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chapter 2&3

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created 2 years ago by ednalznd
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1

First defense against infection

mechanical and chemical barriers

2

mechanical and chemical barriers

skin

mucous membranes

gastirc juices- salivary glycoproteins, lysozyme, oleic acidon the skin, urea

acidity- of the stomach and vagina, kills unwanted bacteria and yeast

bile- aids in fat digestion, a small inhibitory substance against parasites

Antimicrobial peptides-cationic antimicrobial peptides( cathelicdin, defensins, histatins), bacteriocins

lysozyme

interferons

3

skin

skin protects the deeper tissues of the body

4

Mucous membranes

lines the epithelium of the digestive and respiratory tracts- prevents penetration of parasites into tissues

5

Antimicrobial peptides

Cataionic antimicrobial peptides

damage bacterial plasma membranes thru electrostatic interactions

cathelicidin, defensins, histatins

6

Antimicrobial peptides

bacteriocins

plasmid-encoded antibacterial peptides produced by normal bacterial flora; are lethal to related species tru a variety of mechanisms

7

lysozyme

chemical inhibitor of a nonspecific nature. Found in human tears, sweat, saliva. It disrupts the cell wall of gram positive by digesting peptidoglycan

8

interferons

group of substance produced by body cells in response to invasion by viruses. interferons trigger the production of inhibitory substances that interferes with viral replication

9

antimicrobial peptides kill pathogens by

perturbing their membranes

10

physical barriers colonized by microorganism protect against infection by _________ pathogens

commensal

11

What are defensins?

antimicrobial cataionic peptides found in various body secretions that damage bacterial plasma membrane tru electrostatic secretions

12

Complement

A set of more then 20 serum proteins that enhance phagocytosis tru inflammation, opsonize ( mark with special protein) pathogens for phagocytosis and lyse cells tru formation of membrane attack complex

13

Complement produce by

liver

14

membrane attack complex

form large holes in the membrane of many microorganism, especially gram negative bacteria and enveloped virus

15

small peptides released during complement activation

induce local inflammation

16

Alternative complement pathway

  • occurs in response to intravascular invasion by bacteria and some fungi; involves the interaction of complement with the surface of the pathogen forming the membrane attack complex
17

At the start of an infection complement activation proceeds by the

alternative pathway

18

lectin complement pathway also called mannan-binding lectin pathway

occurs when macrophages stimulate liver cells to release acute phase proteins such as manose-binding protein (a lectin), in which then can activate complement via alternative pathway or classical pathway

19

classical pathway

results from antigen-antibody interactions that occur during specific immune responses

20

All 3 pathways lead to

c3 convertase

21

Regulator proteins determine the extent and site of

c3b deposition for opsonization of pathogens

22

Cleavage of C3 to

C3a and C3b

C3b covalently bound to surface of pathogen

23

C5

on activation the soluble C5b fragment initiates assembly of the membrane attack complex in solution

24

C6

Binds to and stabilizes C5b. Forms a binding site for C7

25

C7

Binds to C5b6 and exposes a hydrophobic region that permits attachment to the cell membrane

26

C8

binds to C5b67 and exposes a hydrophobic region that inserts into the cell membrane

27

C9

polymerization on the C5b678 complex to from a membrane-spanning channel that disrupts the cell's integrity can result in cell death

28

Complement receptor (CR1) on macrophages detects

C3b coated on bacteria. Macrophages then engulf the C3b- bacteria complex

29

The membrane attack complex causes

cell lysis. The terminal complement proteins lyse pathogens by forming a membrane pore

30

CD59 important because

on human cells CD59 binds to the C5B678 complex and prevents recruitment of C9 to form the pore

31

The formation the membrane attack complex

1. antibody molecules attach to the antigen on the pathogen's cell membrane

2.complement proteins link two antibody molecules together

3.activated complement proteins attach to the pathogen's membrane in step-by-step sequence

4. the attack complex results in pores in the membrane and lysis by water loss

32

Membrane attack complex consists of which complement proteins?

