Microbio Exam 2

Front 1

Non specific host response

Back 1

non specific host response starts here

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neutrophils or PMN's

Back 2

most numerous WBC's
- indicators of accute inflammation
- increase blood flow by dilating cappilaries.
- phagocytic

Front 3

monocytes (macrophages)

Back 3

phagocytic and they appear a few days after the pmn's

Front 4

basophils

Back 4

not fixed to tissue or circulating

- contain vasoactive substances (like histamine)
- dilation leads to delivery of cells to the site of problems.

Front 5

Eosinophils

Back 5

parasite and fungal infections
- physically bind to parasites and release their toxic granules and eliminate them through lysis.

Front 6

Natural Killer cells

Back 6

lymphocyte like
- kill malignant cells and virus infected cells

Front 7

platelets

Back 7

- involved in blood clotting
- release vasoactive substances
- fibroblast growth factors
- cells that are responsible for making and maintaining conn. tissue
- regenerating CT is an important feature of wound healing.

Front 8

plasma

Back 8

contains soluble defensive elements
- fibrinogen - converted to fibrin in which platelets become embedded --> clot formation
- interferon
- complement
- acute phase proteins
- immunoglobulins (antibodies)

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serum

Back 9

plasma - clotting factors

Front 10

interferon

Back 10

a nonspecific (species) host specific antiviral protein
- interferes with viral replication

- therapeutic dose approaches a toxic dose commonly.

Front 11

alternative complement pathway

Back 11

consists of many proteins that work in concert to destroy bacteria and certain viruses
- complement - a complex of serum proteins that act in a sequence to enhance and amplify:
- phagocytosis
- acute inflammation
- lysis of MO's
- the sequence of rxns. can be
- activated (initiated) nonspecifically
- called the alternative and the lectin pathway
- part of the non specific host resistance

done specifically by classical pathway
- requires activation by antibody

- regardless of the pathway, the biological activities are always the same
- enhance and amplify phagocytosis, acute inflammation, and direct lysis of MO's

Front 12

acute phase proteins

Back 12

increase in response to cytokines (early alarm mediators)
- synthesized in response to infection - triggered by fever and inflammation.

- produced in acute inflammation
- aid in the activation of complement pathways
- example - CRP (complement reactive protein)
-

Front 13

mast cells

Back 13

found in sub conn. tissue and mucosal surfaces (non motie and are bound to CT)
- have vacuoles that contain vasoactive substances (such as histamine)
- cause capillary bed to dilate and become leaky
- function as early warning cells
- respond to trauma by releasing vasoactive substances.

Front 14

lymphatic system

Back 14

lymph nodes - accumulations of WBC's (macrophages, dendritic cells, and lymphocytes) at varoud points along the lymphatic sytem
- very dense population of lymphocytes - initiate the acquired immune response at lymph nodes.

- immune response begins in the lymph nodes
-- they enlarge because lymphocytes are dividing.

Front 15

reticuloendothelial system/ mononuclear phagocyte system

Back 15

- provide a passageway between and within tissues and organs
- these cells are loosely scattered to tissue, adherent to fibers

- cells involved in the reticuloendothelial system
- histocytes
- conn. tissue
- serosal macrophages
- peritoneal cavity
- langerhaans cells
- skin
- dendritic cells
- many tissues as well as lymph nodes
- dendritic cells and lymph nodes macrophages interact with lymphocytes to initiate an acquired immune response.

function - secrete inflam. mediators (cytokines) that stimulate the synthesis of acute phase proteins.
- participate in the initiation of acute inflammation.

Front 16

other soluble factors

Back 16

- defensins and cathelicidins
- broad spectrum antiomicrobial peptides
- defensins - something to replace/ augment antibiotic tx of disease (MO invadors haven't been able to develop resistance to these)

Front 17

phagosomes

Back 17

a bacuole in which cells or cell particles are contained

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lysosome

Back 18

pre exisiting vacuole
- migrates to the scene of the phagosome and fuses with it to form a phagolysosome

THIS IS TH SITE OF KILLING; phagolysosome.

