Innate nonspecific host defenses Flashcards

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1
Q

what are the categories of nonspecific innate immune defenses

A

physical defenses
chemical defenses
cellular defenses

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2
Q

what are examples of physical defenses

A

physical barriers
mechanical defenses
micorbiome

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3
Q

what are examples of chemical defenses

A

chemicals and enzymes in body fluids
antimicrobial peptides
plasma protein mediators
cytokines
inflammation-eliciting mediators

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4
Q

what are examples of cellular defenses

A

granulocytes
agranulocytes

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5
Q

what are barriers at the cellular level

A

cells that are tightly joined to prevent invaders from crossing through deeper tissue

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6
Q

what is an example of cells acting as a physical barrier

A

endothelial cells lining blood vessels have to cell junctions preventing microbes from entering the blood stream

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7
Q

what are cell junctions composed of

A

cell membrane proteins that may connect with the extracellular matrix or with complementary proteins from neighboring cells

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8
Q

what are the types of cell junctions

A

tight
desmosomes
gap

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9
Q

how do microbes attempt to break down junctions

A

using enzymes such as proteases

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10
Q

what does proteases do to cells

A

cause structural damage to create a point of entry for pathogens

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11
Q

what kind of barrier is the skin

A

physical

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12
Q

what are the layers of skin

A

epidermis
dermis
hypodermis

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13
Q

what does the 2nd layer of skin contain

A

hair follicles
sweat glands
nerves
blood vessels

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14
Q

what is in the hypodermis

A

blood and lymph vessesl

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15
Q

what does the epidermis consist of

A

cells packed with keratin that are tightly connected

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16
Q

what does keratin do for the skins surface

A

makes it mechanically tough and resistant to degradation by bacterial enzymes

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17
Q

what can a wound serve as

A

a point of entry for opportunistic pathogens that can infect skin surrounding wound and deeper tissue

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18
Q

what do mucous membranes consist of

A

epithelial cells that with tight junctions, and antimicrobial peptides

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19
Q

what does mucus do

A

protects the more fragile cells and traps debris and particulate including microbes,

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20
Q

what type of defense is ciliated epithelial cells

A

mechanical

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21
Q

what type of defense is the digestive tract

A

physical

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22
Q

what is the mucociliary escalator

A

when respiratory epithelial cells propel mucus with debris up and out of the lungs

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23
Q

what is the intestinal tract lined with

A

epithelial cell with mucus secreting goblet cells

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24
Q

what does the mucus in the intestinal tract do

A

mixes with material, traps it and peristalsis pushes it out

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25
Q

what are endothelia

A

epithelial cells in the urogenital tract, blood vessels, lymphatic vessels and other tissue

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26
Q

what does endothelia of blood brain barrier protect

A

the brain and spinal cord

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27
Q

what do mechanical defenses do

A

physically remove pathogens from the body

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28
Q

what are examples of mechanical defenses

A

shedding of skin, expulsion of mucus, excretion of feces, urine and tears, blinking,

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29
Q

how does the microbiome protect against pathogens

A

through occupation of cellular binding sites and competition for available nutrients

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30
Q

what is an example of microbiome preventing infection

A

bacteria in the vagina protect against candida by limiting nutrients

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31
Q

what happens when macrobiotic is disrupted

A

more susceptible to infection

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32
Q

what do antibiotics do to intestinal tract

A

kill microbiome

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33
Q

what happens when intestinal microbiome is killed

A

c. diff takes over

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34
Q

what are cellular barriers

A

skin, mucous membranes, endothelial cells

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35
Q

function of cellular barriers

A

deny entry of pathogens

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36
Q

examples of mechanical defenses

A

shedding of skin cells, mucociliary sweeping, peristalsis, flushing action of urine and tears

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37
Q

function mechanical defenses

A

remove pathogens from potential sites of infections

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38
Q

examples of microbiome defenses

A

resident bacteria of skin, upper respiratory tract, gi tract, genitourinary tract

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39
Q

function of microbiome

A

computer with pathogens for cellular binding sites and nutrients

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40
Q

what do chemical mediators do

A

inhibit microbial invaders

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41
Q

what does endogenously produced mean

A

proceeded by human body cells

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42
Q

what does exogenously produced mean

A

produced by microbes that are part of the microbiome

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43
Q

what kind of mediators are produced by fluid of the skin

A

endogenous and exogenous

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44
Q

what kind of mediator is sebum

A

endogenous

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45
Q

what does sebum do

A

seals off the pore of the hair follicle preventing bacteria from invading what glands and surrounding tissue

