6B Microorganisms and Immunity Flashcards
immune system
biological processes that identify and kill pathogens
phagocytosis
engulfment and digestion of pathogens by w.b.c
bone marrow
site of B cell maturation
mast cells
immune system cells -> release histamine
T helper cells
release substances to activate …
- B cells
- T killer cells
- macrophages
Tuberculosis
- infectious disease of respiratory system
- caused by Mycobacterium TB
HIV
virus causing AIDS -> infects and destroys T helper cells (host cell)
AIDS
- disease of human immune system
- increases chance of other diseases (infections, cancer)
immunity
having sufficient B and T memory cells to avoid disease
booster injections
re-exposure to antigen
- increases no. B and T memory cells to maintain protective levels so more antibodies
herd immunity
when high enough proportion of pop is vaccinated that those without immunity are PROTECTED
bacteriCIDAL
antibiotics that destroy bacteria
bacterioSTATIC
antibiotics that prevent MULTIPLICATION OF BACTERIA
antigenic drift
changes in antigens due to mutations in pathogen
what is the name of the markers on microorganisms that allow cell-to-cell recognition?
antigens
self antigens
produced by own body
DON’T STIMULATE IMMUNE RESPONSE
what happens after pathogens are engulfed by phagocytosis?
check if right
- phagocytes transfer antigens of digested pathogen to cell surface membrane
- they become antigen presenting cells eg. MACROPHAGES
what do antigen presenting cells
(eg. macrophages) do?
activate specific immune response
-> occurs when lymphocytes bind to presented antigens
macrophage
type of phagocytic w.b.c
long lived
bacteria
- single-celled
- prokaryotic
pathogen
organism that causes disease
diseases caused by pathogens = infectious
describe how HIV affects immune system
what does it mean 2 RNA strands????
HIV replicates inside host T helper cell
- attachment protein attaches to CD4 receptor on cell membrane of T helper cell
- capsid released into cell -> uncoats and releases RNA into cell’s cytoplasm
- inside cell: REVERSE TRANSCRIPTASE used to make COMPLEMENTARY STRAND of DNA from viral RNA template
- from this, DOUBLE STRANDED DNA made and INSERTED into human DNA
- viral proteins assembled into new viruses -> bud from cell and go to infect other cells
inflammation
site where pathogen enters body
describe inflammation process
- immune system cells recognise foreign antigens on surface of pathogen and release HISTAMINE THAT TRIGGERS INFLAMMATION
- histamine causes VASODILATION (widening of ARTERIOLES) around site -> increases blood flow to it
- molecules also increase PERMEABILITY OF CAPILLARIES
- -> increased blood flow = brings loads of immune system cells to site-> increased permeability = allows cells to move OUT OF BLOOD->INFECTED TISSUE
- immune system cells start to destroy pathogen
what are the body’s barriers to prevent infection?
- STOMACH ACID -> acidic conditions (low pH) kill pathogens
BUT some may survive and pass into small intestine where they invade cells of gut wall (eg cholera) - GUT AND SKIN FLORA -> billions of harmless microorganisms -> compete with pathogens for nutrients and space -> harder for pathogens to infect body
- LYSOZYME -> mucosal surfaces (eyes, mouth, nose) produce secretions (tears, saliva, mucus) -> contain enzyme lysozyme -> kills bacteria by damaging cells walls -> makes bacteria burst open (lyse)
what are initial symptoms of AIDS?
- minor infections of mucous membranes (inside of nose, ears, genitals)
- recurring respiratory infections -> caused by lower than normal no. of T helper cells
symptoms of AIDS later on?