C5b, C6,C7, C8, C9

33

other non specific innate resistance mechanisms

moderate fever benefits hosts defenses

natural killer cells

34

moderate fever benefits hosts defenses

low to moderate fever supports the immune system by inhibiting rapid microbial growth, encouraging rapid tissue repair and heightening phagocytosis. Most common cause of fever is viral or bacterial infection due to endogenous pyrogens and inflammatory cytokines ( IL1, IL 6, TNF)

35

Most common cause of fever

is viral infection or bacterial infection due to action of endogenous pyrogens and inflammatory cytokines (IL-1, IL-6 and TNF)

36

Natural killer cells

recognize and kill abnormal cells

defensive lymphocytes that act spontaneously on virus-infected cells, cancer cells, organ transplants

37

When a NK cell recognizes a cell as "nonself" it releases

cytotoxic perforins and granzymes

38

NK cell recognize and target in 3 ways

1.antibody-dependent cell mediated cytotoxicity receptors on NK cells link them to antibody-coated target cells

2. If NK cells bind class I major histocompatibilty (MHC) molecules ( a self antigen) on a cell's surface, killing is inhibited, if there is no class I MHC on the target cell, then killing occurs tru poreforming proteins and cytotoxic enzymes (granzymes)

3. If MIC ligand is expressed by the abnormal cells, then perforins and granzymes are released by NK cells

39

Inflammatory cytokines

raise body temperature and activate the liver to make the acute phase response

IL-1, IL-6, TNF alpha

40

NK cells provide an early defense against

intracellular infections

41

NK cell receptors differ

in the ligands they bind and the signals they generate

42

Cell receptors of innate immunity distinguish

nonself from self

43

natural killer cells are the main circulating lymphocytes that

contribute to the innate immune response

44

Natural killer cells cytotoxicity is activated at sites of

virus infection

45

Phagocytosis

the process by which invaders are recognized, ingested, and killed.

represents part of a second line of nonspecific defense (innate immunity)

and first line of cellular defense against invading microorganism

46

Phagocytic cells

monocytes, tissue macrophages, dendritic cells and neutrophils

Phagocytose infecting organisms

47

Phagocytosis is the process by which

invaders are recognized, ingested and killed

48

Process of phagocytosis

cell eating. A pathogen such as bacteria is engulfed by macrophages and neutrophils

49

Phagocytosis begins with

an invaginaiton, or folding in, of the cell membranes to form a vesicles.

The vesicle pinches off and fuses with several lysosomes, which are organelles that contribute digestive enzymes, proteins and peptides to the digestion process.

50

Chemotaxis

binding of bacteria to macrophages and neutrophils induces chemokines attract other macrophages and neutrophils to the area

51

Opsonins

Opsonization

attach to microbes to increase the ability of phagocytes to adhere

52

Exocytosis

the antigenic remains of invaders can be expelled from the cell (as neutrophils do ) or further processed for antigen presentation on the lymphocyte cell surface (as macrophages and dendritic cells do)

53

Mechanism of phagocytosis

phagocytized microbes are held in a phagosome

The phagosome is acidified, killing or inactivating the pathogen

Phagosomes also fuels with lysosomes (phagolysosome)

Enzymes and other products kill and digest the pathogen

54

Tissue macrophages

carry a battery of phagocytic and signaling receptors

55

Innate immune receptors distinguish features of

microbial structure

56

Innate immunity Depends on

Receptor- Recognition of Common pathogen- Associated molecules

57

Pathogen-associated molecular patterns PAMPs

help the innate immune system recognize pathogens

58

Toll-like receptors are signaling receptors on

macrophages

dendritic cells

endothelial cells

59

Toll like receptors sense the presence of

infection

60

TLRs mediate a specific response

to distinct PAMPs

61

TLR stimulate the secretion

cytokines

62

The TLR response must be regulated to prevent

infection and immune disorders

63

Inflammation plays an important role in fighting infection. Inflammation is a

nonspecific defensive response by the body to an injury in the tissue.

