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Micro and Immuno > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Inflammation consists of a series of reactions by the host in response to tissue injury to…

A
  • prevent tissue damage
  • isolate and destroy the infectious organisms (prevent from getting into systemic infection)
  • repair the damage and restore normal function
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2
Q

four principle characteristics of inflammation described in 2000 by Celsus

A
  1. increase in temperature (calor)
  2. redness (rubor)
  3. swelling (tumor)
  4. pain (dolor)

Virchow later introduced the concept of loss of function

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3
Q

How do innate cells mediate inflammation, i.e., identified by swelling, redness, heat & pain, upon infection?

A

They produce molecules that attract and/or activate other cells

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4
Q

describe 4 basic stages of how innate immune mechanisms establish a state of inflammation at sites of infection

A
  1. healthy skin is not inflamed
  2. surface wound (epithelium has been breached) introduces bacteria, which activates resident effector cells to secrete cytokines
  3. vasodilation and increased vascular permeability allow fluid, protein, and inflammatory cells to leave blood and enter tissues
  4. the infected tissue becomes inflamed, causing redness, heat, swelling, and pain (leukocytes and proteins creating inflammation)
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5
Q

What is the acute inflammatory response?

A

Resident cells secrete various mediators in response to bacterial infection.

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6
Q

What happens in the acute inflammatory response?

A

Microbes and injury activate resident cells (mast cell, DC, macrophage), which then release inflammatory mediations (histamine, cytokines, prostaglandins). The mediators increase capillary permeability, leading to influx of plasma proteins and phagocytic cells. Adhesion molecules and chemokines cause leukocyte migration into tissue, resulting in phagocytosis and killing of microbes.

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7
Q

How do cells at the site of infection alert other innate cells of the immune response?

A

Cytokines attract and activate cells, or induce cellular process

*chemokines are attracting cells

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8
Q

Are produced by innate cells upon interaction with infectious agents and activate or mobilize other cells

A

cytokines

*microbes induce innate cells to produce cytokines, leading to activation of dendritic cells, macrophages, NK cells

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9
Q

Example of process of how cytokines are released and result in activation and recruitment of other cells

A

activate macrophage/dendritic cell to produce IL-12, which then activates NK cells, which then produces IFN-gamma, which then activates macrophage. Macrophage then produces other pro-inflammatory cytokines like TNF, IL-1, chemokines, which then leads to migration and recruitment of other WBCs to infection site.

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10
Q

IL-1beta

A
  • cytokine produced by macrophages upon bacterial infection
  • activates vascular endothelium, activates lymphocytes, local tissue destruction, increases access of effector cells
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11
Q

TNF-alpha

A
  • cytokine produced by macrophages upon bacterial infection
  • activates vascular endothelium and increases vascular permeability, which leads to increased entry of IgG, complement, and cells to tissues and increased fluid drainage to lymph nodes
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12
Q

IL-6

A
  • cytokine produced by macrophages upon bacterial infection
  • lymphocyte activation, increased antibody production
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13
Q

IL-8

A
  • cytokine produced by macrophages upon bacterial infection
  • chemotactic factor recruits neutrophils, basophils, and T cells to site of infection
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14
Q

IL-12

A
  • cytokine produced by macrophages upon bacterial infection
  • activates NK cells, induced the differentiation of CD4 T cells into Th1 cells
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15
Q

4 basic cytokine effects on vascular endothelium

A
  • vasodilation: local small blood vessel enlarges and gets greater blood flow, but lower velocity
  • endothelial wall gains new adhesion proteins specific for interactions with leukocytes (selectins, integrin ligands) (leukocytes move to periphery of blood vessel as a result of increased expression of adhesion molecules)
  • loosening of cell junctions - tight junctions open up to allow passage of leukocytes
  • clotting of micro vessels - restricts exit of infectious agents from the area
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16
Q

systemic effects of inflammatory cytokines

A
  • IL-1, IL-6, TNFalpha affect the liver (serum amyloid protein, C-reactive protein, mannan-binding lectin) causing activation of complement and opsonization
  • IL-1, TNFalpha affect the bone marrow and endothelium to mobilize neutrophils for phagocytosis
  • IL-1, TNFalpha affect the hypothalamus to increase body temp, and affects fat and muscle for protein and energy mobilization to generate increased body temp to decrease viral and bacterial replication
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17
Q

what does a fever inhibit?

