Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

83 Cards in this Set

  • Front
  • Back
Commensal bacteria
They provide SYMBIOTIC BENEFIT to the HOST
Mice in bacteria-free environment
Require 30% more calories than colonized mice to maintain weight.
What do bacteria provide to mice
Metabolic pathways that expand capacity to extract calories and micronutrients from sugar plant diet.

Some bacteria provide vitamins to humans
Symbiotic benefit of nonpathogenic bacteria
out compete pathogenic bacteria for colonizing niche and colonize host
What do bacteria produce that provide symbiotic benefit

E coli and colicins
What are two ways pathogenic bacteria direct kill
1) exotoxins
2) endotoxins
Exotoxin (how bacteria direct kills)
Bacterial secreted molecules- usually act via a cell-surface receptor
induce the phagocytes to secrete inappropriate cytokines, causing local or system symptoms
EXOTOXIN Vibrio Cholerae
Salmonella Typhi
Tyhoid (endotoxin release)
What are the innate mechanisms of protection
Defensins (kill pathogens)
Coagulation system that immobilizes bacteria by prevent COLONIZING
Phagocytosis (Pathogen Recognitition receptors: Cr1, Cr3, lectins, scavenger receptors, TLR) (PAMPS aand PRRs) = Macrophages, neutrophils, monocytes

Inflammatory cytokines
How do inflammatory cytokines of innate system work?
Raise body temperature and induce acute phase proteins

iL1- temperature
iL 6- acute phase proteins
How does the bacteria evade?
Pseudomonus- produces a protein that inactivate C3a and C5a- (complement system) so blocks recruitment of other immune cells

Streptococcus pneumonaiae- produce a capsule that prevents phagocytosis
Streptococcus pneumoniae
capsule prevents phagocytosis
prevents large amount of C' binding on surface

BigMAC can't penetrate
Need antibody to CONTROL pneumoniae
What are the 4 steps of bacterial infection?
1) Attachment to host cells via adhesion molecules
2) proliferation
3) Invasion of host tissue
4) toxins induce damage to host cells
Body fights host cell attachement
host defense
Blocked by igA: prevents them from attaching to surface, lining and therefore bacteria can't colonize and proliferate
How does body prevent proliferation
phagocytosis/ complement lysis (innate or igG molecules)
How does the body prevent bacteria invasion of tissue
Antibody agglutination
Prevent toxin damage to host cells
Antibody neutralizes them
"sponges them all up"
Pathogenic mechanism of exotoxin release
Secreted by bacteria in extracellular space- Toxins hit cell- Kill cell
Endotoxin release
With bacteria, trigger cell to secrete inappropriate cytokines that cause local and systemic symptoms.
How do inflammatory cytokines work in innate protection?
Raise body temperature and induce acute phase proteins

iL-1 Temperature
iL-6 acute phase proteins
Two baceterial evasion mechanisms

streptococcus pneumoniae
Pseudomonus- bacterial evasion
produces a protein that inactivates C3a and C5a that blocks recruitment of other immune cells
Streptococcus PNEUMONIAE
capsule prevents phagocytosis
Prevents large amount of binding C' proteins on surface

BigMAC can't penetrate this capsule
So you need particular Antibody to control streptococcus pneumoniae
Mechanism of Bacterial infection
1) attaches
2) proliferates
3) invasion of host tissue
4) Toxins damage host cells

How can A of APIT be stopped?
attaches via adhesion molecules

Host defense
IgA blocks so prevents bacterial attachement, can't colonize, can't proliferate.
How can P of APIT be stopped?
Phagocytosis/C' lysis

Innate immunity via C3b
how can I of APIT be stopped?
Antibody aggutination
How do you stop toxins in APIT?
Antibodies neutralize these toxins.
Neisseria gonorrhoeae as evasion mechanism
produce proteases that cleave igA (that usually work to prevent bacteria adhesion) to Fab fragments

Cleave igA blocks its ability to AGGULTINATE pathogens for clearance
Extracellular @ interstitial space, blood lymph
Viruses, bacteria, worms require

Extracellular @ epithelial surfaces
Neisseria gonorrhoeae

Antibodies,especially igA
antimicrobial peptides
Two types of intracelllar sites of infection
Cytoplasmic vs. Vesicular
Cytoplasmic intracellular organism
chlamydia spp.

Fight with CTLs and NK cells
Vesicular Intracellular
Salmonella typhimurium

T cell and NK cell dependent MACROPHAGE activation
What cytokines stimulate th2 response?
Primarily iL4

iL 13
iL 5

Antibody production
Eosinophil production
13 and 5 are important for what?
recruitment, growth, survival factors for eosinophils
5 helps with what
"shift to different isotypes"
Eosinophiles are important for
Parasite killing. They secrete superoxide and other proteases

Inducible Nitric Oxide
Oxidative killing involves
NADPH oxidase
Superoxide O2
Hydrogen perioxide
Radical and oxidized chloride (bleach)
nitric oxide

INDUCIBLE Nitric Oxide Synthase
Enzyme that generate nitric oxide
EXTREMELY toxic to bacteria
NO (nitric oxide) and bacteria
NO is EXTREMELY toxin to bacteria
mas toxic to pathogens
What stimulates th1
IFN gamma (virus infected)
so generates

CD8 T cell activation

activation of macrohages to kill intracellular organisms
What determines th1 or th2
The cytokine environment at the time

place of Ag presentation to the naive CD4 by the dendritic cell
T cell receives signal from APC and cytokines present at the time.
Cytokines of dendritic cell or the epithelial cells of secondary lymph node.
il4 and 5 generate
Antibody response
il 12 generate what
CTL and inflammation
What determines cytokine MILIEU that determines kind of response
1) nature of pathogen
2) route of infection
3) amount of antigen/microbes
Nature of the pathogen
TLR or NOD engagement

entracellular or intracellular
Toll Like Receptors
membrane bound one location or at endosomes
Intracellular pattern recognition receptor
Route of infection as a factor that determines cytokine concentration
Where does the Ag traffic to?