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46
Q

how do propionibacterium acnes and malassezia degrade subum

A

using lipase enzymes to degrade it using it as a food source

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47
Q

what is produced when sebum is degraded

A

oleic acid that makes the skin inhospitable to phathogens

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48
Q

what type of mediator is oleic acid

A

exogenously

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49
Q

how does low humidity affect microbiota of the skin

A

decreases sebum production making skin less habitat for microbes that produce oleic acid and more susceptible to pathogens normally inhibited by skins low ph

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50
Q

what mediators does saliva contain

A

lactoperoxidase enzymes

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51
Q

what mediator is excreted by mucus in the esophagus

A

antibacterial enzyme lysozyme

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52
Q

what is a mediator in the stomach

A

acidic gastric fluid

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53
Q

what mediator is in the lower digestive tract

A

intestinal and pancreatic enzymes, antibacterial peptides, bile produced by liver and pantheon cells that produce lysozyme

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54
Q

what do lower digestive tract mediators kill

A

pathogens that survive the acidic ph of the stomach

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55
Q

how does the urinary tract act as a mediator

A

by being slightly acidic

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56
Q

what is lactate in the vagina

A

an exogenously produced mediator

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57
Q

what produces lactate

A

the vagina produces glycogen and lactobacilli ferment it to produce the lactate

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58
Q

what does lactate do for the vagina

A

lowers the ph to inhibit transient microbiota, candida and sti

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59
Q

what chemicals mediators are in tears

A

lysozyme and lactoferrin

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60
Q

what does lysozyme do

A

cleaves the bond between nag and nam in peptidoglycan

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61
Q

what are lysozyme and lactoferrin most effective against

A

gram-positive bacteria

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62
Q

what does lactoferrin do

A

inhibits microbial growth by chemically binding and sequestering iron starving microbes that need iron for growth

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63
Q

how does cerumen have

A

antimicrobial properties due to fatty acids lowering the ph

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64
Q

what does mucus in the nasal passage contain

A

lysozyme, lactoferrin, lactoperoxidase

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65
Q

what do secretions in the trachea and lungs have

A

lysozyme and lactoferrin and others such as surfactant

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66
Q

what is surfactant

A

a lipoprotein complex with antibacterial properties

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67
Q

what are antimicrobial peptides

A

a class of nonspecific cell-derived mediators with broad spectrum antimicrobial properties

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68
Q

when are amp’s produced

A

some routinely and some in response to a pathogen

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69
Q

what do AMP’s induce cell damage

A

by damaging membranes, destoying dna or rna or interfering with cell-wall synthesis

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70
Q

what do AMP’s inhibit

A

some only certain croups and some more broadly

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71
Q

what are defensins

A

AMPS produced by epithelial cells throughout the body

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72
Q

characteristics of defensins

A

may be secreted or act inside a host cell
combat microorganisms by damaging plasma memranes

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73
Q

what are bacteriocins

A

AMP’s produced exogenously by certain members of macrobiotic in gi tract

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74
Q

how are the genes for bacteriocins carried

A

on plasmids and can be passed between different species through lateral or horizontal gene transfer

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75
Q

bacteriocin is secreted by..

A

resident microbiotia

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76
Q

bacteriocins body site

A

GI tract

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77
Q

bacteriocins inhibit?

A

bacteria

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78
Q

mode of action of bacteriocins

A

disrupt membrane

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79
Q

cathelicidin is secreted by…

A

epithelial cells, macrophages and other cell types

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80
Q

cathelicidin body site

A

skin

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81
Q

cathelicidin pathogens inhibited

A

bacteria and fungi

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82
Q

cathelicidin mode of action

A

disrupts membrane

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83
Q

defensins are secreted by

A

epithelial cells, macrophages, neutrophils

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84
Q

defensins body site

A

throughout the body

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85
Q

defensins inhibit

A

fungi, bacteria, many viruses

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86
Q

defensins mode of action

A

disrupt membrane

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87
Q

dermcidin is secreted by

A

sweat glands

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88
Q

dermcidin body site

A

skin

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89
Q

dermcidin pathogens inhibited

A

bacteria and fungi

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90
Q

dermcidin mode of action

A

disrupts membrane integrity and ion channels

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91
Q

histamines secreted by

A

salivary glands

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92
Q

histatins body site

A

oral cavity

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93
Q

histatins pathogens inhibited

A

fungi

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94
Q

histamines mode of action

A

disrupt intracellular function

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95
Q

what does plasma contain

A

electrolytes, sugars, lipids, proteins to maintain homeostasis and proteins involved in blood clotting