A
  • enzyme activity involved in protein synthesis
  • DNA and RNA replication
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18
Q

tooth abscess

A

Root canal infections involving inflammation with formation and discharge of pus. Can lead to apical bone destruction.

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19
Q

Bacteria causing tooth abscess

A

Black pigmented bacterial infection

  • Porphyromonas endodontalis
  • Dialisterinvisus
  • Parvimonas micra
  • Solobacterium moorei
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20
Q

Cytokines involved in tooth abscess

A

TNFalpa, IL1, IL6 in response to LPS and LTA (binding to Toll-Like Receptor 4)

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21
Q

LTA

A

lipoteichoic acid - in bacterial cell wall of G+ bacteria

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22
Q

LPS

A

lipopolysaccharide component of the cell wall of bacteria; forms a toxic component (endotoxin) in Gram-negative bacteria

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23
Q

recruitment of leukocytes: rolling

A

Infection in tissue is recognized by a macrophage, which releases cytokines TNF and IL-1. These cytokines activate the endothelium to express adhesion molecules Integrin ligand (ICAM-1 and VCAM-1) and E-Selectin and P-selectin. Rolling of leukocytes occurs because they express selectin ligands (Sialyl Lewis-X) and thus can interact with the endothelial cell.

Integrin (LFA-1, VLA-4) is on the surface of the leukocyte. These can interact with ICAM-1 and VCAM-1 on the surface of endothelial cells. This is a low-affinity state, and thus the adhesion is not very stable. Leukocyte stops and re-attaches as the blood flows, resulting in rolling.

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24
Q

recruitment of leukocytes: integrin activation by chemokines

A

Chemokines produced by the macrophage can bind to proteoglycans on the endothelial cell. Recognition of chemokines by the chemokine receptor on the surface of the leukocyte then occurs. This impacts the affinity state of the integrin on the surface of the leukocyte - they are now high affinity. Stable adhesion on the surface of the endothelial cell occurs.

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25
Q

Recruitment of Leukocytes: Stable adhesion

A

High affinity state of Integrin causes leukocytes to stop moving across endothelial cells. Stable adhesion

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26
Q

Recruitment of leukocytes: migration through endothelium

A

With stable adhesion, the cytoskeleton is reorganized, allowing the leukocyte to pass through the interendothelial spaces into the CT of the tissue. The WBC follows the chemokine gradient to the site of the infection.

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27
Q

Why do neutrophils get to the site of infection first?

A

There is a temporal difference in expression that triggers different waves of cells. Neutrophil-specific Integrin Ligand are upregulated first. Takes hours to get to site.

  • express carbohydrate ligands for P and E-selectin
  • express LFA-1 that binds to ICAM-1
  • express CXCR1/2 that binds to CXCL8
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28
Q

In which BVs do leukocytes move from?

A

Veins - do not crawl from arteries

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29
Q

Host cells seen in tooth abscess

A

Neutrophil and monocytes

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30
Q

How do plasma proteins play a role in inflammation?

A

Function as opsonin and induce phagocytosis or induce inflammatory cell recruitment

(mostly produced by liver)

31
Q

What are acute phase reactants?

A

Factors whose serum concentrations change significantly in response to inflammation. Once cytokines are produced, these reactants immediately get into the blood.

Liver plasma proteins: SAP, CRP, MBL

Function as opsonin, targeting microbes for phagocytosis.

