Microorganisms and Immunity Flashcards
how do prokaryotes differ from eukaryotes
A cytoplasm that lacks membrane-bound organelles
Ribosomes that are smaller (70 S) than those found in eukaryotic cells (80 S)
No nucleus, instead having a single circular bacterial chromosome that is free in the cytoplasm
A cell wall that contains the glycoprotein murein / peptidoglycan
cell membrane that contains folds known as mesosomes
Loops of DNA known as plasmids
Capsules
Flagella
Pili
what does a capsules / slime capsule do
protect bacteria from drying out and from attack by cells of the immune system of the host organism
what does flagella do
Long, tail-like structures that rotate, enabling the prokaryote to move
what does Pili do
Thread-like structures on the surface of some bacteria that enable the bacteria to attach to other cells or surfaces
describe the structure of a virus
A nucleic acid core
Their genomes are either DNA or RNA, and can be single or double-stranded
A protein coat called a ‘capsid’
do not possess a plasma membrane, cytoplasm, or ribosomes
an outer layer called an envelope formed from the membrane-phospholipids of the cell they were made in
contain attachment proteins that sticks out from the capsid or envelope
This enables the virus to attach itself to a host cell
structure of HIV
contains RNA and is a retrovirus
what is a helper T cell
a type of white blood cell that is normally responsible for activating antibody-producing B cells
how is HIV replicated
enters the helper T cells by attaching to a receptor molecule on the host cell membrane
The capsid enters the helper T cell and releases the RNA
The viral RNA is used as a template by reverse transcriptase enzymes to produce a complementary strand of DNA
Once this single-stranded DNA molecule is turned into a double-stranded molecule it can be successfully inserted into the host DNA
uses the host cell’s enzymes to produce more viral components which are assembled to form new viruses
enter the blood, where they can infect other helper T cells repeat the process
individual is HIV positive and may experience flu-like symptoms
individual enters the latency period after replication rate drops
what happens when virus reduces the number of helper T cells
B cells are no longer activated
No antibodies are produced
What are the four ways pathogens enter body
Broken skin
digestive system
respiratory system
Mucosal surfaces
what are the four barriers to infections
skin : blood clotting mechanism of the body plays an important role in preventing pathogen entry in the case of damage to the skin
microorganisms of the gut and skin: gut or skin flora they compete with pathogens for resources, thereby limiting their numbers and therefore their ability to infect the body
stomach acid : HCl creates an acidic environment that is unfavourable to many pathogens
lysozyme : damage bacterial cell walls, causing them to burst, or lyse
what is a specific response
response specific to a particular pathogen
recognise specific pathogens due to the presence of antigens on their cell surface
what is an antigen
molecules such as proteins or glycoproteins located on the surface of cells; their role is to act as an ID tag, identifying a cell as being ‘self’ or ‘non-self’
what is included in a non-specific immune response
Inflammation
Interferons
Phagocytosis
explain inflammation
surrounding area of a wound can sometimes become swollen
mast cells respond to tissue damage by secreting the molecule histamine
Histamine is a chemical signalling molecule that enables cell signalling
Histamine stimulates
Vasodilation increases blood flow through capillaries
Capillary walls more permeable
Phagocytes leave the blood and enter the tissue to engulf foreign particles
Cells release cytokines, another cell signalling molecule that triggers an immune response in the infected area
explain interferons
Cells infected by viruses produce anti-viral proteins called interferons which prevent viruses from spreading
inhibit the production of viral proteins, preventing the virus from replicating
They activate white blood cells involved with the specific immune response to destroy infected cells
They increase the non-specific immune response e.g. by promoting inflammation
