectin pathway
1) Lectin beings to invading cell (and combines to carb on cell membrane containing mannose) 2) bound lectin splits C2 into C2b and C2a and C4 into C4a and C4b 3) C2a and C4b coning and activate C3 -Results: opsonization, cytolysis, inflammation
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Consequences of activation: cytolysis
-C5,6,7 and 9 -Bursting of microbe due to inflow of extracellular fluid through transmembrane channel formed by membrane attack complex- lysis
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Consequences of activation: opsonization
Phagocytes have C3b receptors Enhancement of phagocytes (adherence step) by coating w/ C3b C3> C3a and C3b
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Inflammation stimulated by complement
-Histamines releases -Triggered by C5a and C3a binding -Chemotactic factor
45
Complement
A group of serum proteins involved in phagocytosis and lysis of bacteria -Activated by classical pathway, alternative pathway, or lectin pathway -Deactivated by host-regulatory proteins -Inherited complement deficiency (C3 deficiency) can result in an increased susceptibility to disease -Rare
46
Some bacteria evade complement
-Capsules -Length surface lipid-carb -gram-(-) bacteria- prevent insert of C5- C9a coating w/ C3b) -Enzymatic digestion of C5a -Gram-(+) bacteria
47
Interferons
Specific group of cytokines. Alpha and beta INF are antiviral proteins produced by certain animal cells in response to a viral infection. Gamma-INF stimulates macrophage activity -Host-cell specific -Not virus-specific
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Antiviral action: alpha and beta INF
1) viral RNA from and infecting virus enters the cell 2) The virus induces the host cell to produce interferon mRNA (INF-mRNA), which is translated into alpha and beta interferons 3) Interferons make contact w/ uninfected neighboring host cells, where they bind either to the plasma membrane or to nuclear receptors. Interferons induce the cells to synthesize antiviral proteins (AVPs) 4) AVP’s degrade viral mRNAand inhibit protein synthesis and thus interfere w/ viral replication
49
Alpha and Beta INF
-Produced by viral-infected cells -Induce the uninfected neighboring cells to make antiviral proteins
50
Gamma INF
-Produced by lymphocytes -T lymphocytes and Natural killer cells (NK cells) -Activated neutrophils and macrophages -Increase antigen presentation -Upregulate MHC expression
51
Interferon gamma release Assays (IGRAs)
-Whole blood test to detect M. tuberculosis infection by measuring gamma IFN release -QuantiFERON TB Gold in test tube and T. SPOT
52
Iron-binding proteins
-antimicrobial peptides -Transferrin, lactoferrin, ferritin -Inhibit cell wall synthesis, lyse microbial cells, destroy DNA and RNA
53
Describe the role of the skin and mucous membranes in non-specific resistance.
non- specific mechanical barriers to infection. composition- physical/mechanical defenses of the skin and mucous membranes. Innate immunity, nonspecific Nonspecific Resistance: -AKA innate immunity -the defense of our body from any kinds of the pathogens Skin: -mechanical barrier -breaches of it may allow microbes to enter blood -if pathogens are detected by langerhans cells, they phagocytize it & induce an acquired immune response -sweat and sebaceous glands produce lactic acid, fatty acids and lysozyme Mucous Membranes: -produce mucous that traps microbes -membranes with ciliated epithelial cells line the respiratory tract to sweep out particles -particles can be removed from body by sneezing, coughing, or being swallowed and killed by stomach acid
54
Differentiate between physical and chemical factors, and list five (5) examples of each.
a physical barrier relies on the material it is made of to block the passage of "whatever" in and out or through the barrier. What can or cannot pass through is dictated by the size of the spaces between the molecules, or holes, in the physical barrier. A chemical barrier is made up of chemicals, or enzymes, and more, than do not allow certain chemicals to pass through, For example, the chemical kills the germ before it can pass into a cell, or the barriers of the cell, and parts inside the cell , dictate what can and cannot penetrate the cell, if all works well. examples: skin (epidermis, dermis) mucous membranes, hairs, cilia, peristalsis, defecation, vomiting. chemical factors- vaginal secretions, gastric juice, perspiration, sebum, urine
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Phagocytes
A cell capable of engulfing and digesting particles that are harmful to the body
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Differential WBC count
The # of each kind of leukocyte in a sample of 100 leukocytes
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Macrophage
A phagocytic cell; a mature monocyte.
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Opsonization
The enhancement of phagocytosis by coating microorganisms w/ certain serum proteins (opsonins) “Immune adherence”
59
Describe the process of phagocytosis, and include the stages of adherence and ingestion.
1. Chemotaxis and Adherence Chemotaxis = chemical attraction of phagocyte to microbe; attracted by microbial products, damaged cells, cytokines, and/or complement Adherence = attachment of plasma membrane of phagocyte to microbe; Toll-like receptors (TLRs) on phagocyte membrane bind to pathogen-associated molecular patterns (PAMPs) on microbe Adherence made easier by opsonization Opsonization = coating of the microbe with antibodies or complement proteins 2. Ingestion: phagocyte extends pseudopods around microbe 3. Phagosome formation: fusion of pseudopods around the microbe encloses it in a phagocytic vesicle called a phagosome which now floats in the cytoplasm 4. Phagolysosome formation: the phagosome fuses with a lysosome creating a phagolysosome putting the microbe in contact with digestive enzymes and bacteriocidal substances 5. Digestion: most microbes are killed and hydrolyzed in 10-30 min Oxidative burst kills the microbe: toxic oxygen radicals (superoxide, hydrogen peroxide) Enzymes and acids hydrolyze the microbe into component organic molecules 6. Formation of the residual body: useful small organic molecules are absorbed into the cytoplasm and the acids and enzymes are neutralized. Residual body = all remaining undigested material in a vesicle 7. Exocytosis: residual body contents are discharged outside the cell
60
List the stages of inflammation
1) redness 2) swelling 3) heat 4) pain 5) loss of function (a.) damage to otherwise healthy tissue- in this case skin (b.)vasodilation and increased permeability of blood vessels (c.) phagocyte migration and phagocytosis of bacteria and cellular debris by macrophages and neutrophils. Macrophages develop from monocytes (d.)the repair of damage tissue
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Cytokines and ex of cytokines
A small protein released from human cells that regulates an immune response; directly or indirectly may induce fever, pain, or T cell proliferation Ex. interleukins, interferons
62
Describe phagocyte migration and emigration (diapedesis).
They can migrate out of the bloodstream. In fact leucocytes spend most of their life outside of the blood. When activated, they attach to the endothelial lining of the blood vessel, and eventually pass between endothelial cells into the interstitial fluid.
63
List and describe the major events of inflammation
Mast cells call the chemical messengers when faced against a foreign bacteria. chemical messengers cause vasodilation Diapedesis- monocyte squeezes between epithelial tissue Monocyte converts to macrophages and engulf the bacteria and this generates heat. (breaking down of cells always releases heat)
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How does inflammation differ from a fever?
Fever raises the temperature of the body, and local inflammation can raise the temperature of surrounding tissues.
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Gamma INF
-Produced by lymphocytes -T lymphocytes and Natural killer cells (NK cells) -Activated neutrophils and macrophages -Increase antigen presentation -Upregulate MHC expression
67
which cells directly attack abnormal cells in the body?
Cytotoxic T cells
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antibodies directly interact with which innate defenses?
Phagocytes and complement system