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96
Q

what proteins in plasma are involved in nonspecific innate immune response

A

acute-phase proteins
complement proteins
cytokines

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97
Q

describe acute phase proteins

A

antimicrobial mediators produced by the liver and secreted into the blood in response to inflammation molecules from the immune system

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98
Q

examples of acute phase proteins

A

c reactive protein
serum amyloid a
ferritin
transferrin
fibrinogen
mannose binding lectin

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99
Q

function of c reactive protein and serum amyloid a

A

coats bacteria, preparing them for ingestion by phagocytes

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100
Q

function of ferritin and transferrin

A

bind and sequester iron inhibiting growth of pathogens

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101
Q

function of fibrinogen

A

involved in formation of blood clots that trap bacterial pathogens

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102
Q

function of mannose-binding lectin

A

activates complement cascade

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103
Q

what is the complement system

A

a group of plasma protein mediators that act as nonspecific defense while also serving to connect innate and adaptive immunity

104
Q

what is the complement system composed of

A

more than 30 proteins that circulate as precursor proteins in blood

105
Q

when do precursor proteins become activated

A

when stimulated or triggered by factors including the presence of microorganisms

106
Q

why are complement proteins considered part of innate nonspecific immunity

A

they are always present in blood and tissue fluids allowing them to be activated quickly

107
Q

what is the process by which circulating complement precursors become functional

A

complement activation

108
Q

how is complement activation triggered

A

by one of 3 defense mechanisms

alternative
classical
lectin pathway

109
Q

how is the alternative pathway initiated

A

by spontaneous activation of the complement protein C3

110
Q

what does hydrolysis of C3 produce

A

C#a and C3b

111
Q

what happens to c3b if no invaders are present

A

it is degraded in a hydrolysis reaction using water in the blood

112
Q

what happens to c3b if invaders are present

A

it attaches to the surface of the microbe and recruits other complement proteins

113
Q

what does the classical pathway depend on

A

production of antibodies by the specific adaptive immune defenses

114
Q

how is the classical pathway initiated

A

a specific antibody must bind to the pathogen to for form an antibody-antigen complex activating the c1 complex

115
Q

what is the c1 complex

A

a multipart protein complex where each component participates in the full activation of the overall complex

116
Q

what happens after activation of the c1 complex

A

the remaining classical pathway complement proteins are recruited and activated in a cascading sequence

117
Q

what triggers the lectin activation pathway

A

the binding of manes-binding lectin to the carbohydrates on the microbial surface

118
Q

how are lectins produced

A

by liver cells

119
Q

when are lecitins upregulated

A

in response to inflammatory signals received by the body during infection

120
Q

what do complement activation pathways provide

A

opsonization, inflammation, chemotaxis, and cytolysis

121
Q

what is opsonization

A

the coating of a pathogen by a chemical substance that allows phagocytic cells to recognize engulf and destroy it more easily

122
Q

what are opsonins from the complement cascade

A

c1q, c3b, c4b, mannose binding proteins and antibodies

123
Q

what are c3a and c5a

A

complement fragments with anaphylatoxins wit potent pro inflammatory functions

124
Q

what do anaphylatoxins do

A

activate mast cells causing degranulation and the release of inflammatory chemical signals, including meditators that cause vasodilation and increased vascular permeability

125
Q

what is an additional role of c5a

A

chemoattractant for neutrophils and other white blood cells

126
Q

what is a membrane attack complex composed of

A

c7, c7, c7 and c9

127
Q

what does the membrane attach complex allow

A

c9 to polymerize into pores in the membranes of gram-negative bacteria

128
Q

what do the pros from c9 do

A

allow water, ions and other molecules to move freely in and out of targeted cell leading to cell lysis and death of the pathogeb

129
Q

what is Mac effective against

A

only gram-negative it cannot penetrate wall of gram-positive bacteria

130
Q

what is more important for gram-positive bacteria

A

mediated opsonization

131
Q

what are cytokines

A

soluble proteins that act as communication signals between cells

132
Q

what is the role of cytokines in nonspecific innate immune respones

A

stimulate production of chemical mediators or other funcitions such as cell proliferation, cell differentiation, inhibition of cell division, apoptosis and chemotaxis