explain phagocytosis
idea of binding of {bacteria / virus / pathogen / microorganism / antigen / non-self / foreign matter / eq} to (phagocytic) cell;
idea that {bacteria / virus / pathogen / microorganism / antigen / eq} is {engulfed by / taken into / endocytosis into
} (phagocytic) cell;
idea of bacteria being inside a {vacuole / phagosome /
mode of action of phagocytosis
Chemicals released by pathogens, as well as chemicals released by the body cells under attack. Histamine, attract phagocytes to the site where the pathogens are located
Phagocytes move towards pathogens and recognise the antigens on the surface of the pathogen as being non-self
cell surface membrane of a phagocyte extends out and around the pathogen, engulfing it and trapping the pathogen within a phagocytic vacuole known as endocytosis
Enzymes are released into the phagocytic vacuole when lysosomes fuse with phagosome
These digestive enzymes, which includes lysozyme, digest the pathogen
After digesting the pathogen, the phagocyte will present the antigens of the pathogen on its cell surface membrane
presentation of antigens initiates the specific immune response
what are phagocytes also known as
antigen presenting cell
what do antigens do
allow cell-to-cell recognition
what happens to the antigens of the engulfed pathogen
phagocytes transfer the antigens of the digested pathogen to their cell surface membrane, becoming antigen presenting cells
what do antigen presenting cells do and how
apc=sir
Antigen presenting cells such as macrophages activate the specific immune response
This occurs when the white blood cells of the specific immune response, known as lymphocytes, bind to the presented antigens with specific receptors on their cell surface membranes
what are the Y shaped antibodies also known as
immunoglobulins
how many polypeptides do antibodies consist of
four polypeptide chains; two ‘heavy’ chains attached by disulfide bonds to two ‘light’ chains
what does each polypeptide consist of
a constant region and variable region
The amino acid sequences in the variable region are different for each antibody
what is there at the end of each variable region
a site called the antigen binding site
The antigen binding sites vary greatly, giving the antibody its specificity for binding to antigens
what does variable region do
where the antibody binds to an antigen to form an antigen-antibody complex
what is the hinge region
where the disulfide bonds join the heavy chains, gives flexibility to the antibody molecule provides flexibility to the molecule and allows the molecule to change shape which is helpful in binding to antigens of different shapes and sizes.
what do membrane bound antibodies have
an extra section of polypeptide chain within their heavy chains which forms the attachment to lymphocytes
what can the gene that codes for heavy chain antibodies in non membrane bound antibodies do
undergo a process called alternative splicing to remove this extra section in non-bound antibodies removes coding sections called exons
what are the three ways antibodies deal with pathogens
antibodies can bind to the receptors of host cell, preventing pathogens from infecting host cells
act as anti-toxins by binding to toxins produced by pathogens
cause pathogens to clump together, a process known as agglutination; this reduces the chance that the pathogens will spread through the body and makes it possible for phagocytes to engulf a number of pathogens at one time
What are T cells and where are they produced
a type of white blood cell
produced in the bone marrow and finish maturing in the thymus, which is where the T in their name comes from
what do mature T cells have
specific cell surface receptors called T cell receptors
have a similar structure to antibodies and are each specific to a particular type of antigen
when are t cells activated
Bacterium is engulfed by a macrophage. Antigens are displayed on the surface of the macrophage
The macrophage acts as an antigen-presenting cell (APC).
Macrophage APC binds to T Helper cell with complementary receptor proteins.
The T Helper cell is ‘activated’ and divides by mitosis to form T memory cells and active T helper cells.
