Microbiology: Immunity

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Physical barriers

Skin and mucous membranes are the physical barriers
Physical barriers often in association with chemical barriers

Chemical barriers

Stomach acid (HCl)
Lysozyme (saliva and tears)
Fatty acids and oils (skin)

2nd line of defense

Phagocytes, inflammation, complement system, interferon

3 types of phagocytes

neutrophils, macrophages, dendritic cells

steps of engulfing and killing

Endocytosis with microbe being contained in phagosome
Lysosome fuses with phagosome
Degradative enzymes along with reactive oxygen products kill microorganism
Release of debris

5 cardinal signs of inflammation

injury, rubor, tumor, dolor, loss of function

Mast cells

release chemical mediators:
vasodilation, increased permeability, pain, chemotaxis

Histamine

chemical mediator that causes vasodilation and increased permeability

Complement system

A set of blood proteins that when "triggered/activated"
undergo a series of chemical reactions that lead to the
killing of microorganisms, stimulate inflammation (mast cells, neutrophils), opsonization (stimulates and helps phagocytes)

Classic pathway

antibody on surface of microbe

Lectin pathway

mannose on surface of microbe

Alternative pathway

other molecules on surface of microbe

All pathways lead to:

the MAC, membrane attack complex

MAC

membrane attack complex, composed of many C9, C5-C8 molecules, leads to holds in the membrane of the microbe

Interferon

chemicals produced in response to viral infection,
act to: stimulate phagocytic T andB cells
slow viral replication in infected host cells
inhibit cancer cells

Antigens

large complex molecules, organic, usually proteins, foreign particles, found on surface of pathogen, lymphocytes recognize pathogens by binding to antigens, lymphocytes have receptor molecules that bind to specific antigens

plasma cells

b-lymphocyte that produces antibody

antibody

a protein
IgG 2 bonding sites, (80%)more commonly found, smallest, lives longest, crosses placenta, fixes complement, binds to phagocytes, long term immunity
IgA 2-4 bonding sites, (13%), binds to epithelial cells
IgM 10 bonding sites, (6%)less commonly found, largest, dies fastest, fizes complement, binds to NA, first response

How antibody works

opsonization
complement fixation
agglutination
neutralization (viruses)
precipitation of free molecules (toxins)

Cell mediated response effector

cytotoxic t cells (CD-8 cells)

What is needed to activate t-cells?

antigen presenting cells

Cell mediated response is the primary defense against what pathogens?

intracellular pathogens

Antibody mediated response is the primary defense against what pathogens?

extracellular pathogens

Cytotoxic t cells recognize cells with ________ pathogens, infected host cell has _______ on surface with ___________ molecule

intracellular, antigen, class 1 MHC

Once bounce CD-8 cells produce

lymphotoxins

Lymphotoxins act on infected cell by...

disrupt cell membrane
disrupt metabolism
initiate apoptosis

What type of cell is an APC?

phagocytic cells like macrophages and dendritic cells primarily

What is the APCs process?

Engulf pathogen →digest pathogen→processes antigen→presents antigen on its surface

Class 1 MHC is associated with what cells?

CD8 cells

Class 2 MHC is associated with what cells?

TH1, TH2

What do TH1 cells do?

help cytotoxic t cells (CD-8)

What do TH2 cells do?

helps B-lymphocytes

What is another name for a t-helper cell?

CD-4

What do t-helper cells produce?

Lymphokines which stimulate other lymphocytes

lymphokines

produced by CD-4 cells to stimualte other lymphocytes

Immune avoid mechanisms

rapid reproduction
prevention of phagocytosis-due to capsule
--Klebsiella pneumoniae, Streptococcus pneumoniae
survival w/in phagocytes
--Mycobacterium tuberculosis, Trypanosoma cruzi (chagas disease)
intracellular pathogens
--rickettsia, chlymidia
changing antigens
--Borrelia hermsii (relapsing fever), Trypanosoma bruceii (sleeping sickness)

Killed and inactivated vaccines

pathogen subjected to chemical/radiation treatment
antigens intact but pathogen destroyed
advantages-safe, no symptoms
disadvantages-requires larger dose/ frequent application
--adverse reactions
ex) pertussis, typhoid, cholera

Live/attenuated vaccines

pathogen made virulent by modifying growth conditions in lab
antigen intact pathogen capable of replicating
advantages-produce strong immune response
--less adverse reactions
disadvantages-possible mild symptoms, might become virulent again, transmissible
ex) polio(oral), measles, mumps, rubella

Subunit vaccines (acellular)

contain only antigenic portion of microbe
bacterial capsules, cell walls
advantages- few adverse reactions
--good to excellent immune response
disadvantages-newer vaccines expensive
ex) pneumococcus, HIB, hepatitis A

Toxoid vaccines

chemically denatures pathogen toxin
non-toxic and stimulates IR
ex)tetanus, diphtheria

post exposure preventative

hepatitis B, rabies

therapy for immunocompromised patients/
treatment of diseases due to toxins

ex) tetanus, diphtheria
bite from poisonous snake

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