Front 19

Oxidative killing

Back 19

don not always kill this way , must be provoked by products of the complement pathway to engage in oxidative killling
- more rapidly lethal
- increased O2 consumption (respiratory burst)

- synthesis of ROS
-
Secretion of ROS and RNS, causes a large amount of collateral damage to tissues

Front 20

intrecellular survival of some mo's

Back 20

TB can exist inside of the phagocyte

Front 21

acute inflammation

Back 21

- for the containment, destruction and removal of foreign material
- complex but well orchestrated sequence of events
- increased vascular permeability
- capillaries have dilated in response to anaphylotoxins
- vasodilation - increases blood flow to area of damage, which facilitates the influx of immune components (also causes redness and warmth)

edema

Leukocytosis
- migration of cells from circulation into tissue
- PMN's follow C3a, C5 a to their source

Front 22

closer look at the acute inflammation process

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1. vasoconstriction
2. relaxation of the arteriole side occurs within seconds
3. increased blood flow engorges cappilaries and venuoles
4. as capillaries and venuoles begin to dilate, endothelial cells begin to contract
5. plasma exits (forced) into tissue(edema)
- what is plasma delivering
a. RBC conc. increases
b. endothelial cells begin to synthesize intercellular adhesion molecules
c. PMN's and later macrophages bind to ICAM's on endothelial cells
d. detect gradient of chemotactic factors and migrate toward the battlefield to engage the enemy (leucocytosis)
e. multiple neutrophils responding to special signaling molecules converge on the injured site.
f. chemotactic factors C3a and C5a , leukotrienes, cytokines form activated macrophages.

Front 23

plasma

Back 23

contains
- fibrinogen
- converted to fibrin in which platelets become embedded --> clot formation
- interferon
- complement
- acute phase proteins
- immunoglobulin
- serum = plasma - clotting factors
- interferon - antiviral protein
- alternative complement pathway
- amplify PHAGOCYTOSIS
- acute inflammation
- lysis of MO's

Front 24

non specific alternative (lectin) pathway

Back 24

amplifies phagocytosis, acute inflammation and direct lysis of MO's.

Front 25

acute phase proteins

Back 25

increase greatly in concentration in response to early alamr mediators - cytokines

- produced in acute inflammation
- aid in the activation of complement pathway.

Front 26

mast cells

Back 26

- found in subq connective tissueand mucosal surfaces
- non motile and are bound to CT

-have vacuoles that contain vasoactive substancesw (such as histamine)
- cause capillary bed to dilate, become leaky
- function as early warning cells
- respond to trauma by relaeasing vasoactive substances

Front 27

lymphatics sytem

Back 27

enlarged lympho nodes mark the beginning of the immune response... caused by dividing of lymphocytes.

Front 28

reticuloendothelial system

Back 28

- histocytes - connl. tissue
- kupfer cells - liver and spleen
- alveolar macrophages - lungs
- serosal macrophages - peritoneal cavity
- microglia - brain
- osteoclasts - bone
- langerhaans cells - skin
- dendritic cells - many tissues asa well as lymph nodes

FUNCTION of RES - participate in teh initiation of acute inflammation
- secrete inflammatory mediators (cytokines) which stimulate the synthesis of acute phase proteins.
-

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To initiate an acquired immune response

Back 29

dendritic cells and lymph node macrophages interact with lymphoctye to initiate this.

Front 30

defensins and cathelicidins

Back 30

- broad spectrum antimicrobial peptides
- Defnesins - something to replace/ augment antibiotic tx of disease. (MO invaders havent' been ablo to develop resistance to these)

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phagocytosis

Back 31

- PMNS, macrophages and dendritic cells

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dynamics of phagocytosis

Back 32

- opsonization - coats the surface of MO's with antibodies or complement, facilitating recognition and engulfment.

acute phase proteins - CRP and MLB and C3b, function as opsonins (bridge between phagocyte and MO)

- opsonins increase the macrophages and dendritic cells ability to interact with lymphocytes.