what could antigen presenting cell be
a macrophage, an infected body cell, or the pathogen itself
how do t cells increase in number
Dividing by mitosis produces genetically identical cells, or clones, so all of the daughter cells will have the same type of T cell receptor on their surface
what happens as t cells divide by mitosis
differentiate into three main types of T cell
T helper cells
T killer cells
T memory cells
what is a T helper cells
Release chemical signalling molecules that help to activate B cells
what is a T killer cells
Bind to and destroy infected cells displaying the relevant specific antigen
what is a T memory cells
Remain in the blood and enable a faster specific immune response if the same pathogen is encountered again in the future
where are b cells found
B cells remain in the bone marrow as they mature, hence the B in their name
what do b cells have
specific receptors on their cell surface membrane
The receptors are in fact antibodies, and are known as antibody receptors
Each B cell has a different type of antibody receptor, meaning that each B cell can bind to a different type of antigen
what happens when b cell binds to antigen and
forms an antigen-antibody complex
what does daughter cells of B cell differentiate to
Effector cells, which go on to form plasma cells
Plasma cells produce specific antibodies to combat non-self antigens
Memory cells
Remain in the blood to allow a faster immune response to the same pathogen in the future
what do eukaryotic cells transcribe
both introns and exons to produce pre-mRNA molecules
what happens before pre-MRNA exit nucleus
splicing occurs
The non-coding intron sections are removed
The coding exon sections are joined together
The resulting mRNA molecule contains only the coding sequences of the gene
Since these modifications are made after transcription occurred, they are called post-transcriptional modifications
what is alternative splicing
exons of genes can be spliced in many different ways to produce different mature mRNA molecules
a single eukaryotic gene can code for more than one polypeptide chain
what happens when a new antigen is encountered
primary immune response consisting of a non specific response then specific response
if it is the first time the immune system has encountered an antigen what would you expect for the number if T and B cells
T and B cell number with correct membrane receptor present in blood will be low
why does person get symptoms for disease first time they contract it
takes time for correct T and B cells to be activated and to divide and differentiate into different cell types
plasma can take days to develop and produce antibodies
what allows someone to be immune to a pathogen
memory cells during primary response
HIV evasion mechanism
Virus kills helper T cells after it infects them which reduces number of cells that could detect the presence of a virus and produce antibodies
High antigenic variability due to high mutation rate in genes coding for antigen proteins - memory cells for one strain wont recognise antigen for another strain
Virus prevents infected cell from presenting antigens on cell surface membrane making it difficult for WBC to recognise and destroy the infected cells
Disrupts antigen presentation in infected phagocytes making it difficult for immune system to recognise and destroy the cells
TB evasion mechanism
once engulfed by phagocyte in lungs the bacteria produces substances which prevent lysosomes from fusing with phagocytic vacuole preventing bacteria from being broken down by digestive enzymes making them multiply
How do antibiotics work
interfering with growth or metabolism of target bacterium
why will mammalian cells not be damaged by antibiotics
eukaryotic with no cell walls, different enzymes and different ribosomes
why wont viruses be affected by antibiotics
no enzymes ribosomes or cell walls
explain effect of increasing interferon dosage on survival from influenza virus
increasing dose of interferon increases the survival time of the mice
because interferon inhibits viral replication (inside cells)
the greater the dose of interferon the fewer virus particles {produced / released} (to infect other cells)
what is bactericidal antibiotics
kill bacteria by destroying their cell wall causing lysis (burst)
what is bacteriostatic antibiotics
inhibit growth of bacteria by stopping protein synthesis and production of nucleic acid so bacteria cant divide and grow
devise an experiment to investigate the effects of different antibiotics
Set up your sterile work area by wiping surfaces with disinfectant and setting up a Bunsen burner
Transfer some of the bacterial culture on to an agar plate using a sterile pipette and spread it out using a inoculating loop
Soak similar sized paper discs in different types of antibiotics