64

Inflammation develops

after mechanical injury, such as an injury or blow to the skin, or from an exposure to a chemical agent, such as acid or bee venom

65

Activation of resident macrophages

induces inflammation at sites of infection

66

An inflammatory response also may by due to

an infection by a living organism such as a parasite.

67

Processes of inflammation 1.

tissue injury or parasite infection triggers the release of chemical mediators such as histamines, which in turn triggers vasodilatation and increase capillary permeability at the site of infection. Macrophages and neutrophils march in to take care of business... that is clearing of the parasite.

68

Neutrophils are dedicated phagocytes

that are summoned to sites of infection

69

Inflammatory cytokines recruit

neutrophils from the blood to the infected tissue

70

The homing of neutrophils to inflamed

tissues involves altered interactions with vascular endothelium

71

Neutrophils are potent killers of pathogens and are themselves

programmed to die

72

Pus is a product of

phagocytosis during inflammation... when pus becomes enclosed in, a wall fibrin forms a sec, this sac is an abscess or boil

73

Which of the following pairs is mismatched?

B + T Lymphocytes innate immune response

Natural Killer cells, kill virus infected cells

Macrophages phagocytosis and killing microbes

B + T Lymphocytes

74

Process of inflammation

1.

A thorn pierces the skin causing a mechanical injury and bringing bacteria into the tissue

75

Process of inflammation

2.

Capillary walls open (dilate) and plasma flows to the site of injury making it red, swollen and warm

76

Process of inflammation

3.

Phagocytes (neutrophils and macrophages) arrive and begin phagocytosis

77

Process of inflammation

4.

A fibrin wall accumulates around the mixture of plasma leukocytes, bacteria, and tissue cells, collectively called pus. An access becomes apparent .

78

Process of inflammation

5.

Lacing of the abscess releases the pus

79

Kallikrein

an enzyme that catalyzes formation of bradykinin

80

Bradykinin

binds capillary walls, causing movement of fluid and leukocytes into tissue and production of prostaglandins (cause pain)

Binds mast cells, causing release of histamine and other inflammation mediators

81

Histamine

promotes movement of more fluid, leukocytes, bradykinin, and kallikrein into tissue

82

Pro-inflammatory cytokines are released by

macrophages upon activation

AT THE SITE OF INFECTION RESIDENT MACROPHAGES SECRETE INFLAMMATORY CYTOKINES

83

IL- 1B

TNF ALPHA

Induce blood vessels to become more permeable, enabling effector cells and fluid containing soluble effector molecules to enter infected tissue

84

IL 6

Induces fat and muscle cells to metabolize, make heat and raise the temperature in the infected tissue

85

CXCL8

RECRUITS NEUTROPHILS FROM THE BLOOD AND GUIDES THEM TO THE INFECTED TISSUE

86

IL-12

Recruits and activates natural killer cells that in turn secrete cytokines that strengthen the macrophages response to infection

87

Activation of resident macrophages

induces a state of inflammation at sites of infection

88

interferon

group of substances produced by body cells in response to invasion by viruses. interferons trigger the production of inhibitory substances that interfere with viral reproduction

89

1i interferon

inhibit viral replication and activate host defenses

90

internal detection of viral infection induces cells to

make an interferon response

91

plasmacytoid dendritic cells are factories making large quantities

of type 1 interferon

92

interferon response IFN ALPHA IFN BETA

induce resistance to viral replication in all cells

increases expression of ligands for receptors on NK cells

activate NK cells to kill virus infected cells

93

NK cells and macrophages activate

each other at sites of infection

94

Interaction between dendritic cells and nk cells influence

the immune response

95

Which cytokine is directly important in induction of resistance to viral replication ?

interferon alpha and beta


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