What cells are present?
Amount of antigen/microbes as a factor the influences cytokines
peptide: MHC complexes

The dnesity and affinity of these antigens/microbes.
The nature of the pathogen is intracelllular
Viruses and some bacteria induce dendritic to secrete iL 12 that activate NK cells

NK cells produce IFN gamma

Naive CD4 T Cells with iL12 and IFN gamma are comitted to th1
Intracellular nature of the pathogen
Macrophage activation
because iL12 is inducing NK cells
produce IFN gamma
Gamma interacts with CD4
drive naive to th1
Extracellular pathogen
Worms, bacteria, viruses do not induce dC iL12 but induce NK1.1+ T cells to synthesize and secrete iL 4

Naive plus iL 4 differentiate into th2
Producing 13 and 5
Extracellular pathogen that makes dC's make cytokines
Seeing worm antigens
Present to naïve cd4 cell
Il-4 producing
Th2 cell
Secrete more 4, 13, 5
Peyer's patch DC produce higher levels of what cytokine? compared to what other location?
il10 ---- Ab production

Compared to spleen
iL 10 is inhibitory to what response
Blocks adherence and cohesion
Neutralizes toxins
Mechanism of Peyers patches
Polymeric igA is transported to gut through epithelial cells

igA binds to mucus layer overlying epithelium

IgA in gut neutralizes pathogens and bacterial toxins
Peyer's Patches and iGA
Allows plasma cells to generate and secrete igA
F c alpha receptors
Transported through epithelial cells
Line epithelial cell layer (within mucus membrane)
Prevent colonization of bacteria in gut (adherence to walls)
Neutralize toxins in the gut
Recap what are the three factors that determine cytokine milleus
1) nature of pathogen
2) location
3) amount or concentration
Amounts and concentrations of antigen or microbes help determine cytokines
Low abundance/affinity vs. high abbudance/high affinity
Low abundance/ low affinity
APC presents peptide with weak binding to TCR
Naive CD4T cell differentiates into th2

iL 4 and 5
High affinity and high abundance
APC presents peptide that binds strongly to TCR

Naive differentiates into th1

makes 2, gamma, TNF Beta
th1 cytokines again
il2, ifn gamma, tnf beta
th2 secretes TGF- beta and iL 10
These inhibit activation and growth of Th1 cells
Th1 cells secrete ifN gamma
inhibits proliferation of th2 cells
T reg's
T reg control th1 response
Turn off production of T cells whne there is no longer pathogen.

T reg are CD4 Cd25+
Aka suppressor cells
Type of Cd4, function to inhibit th1
By Secreting beta and 10

Lack these regS- autoimmune disorders
Disease progression depend on th1 or th2 balance
1) Leprosy:
Tuberculoid vs. Lepromatous

2) Leishmania major: requires th1 protection

high affinity, high abundance
il2, TGF beta, IFN gamma
growth well controlled by th1 like cells that activate infected macrophages

Lesion contains granulomas and is inflammed
Local inflammation- local effects (Peripheral nerve damage)
Tuberculoid leprosy granuloma
Granuloma: large number of infiltrating cells (dark brown stain)
Low numbers of organisms that are present, undetectable levels
Low activity as a result

Growth of microbacteria
Limited in Tuberculoid leprosy
Because you generated a th1 type of cell
Local inflammation
Don't have large systemic effects
No local nerve damage
Lepromatous leprosy
Widely disseminated
Not so many cells infiltrating
Don't wall off
High activity bc of organisms
Can go beyond local environment

Didn't generate cytokines that drove th1 response to kill intracellular pathogens

4, 13, 5? Are made (wrong cytokines) these generate th2 response ( Antibody production)
What cytokines dominate in the tuberculoid form
th1 cytokines
IFN gamma
TNF betta
What cytokines dominate in LEPROMATOUS FORM
th2 cytokines
iL 4
iL 5
iL 10 dominate
IFN gamma would be expected to actiave macrophages
Enhances killing of M. leprae
actually inhibits induction of bactericidal activity in macrophages
Modifying the immune response to Leishmania (intracellular)
Treat with anti-iL 4 antibody at time of infection allows normally susceptible mice to clear infection
Leishmania and anti-4 antibody
Scarf up all il 4
Allow th1 response to become visible and propogate
Ifn gamma, tnf, inos generation
Allows normally susceptible mouse to fight it
Leishmania and Balb/c
Very susceptible to Leishmania by generating a lot of iL 4
C57/BL6 and not Balb/c
doesn't kill them, considered a th1 mouse, totally resistant to Leishmania