Add a negative control to the investigation by soaking a disc in distilled water
Space the discs apart on the agar plate using sterile forceps
Lightly tape a lid onto the petri dish, invert and incubate at 25 °C for 24 to 48 hours
Any clear patches in the lawn will indicate where bacteria could not grow - This is called the clear zone
why lightly tape than sealing lid
why invert the dish
why incubating at room temperature
ensures oxygen is available to bacteria
prevents condensation from dripping onto the agar, potentially contaminating the dish
prevents the growth of harmful pathogens
what is the use of the bunsen burner in experiment
updraft and prevent microorganisms in air from landing in the work area
what does a larger clear zone indicate
more effective antibiotic was at inhibiting bacterial growth
characteristics of antibodies
reference to glycoprotein;
credit detail of structure e.g. specific (3D) shape, L and H regions, Y-shape, 4 (peptide) chains, disulphide bridges between peptides, hinge region
reference to {antigen-binding site / variable region / Fab (region) / eq };
idea of antibodies have a {similar / constant / Fc / eq } region;
produced by plasma cells / present on B cells;
role of antibody described e.g. opsonisation, immobilisation, agglutination, lysis ;
what is active immunity
when an antigen enters the body triggering a specific immune response
what is active natural
acquired through exposure to pathogens
what is active artifical
acquired through vaccination
what is passive immunity
acquired without an immune response; antibodies are gained from another source, not produced by the infected person
what is passive natural
Foetuses receive antibodies across the placenta from their mothers
Babies receive antibodies in breast milk
what is passive artificial
People can be given an injection / transfusion of antibodies
what is antigenic variation
memory cells do not detect the altered antigens and are no longer effective against the pathogen
explain how phagocytosis and lysosome action lead to antigen presentation by macrophages
pathogen taken into macrophage
phagosome fuses with lysosome
lysosome digests the bacteria
antigen / bacteria is presented on the surface of the macrophage
difference between totipotent and pluripotent
totipotent cells can { give rise to / differentiate to become } { any cell / extra embryonic tissues / eq };
pluripotent cannot { give rise to / differentiate to become } { all cells in the body / extra embryonic tissues / eg };
idea that only totipotent cells can give rise to other totipotent cells;
idea that totipotent cells can give rise to an entire human being, pluripotent cells cannot;
Give two differences between the genetic material of bacteria and viruses.
bacteria have DNA, viruses have DNA or
RNA ;
2. idea that bacteria have {circular / eq}
genetic material, viruses have {linear /
straight} ;
3. bacterial DNA is double-stranded, viral {DNA
/ RNA} is single (or double) stranded / eq;
4. bacteria (may) have plasmids, viruses do
not have plasmids
Describe how a B cell is activated.
{antigen / bacteria / virus / pathogen} {binds / eq} to B
cell ;
2. {antigen / bacteria / virus / pathogen} {binds / eq} to
MHC (antigen) ;
3. T helper {lymphocytes / cells} {bind / eq} (to B cell) ;
4. reference to cytokines (from T helper cells)
how do macrophages present antigen to helper T cells
macrophage {binding/ eq} to T (helper) {cell /
lymphocyte} ;
- reference to {MHC / major histocompatibility complex }
(on macrophage) ;
as antigen is presented on MHC
How does HIV enter T helper cells
(glycoproteins / GP120} on the (surface of the) virus(1)
bind to (CD4) receptors on the (surface of the) T (helper) cells(1)
viral envelope fuses with cell membrane of T helper cell (1)
viral RNA enters the cell
Explain why the presence of microorganisms on the skin and in the gut helps to prevent pathogenic organisms multiplying in the body.
flora in the gut and skin are better adapted to the conditions (1)
* therefore they can outcompete pathogenic organisms (1)
* bacteria in the gut secrete {chemicals /lactic acid} which help to destroy pathogens (1)
Devise a laboratory procedure to compare the effectiveness of penicillin with one of the new antibiotics.
prepare agar plates with bacterial cultures / bacterial lawn / seeded with bacteria -use bacteria that are resistant to other antibiotics
prepare solutions of new antibiotic and penicillin
place onto paper discs / into wells in the agar /
prepare mast rings control time and temperature of incubation
same concentration and volume of both antibiotics
measure the area of inhibition
repeat for effective antibiotics
description of serial dilution of each antibiotic range of dilutions on each plate-one antibiotic per plate
statistical test to determine which is the most effective
repeat with different strains of resistant bacteria