133
Q

how can the function of a cytokine be described

A

autocrine, paracrine, or endocrine

134
Q

what happens in autocrine function

A

the same cell that releases the cytokine is the recipient of the signal ( self stimulation)

135
Q

what does paracrine function involve

A

the release of cytokines from one cell to other nearby cells stimulating some response from recipient cells

136
Q

what is endocrine function

A

when cells release cytokines into the bloodstream to be carried to target cells further away

137
Q

what are the most important classes of cytokines

A

interleukins, chemokine, interferons

138
Q

what do interleukins modulate

A

almost every function in the immune system

139
Q

what are chemokines

A

chemotactic factors that recruit leukocytes to sites of infection, tissue damage and inflammation

140
Q

how are chemokine different from chemotactic factors

A

chemokine are very specific in the subsets of leukocytes they recruit

141
Q

what are interferons

A

group of immune signaling molecules that defend against viruses

142
Q

what are type 1 interferons

A

interferon a and b produced band released by cells infected with virus

143
Q

what do type 1 interferons do

A

stimulate nearby cell to stop production of mRNA, destroy rna already produced and reduce protein synthesis.

stimulate various immune cells involved in viral clearance to more aggressively attack virus infected cells

144
Q

what are the effects of type 1 interferons

A

inhibit biral replication and production of mature virus slowing the spread,

145
Q

what do type 2 interferon (Y) do

A

activator of immune cells

146
Q

what happens to cytokine that bind mass cells and basophils

A

they release histamine

147
Q

what is histamine

A

a pro inflammatory compound

148
Q

where are histamine receptors found

A

a variety of cells

149
Q

what pro inflammatory events does histamine activate

A

bronchoconstriction and smooth muscle contractions

150
Q

what releases leukotrienes

A

mast cells

151
Q

what are leukotrienes

A

lipid based pro inflammatory mediators produced from the metabolism of arachidonic acid in the cell membrane of leukocytes and tissue cells

152
Q

how does the pro inflammatory effects of histamine compare to leukotrienes

A

leukotrienes are more potent and longer lasting

153
Q

what do histamine and leukotrienes do together

A

induce cough, vomiting, diarrhea to expel pathogens

154
Q

what are prostaglandins

A

chemical mediators the promote the inflammatory effects of kinins and histamines

155
Q

what do prostaglandins help to do

A

set the body temperature high to promote activities of white blood cells and inhibit growth of pathogens

156
Q

what is bradykinin

A

an inflammatory mediator that contributes to edema

157
Q

how does bradykinin work

A

it binds to receptors on cells in capillary walls, causing capillaries to dilate and become more permeable to fluids

158
Q

what are the three categories of formed elements

A

erythrocytes
platelets (thrombocytes)
leukocytes

159
Q

what are platelets

A

cellular fragments that participate in blood clot formation and tissue repair

160
Q

where do formed elements of blood come from

A

pluripotent hematopoietic stem cells in the bone marrow

161
Q

what is hematopoiesis

A

differentiation of HSC into different types of blood cells

162
Q

what dooms HSCs become

A

erythrocytes

163
Q

how can leukocytes be divided

A

granulocytes and agranulocutes

164
Q

where are granules in granulocytes

A

in the cytoplasm

165
Q

how can granulocytes be distinguished from one another

A

by the appearance of their nuclei and the contents of their granules, that have different traits functions and staining properties

166
Q

describe the nucleus of a granulocyte

A

has a nucleus with three to five lobes and small numerous lilac colored granules

167
Q

how are the lobes of the nucleus in neutrophils connected

A

by a thin strand of material

168
Q

describe the nucleus of eosinophils

A

fewer lobes in the nucleus (2-3) and larger granules that stain reddish-orange

169
Q

describe nucleus of basophils

A

two lobed nucleus and large granules that stain dark or purple

170
Q

what are the granulocytes

A

neutrophils
eosinophils
basophils

171
Q

what are neutrophils involved in

A

the elimination and destruction of extracellular bacteria

172
Q

what are neutrophils capable of

A

migrating through the walls of blood vessels to areas of bacterial infection and tissue damage where they seek out and kill infectious bacteria

173
Q

what do PMN granules contain

A

defensins and hydrolytic enzymes that help them destroy bacteria through phagocytosis