Activate complement: classical pathway (CRP-SAP); lectin pathway (MBL)

32
Q

opsonin

A

Molecules coating the microbe surface; “tag” for destruction

33
Q

Opsonization

A

process of coating microorganisms or other particles with specific antibodies so they are more readily recognized for ingestion

34
Q

opsonins simultaneously bind to…

A

microbe and phagocyte receptor

35
Q

C-reactive protein (CRP)

A

Binds phosphocholine on bacterial surfaces, acting as an opsonin and as a complement activator.

*Serum amyloid P (SAP)/CRP bind phagocyte scavenger receptor

36
Q

Mannose-binding lectin (MBL)

A

Binds to carbs on bacterial surfaces, acting as an opsonin and as a complement activator.

MBL binds phagocyte C1q receptor.

37
Q

what is the complement system?

A

also known as complement cascade, is a part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen’s cell membrane

38
Q

Consists of several heat-sensitive plasma proteins produced by the liver

A

compliment system

39
Q

Initiation of complement activation by microbes occurs in what three ways?

A
  1. classical pathway: mediated by antibody binding on the surface of a microbe
  2. lectin pathway: recognition of mannose-binding lectin
  3. alternative pathway: binding of C3 on surface of the microbe

*all pathways lead to cleavage of C3 by C3 converts into C3b (opsonin) and C3a (anaphylatoxin)

40
Q

Describe how C3a and C5a induce local inflammatory responses

A
  • anaphylatoxins act on BVs to increase vascular permeability
  • increased permeability allows increased fluid leakage from BVs and extravasation of complement and other plasma proteins at the site of infection
  • migration of monocytes and neutrophils from blood into tissues is increased. Microbicidal activity of macrophages and neutrophils is also increased
41
Q

Which process triggered by opsonization leads to microbe ingestion?

A

phagocytosis

42
Q

the only cells in the immune system that can ingest microbes

A

neutrophils
macrophage
dendritic cells (main function is actually to present antigen in lymph node to T cell)

43
Q

What is phagocytosis?

A

Process of ingestion of opsonin-coated or receptor-bound microbes

Recognition of microbes via binding to receptors involved in phagocytosis

Ingestion inro vesicles

44
Q

steps of phagocytosis

A
  1. microbes bind to phagocyte receptors (lectin receptor/C3 receptor)
  2. phagocyte membrane zips up around microbe
  3. microbe ingested in phagosome
  4. fusion of phagosome with lysosome
  5. killing of microbes by ROS, NO, and lysosomal enzymes in phagolysosomes
45
Q

How are microbes killed once phagocytosed?

A

production of toxic products kill microbes

46
Q

what is oxidative or respiratory burst?

A

is oxygen dependent intracellular killing and produces oxygen-containing compounds which kills the bacteria; generation of O2- and reactive oxygen species (H2O2, OCl-, -OH) toxic for microbes

47
Q

What mediates the oxidative or respiratory burst?

A

Ingestion of microbes induces assembly of phagocyte or NADPH oxidase in phagolysosome: activated NADPH oxidase converts O2 molecules to the superoxide ion O2-

A second enzyme, superoxide dismutase, converts the superoxide to hydrogen peroxide.

Peroxidase enzymes (myeloperoxidase) and iron further convert the hydrogen peroxide to hypochlorite ions and hydroxyl radicals

48
Q

What happens in deficiency in NADPH oxidase?

A

Chronic granulomatous disease: accumulation of granulocytes because cannot kill microbe

49
Q

what are the two free-radical generating systems for killing microbes?

A
  1. phagocyte oxidase system
  2. inducible nitric oxide synthase (iNOS)

*both induced by IFNgamma, complement and signals from TLR. Generation of ROS and NO and reactive peroxynirite radicals that are toxic.

50
Q

Proteolytic enzymes which are involved in the killing of microbes by lysosomal enzymes in phagolysosomes

A
  • elastase
  • Cathepsin G
  • lysozyme
  • acid hydrolase
  • activity dependent on increase in pH and osmolarity
51
Q

How do neutrophils and macrophages compare in terms of enzymes and bactericidal agents produced?

