How can we help?

You can also find more resources in our Help Center.

42 terms

Microbiology: Immunity

STUDY
PLAY
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