- phagosome and phagolysosome formation
- phagosome - where particles are located
lysosome - pre existing vacuole

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how phagocytosis works

Back 33

- non oxidative killing - slower process involviing bactericidal peptidases and enzymatic degradation.

- oxidative killing

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oxidative killing

Back 34

- synthesis of ROS
- HCLO
- O2
- H2O2

Front 35

acute inflammation

Back 35

for the containment, destruction and removal of foreign material

Front 36

sequence of acute inflammation events

Back 36

- increased vascular permeability
- dilated in response to anaphylotoxins
- vasodilation - increases blood flow to area of damage, which facilitates the influx of immune components
- edema - movement of fluid into endothelial tissue (delivers fibrinogen and antibodies)
- leucocytossi - migration o fcells from circulation to tissue
- PMN's follow C3a and C5a to their source.

Front 37

PMN DNA does what?

Back 37

serves to maintain the viscosity of the inflammatory exudates.

Front 38

chronic inflammation

Back 38

for containment, destruction and removal of persistent foreign material.

- T lymphocytes - also calle t cells
- active T cells are active in CELL MEDIATED IMMUNITY.

Front 39

c3b

Back 39

opsonin ability

Front 40

antigen presenting cells

Back 40

- macrophages and dendritic cells

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T lymphocytes

Back 41

- Two types
1. T helper cells - assist effector T cells and B cells
2. are the on switch of the immune system.
3. HIV infects TH cells.
Effector T cells - attack teh enemy directly
- CELL MEDIATED IMMUNITY

- B lymphocytes -

Front 42

B lymphocytes

Back 42

- following antigen stimulation they differentiate into plasma cells wthich synthesize antibodies.

- acquired immune response begins in the Lymph nodes.

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heavy chain switch

Back 43

- occurs at the level of teh B cell, not the plasma cell.

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T cells don't have

Back 44

immunoglobulins on their surface.

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T cell receptors bind to

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Major histocompatibility receptors

Front 46

if antigen presentation is in high density

Back 46

th 0 --> th1 = inflammatory T cells

- Th1 cells interacti with macrophages as effector T cells in the cell mediated immune response.

Front 47

if antigen presentation is in low density

Back 47

- th2 lymphocytes interact with b cell in the humoral response (synthesis and secretion of antibody)

Front 48

cytokines

Back 48

t and be cells interact in an immune response with each other thgouth these soluble molecules.

Front 49

MHC 1

Back 49

- attach to proteins synthesized in a host cell
- all nucleated cells express class 1 MHC (RBC's) don't therefore.

- effectore te cell smust recognize BOTH the antigenic determinang and class one MHC in order to become aroused.

-

Front 50

Class 2 MHC

Back 50

- attach to proteins PROCESSED by mcarophages and dendritic cells.

Front 51

primary congenital disorders

Back 51

- B cell deficiency

T Cell deficiency

- SCID
Complement deficiencies
phagocytic defects

Front 52

type 2 hypersensitivity

Back 52

- mediated by IGM and IGG, complement, pmn's and macrophages

- target tissue - usually RBC's platelets and cells of other tissues.

- complement pathway is initiated resulting in complement mediated cytosis.

Front 53

type 3 or immune complex hypersensitivity

Back 53

- mediated by Igm and IgG, complement and macrophages adn PMN's soluble antigen reaction with antibody, latticle like structure of AGN and Aby
- these complexes form in such excess ha they can't be effectively removed by cells of the RES
- these complexes are then deposited in teh vascular endothelium, basement membrans of the glomeruli adn sinovial membranes of joints.
- buld of damage due to PMNS which cause tissue damage.

Front 54

Type 4 hypersensitivity

Back 54

- Th lymphocyte, macrophages and some Tctl involvement

- occurs 1-3 days after exposure. wait for cesll to accumulate, macrophages to get activated,
- lymphokines activate macrophages which relaeas mediators of oxidateve and on oxidative killing.