A

Macrophages do not produce MPO, thus do not have the oxygen derived products of OCl- and OH

52
Q

Neutrophils can kill microbes intracellularly and extracellularly using…

A

ROS and degranulation and NETs (neutrophil extracellular traps)

53
Q

Neutrophil Extracellular Traps (NETs)

A

Networks of extracellular fibers composed of DNA that bind microbes. High local concentration of antimicrobial components that kill microbes extracellularly.

54
Q

In regards to inflammation, what are the four principal effects?

A

-Increase in temperature (calor)
-Redness (rubor)
-Swelling (tumor)
-Pain (dolor)

55
Q

Describe the acute inflammatory response

A

-Resident cells secrete various mediators (histamine, prostaglandins, TNFalpha)
-Mediators increased capillary permeability leading to influx of plasma proteins and phagocytic cells, contributing to swelling, redness, heat and pain

56
Q

How are cytokines produced?

A

By innate cells upon interaction with infectious agents and activate or mobilize other cells

57
Q

How does cytokine effect vascular endothelium?

A

Endothelial wall gains new adhesion proteins specific for interactions with leukocytes (ex: selectins, integrin ligands)

58
Q

Describe the systemic effects of inflammatory cytokines on the liver

A

IL-1, IL-6, and TNFalpha act on the liver –> leads to activation of complement Opsonization

59
Q

Describe the systemic effects of inflammatory cytokines on the hypothalamus

A

IL-1 and TNFalpha act on the hypothalamus –> leads to increased body temp –> which leads to decreased viral and bacterial replication

(fever inhibits enzyme activity involved in protein synthesis and DNA and RNA replication)

60
Q

Describe the systemic effects of inflammatory cytokines on fat and muscle

A

IL-1 and TNFalpaha act on fat and muscle –> leads to protein and energy mobilization to generate increased body temperature –> leads to decreased viral and bacterial replication

(fever inhibits enzyme activity involved in protein synthesis and DNA and RNA replication)

61
Q

What is the order of the recruitment of leukocytes to sites of infection: transmigration

A
  1. Rolling
  2. Integrin activation by chemokines
  3. Stable adhesion
  4. Migration through endothelium

**Video on Bb if better explanation is needed

62
Q

What are the liver plasma proteins?

A

SAP, CRP, MBL

63
Q

Describe acute phase reactants

A

-Function as opsonin, targeting microbes for phagocytosis (opsonins simultaneously bind to microbe and phagocyte receptor)
-Activate complement

64
Q

Opsonin

A

Molecules coating microbe surface (opsonins simultaneously bind to microbe and phagocyte receptor)

65
Q

Opsonization

A

Process of marking microbe for ingestion

66
Q

All pathways of the complement system lead to what?

A

Cleavage of C3 by C3 convertase into C3b (opsonin - involved in binding) and C3a (anaphylatoxin - involved in recruitment)

67
Q

C3a and C5a induces local inflammatory responses. Describe the responses

A

-Increased vascular permeability
-Increased microbicidal activity

68
Q

What is meant by phagocytes being the “PAC-MAN” of the immune system?

A

They ingest microbes. From there, neutrophils/macrophages will kill microbes and DC will process antigens

69
Q

Process of ingestion of opsonin-coated or receptor-bound microbes

A

Phagocytosis

-Creates a phagosome that must bind with other components in cell
-Fusion of these vesicles with organelles containing toxic molecules/enzymes where the microbes are destroyed

70
Q

Oxidative or respiratory burst

A

Generation of O2- and reactive oxygen species (ROS: H2O2, OCl-, and OH-) toxic for ingested microbes

71
Q

How are microbes killed?

A

Generation of ROS and NO and reactive peroxynitrite radicals that are toxic

72
Q

What does pus indicate?

A

dying neutrophils

73
Q

***understand the interaction of the innate immune system components upon infection

A

(chart on slide 32)

Micro and Immuno (17 decks)

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