174
Q

what happens when neutrophils are brought into an infected area

A

they can be stimulated to release toxic molecules into the surrounding tissue to better clear infectious agents (degranulation)

175
Q

What are neutrophil extracellular traps

A

extruded meshes of chromatin that are closely associated with antimicrobial granule proteins and components

176
Q

what is chromatin

A

dna with associated proteins

177
Q

what does creating and releasing a mesh or lattice like structure of chromatin, coupled with antimicrobial proteins, allow neutrophils to do

A

mount a highly concentrated and efficient attack against nearby pathogens

178
Q

what proteins re associated with NET

A

lactoferrin
gelatinase
cathepsin g
nyeloperoxidase

179
Q

what is pus

A

visible accumulation of leukocytes, cellular debris and bacteria at the site of infection

180
Q

what does the presence of pus indicate

A

immune defenses have been activated against an infection

181
Q

what are eosinophils

A

granulocytes that protect against protozoa and helminths and play a role in allergic reactions

182
Q

what do eosinophils contain

A

histamine
degradative enzymes
major basic protein

183
Q

what does major basic protein do

A

binds to the surface of carbohydrates of parasites and the binding is associated with disruption of the cell membrane and membrane permeability

184
Q

what do activated complement fragments c3a and c5a act as

A

anaphylatoxins

185
Q

when are c3a and c5a fragments produced

A

in the activation cascades of complement proteins

186
Q

how do c3a and c5a act as anaphylatoxins

A

by inducing degranulation of basophils and inflammatory responses

187
Q

what are basophils important in

A

allergic reactions and other responses that involve inflammation

188
Q

what is the most abundant components of basophil granules

A

histamine

189
Q

what makes mast cells and basophils similar

A

they have the same components and play an important role in allergic reactions and inflammatory response

190
Q

how are mast cells different from basophils

A

mast cells leave circulation blood and are found in tissue

191
Q

what are art cells associated with

A

blood vessels and nerves or found close to surfaces that interface with the external environment

192
Q

how can agranulocytes be categorized as

A

as lymphocytes or monocytes

193
Q

what do lymphocytes include

A

B cells
t cells
natural killer cells

194
Q

how do monocytes differentiate

A

into macrophages and dendritic cells

195
Q

what makes natural killer cells different from other lymphocytes

A

they use nonspecific mechanisms to recognizes and destroy cells

196
Q

what types of cells do natural killer cells target

A

cancer cells and cells with viruses

197
Q

what are mhc markers

A

marks that say a cell is part of self

198
Q

how does a natural killer cell know to attack another cell

A

it lacks the mhc marker

199
Q

how do natural killer cells make another cell suicide

A

by expressing cytotoxic membrane proteins and cytokines that stimulate the target cell to undergo apoptosis

200
Q

what two toxins are used in perform mediated cytotoxicity

A

perforin and granxymes

201
Q

what is perforin

A

a protein that creates pores in the target cell

202
Q

what are granzymes

A

proteases that enter through pores in to the target cells cytoplasm and triggers a cascade of protein activation leading to apoptosis

203
Q

why aren’t natural killer cells considered granulocytes

A

because their granules a re less numerous than those in true granulocytes

204
Q

describe monocytes

A

largest of white blood cells and has a nucleus that lacks lobes, also lacks granules

205
Q

where do dendritic cells live

A

in skin and mucous membranes

206
Q

what macrophage lives in bran and CNS

A

microglial cells

207
Q

what macrophage lives in liver

A

kupffer cells

208
Q

what macrophage lives in lungs

A

alveolar macrophages

209
Q

what macrophage lives in peritoneal cavity

A

peritoneal macrophages

210
Q

what is the main function of phagocytes

A

to seek ingest and kill pathogens

211
Q

what is extravasation/diapedesis

A

when leukocytes pass through walls of capillaries to reach infected tissue

212
Q

what initiates extravasation

A

complement faster c5a and cytokines released into area by resident macrophages and tissue cells responding to infectious agent

213
Q

what is transendothelial migration

A

when cytokines reach the cellular junction, bind to adhesion molecules, flatten out and squeeze through their cellular junction

214
Q

what allows leukocytes to exit the blood stream and enter infected areas where they can begin phagocytosis invading pathogens

A

rolling adhesion

215
Q

does extravasation occur in arteries or veins

A

no because they have thicker multilayer walls and arterial blood flow is too turbulent for rolling adhesion

216
Q

how long does it take neutrophils to respond?

A

hours

217
Q

how long does it take monocytes to respond

A

several days

218
Q

what are pathogen associated molecular pathways

A

molecular structures common to groups of pathogens

219
Q

what are some pamps

A

peptidoglycan
flagellin
lipopolysaccharides
lipopeptides
nucleic acids

220
Q

what are pattern recognition receptors

A

structures that allow phagocytic cells to detect pamps

221
Q

what do toll like receptors do

A

bind to pamps and communicate with the nucleus of the phagocyte, some embed in the membranes of interior compartments and organelles

222
Q

what are toll like receptors useful for

A

binding and recognition of intracellular pathogens that may have gained access to inside the cell before phagocytosis could take place

223
Q

what is phagocytosis

A

when a pathogen is engulfed in a vesicle and Brough into the internal compartment of a phagocyte

224
Q

how do prr’s aid in phagocytosis

A

by binding to the pathogens surface

225
Q

how does a phagocyte engulf a pathogen

A

by forming a pseudopod that wraps around the pathogen and pinches it offf into a membrane vesicle called a phagosome

226
Q

what happens when the phagosome has the pathogen

A

it fuses with one or more lysosome to form a phagolysosome

227
Q

what does formation of the phagolysosome do

A

enhance the acidification which is essential for activation of ph dependent digestive lysosomal enzymes and production of hydrogen peroxide and toxic reactive oxygen species

228
Q

what digests pathogens

A

enzymes such as lysozyme
phospholipase and protease

229
Q

what happens during a respiratory burst

A

phagocytes increase their uptake and consumption of oxygen

230
Q

why do phagocytes increase oxygen if not for energy

A

to produce superoxide anion, hydrogen peroxide, hydroxyl radicals and other reactive oxygen species that are antibacterial

231
Q

what triggers inflammation

A

a cascade of chemical mediators and cellular responses that may occur when cells are damaged and stressed or when pathogens successfully breach the physical barriers of innate immune system

232
Q

what does inflammation allow for

A

recruitment of cellular defenses needed to eliminate pathogens, remove damaged cells and initiate repair mechanisms

233
Q

what can excessive inflammation lead to

A

local tissue damage and death

234
Q

what happens immediately following an injury

A

vasoconstriction of blood vessels to minimize blood loss

235
Q

what happens after vasoconstriction

A

vasodilation and increased vascular permeability

236
Q

what causes vasodilation

A

the release of histamine from mast cells

237
Q

what does increased blood flow and vascular permeability do

A

dilute toxins and bacterial products at the site of injury or infection, associated with influx of phagocytes at site

238
Q

what are the signs of the inflammatory process

A

erythema, edema, heat, pain, altered function

239
Q

how does the complement system enhance the inflammatory process

A

through production of anaphylatoxin ca5

240
Q
A
241
Q

what does the release of bradykinin cause during inflammation

A

capillaries to remain dilated, flooding tissues with fluids leading to edema

242
Q

what happens during period of inflammation

A

bradykinin is released
neutrophils are recruited
pus forms
macrophages clear out pus
tissue repair begins

243
Q

what causes chronic inflammation

A

an on going and lower level battle between the host and pathogen, it may appear healed but pathogens are present in deeper tissue

244
Q

what can chronic inflammation be involved in

A

alzheimers, parkinsons, heart disease metastatic cancer, granulomas

245
Q

what are granulomas

A

pockets of infected tissue walled off and surrounded by WBC

246
Q

what infection can cause chronic inflammation

A

TB, it causes granulomas in lung tissue

247
Q

what is a fever

A

inflammatory response that affects the entire body

248
Q

what normally maintains body temperature

A

hypothalmus

249
Q

how do bacterial and viral infections create fever

A

by producing pyrogens

250
Q

what are pyrogens

A

chemicals that alter they hypothalamus to elevate body temp

251
Q

how does fever enhance innate immune defenses

A

by stimulating leukocytes to kill pathogens, stimulate the release of iron sequestering compounds from liver to starve ones that need iron out

252
Q

what happens during a fever

A

skin is pale due to vasoconstriction in skin, shivering muscles are stimulated,

253
Q

what is the crisis phase

A

when fever breaks

254
Q

how do superantigens cause life threatening fevers

A

by causing excessive activation of T cells and release of cytokines overstimulating the inflammatory response

255
Q

what can produce superantigens

A

staphylococcus aureus and Streptococcus pyogenes

256
Q
A