- as AIDS progresses = less and less T helper cells
- patients become prone to more serious infections eg. chronic diarrhoea and TB
passive immunity
acquired without an immune response
antibodies gained are from another source e NOT OWN BODY
artificial passive immunity
injection / transfusion of antibodies e.g. the tetanus antitoxin
artificial active immunity
vaccination
natural active immunity
exposure to a pathogen
natural passive immunity
antibodies received from another organism eg. from placenta or breastmilk
role of T helper cells in developing immunity after a vaccine
- T helper cells BIND to APC
- leads to production of ACTIVE T- helper cells
- T helper cells activate B cells to become PLASMA CELLS
specific immune response
secondary response
DELAYED response directed at SPECIFIC pathogen
non-specific immune response
primary response
IMMEDIATE response directed at ALL pathogens
suggest how antihistamines work
bind to histamine receptors and BLOCK histamine from binding
explain why someones wound may become hot, red and swollen
hot -> increase in metabolic rate and lots of cells RESPIRING
red -> increased blood flow
swollen -> leakage of fluid from CAPILLARIES
interferons
- anti viral proteins
- made by cells when infected with virus
- prevent virus spreading to uninfected cells
how do interferons prevent virus from spreading to uninfected cells?
- stop production of viral proteins
- ACTIVATE CELLS involved in SPECIFIC IMMUNE RESPONSE to kill infected cells
- activate mechanisms of non-specific immune response
eg. PROMOTE INFLAMMATION by bringing immune system cells to site of infection
2 main types of lymphocytes
- B cells
- T cells
neutrophils
type of phagocyte
short lived
lysosomes
membrane organelles
contain digestive enzymes called lysozymes -> digest unwanted material present in cells
pus is a sign of what?
dead neutrophils
B cells divide to produce two clones of cells …
- B effector cells
- B memory cells
B effector cells
differentiate into plasma cells* and release ANTIBODIES into blood and lymph in response to antigen
short lived, last a few days
*they specialise to become plasma cells -> plasma = B effector
B memory cells
remain in body for years
enable organism to respond quicker to same antigen in future
cell clonal selection
process of B cell division
antibodies
- secreted by plasma cells
- bind to specific antigens identifying them for easier destruction
- and agglutinating them so phagocytosis is quicker
granuloma
anaerobic masses of tissue containing dead bacteria and macrophages
T cells
immature T cells leave bone marrow to mature in thymus
mature T cells have specific cell surface receptors
(T cell receptors) -> similar structure to antibodies and are each SPECIFIC TO ONE ANTIGEN
T killer cells
bind to antigens and destroy their infected cells
T memory cells
remain in blood
-> enable faster specific immune response if same pathogen encountered again in future
what role to cytokines play in making sure there are enough
T killer cells?
is this answer right???
stimulate differentiation of T cells
(compare and contrast B and T cells)
check if this is right
- both are WBCs
- B cells mature in bone marrow and T cells mature in thymus
- B cells respond to foreign cells OUTSIDE BODY CELLS, bacteria, virus whereas T cells respond to foreign material INSIDE BODY CELLS
compare and contrast bacteria and viruses
- both have nucleic acids (DNA or RNA in viruses and only DNA in bacteria)
- bacteria are small prokaryotes whereas viruses are not cells
-> just particles - bacteria may have plasmids whereas viruses do not have them
- bacterial DNA is double stranded whereas viral (DNA / RNA) is single / double stranded
what are the 4 entry points for pathogens?
- broken skin -> access to tissues and bloodstream
- dig system -> contaminated food / drink
- respiratory system -> inhaling
- mucosal systems eg. inside of nose, mouth, genitals
histamine
chemical signalling molecule that enables cell signalling / communication between cells
stimulates:
- vasodilation
- leaky capillary walls
- phagocytosis
what does the non-specific immune response include?
happens first!!
- inflammation
- interferon production -> prevents virus spreading to uninfected cells
- phagocytosis -> WBCs engulf pathogens
- lysozyme action -> kills bacteria cells by damaging cell wall
describe the process of phagocytosis
- phagocyte recognises antigen on pathogen
- engulfs pathogen
- pathogen contained in phagocytic vacuole
- lysosome fuses with phagocytic vacuole …
- … and lysozymes break down pathogen
- phagocyte presents antigen to activate other immune system cells - now an APC
what does the specific immune response include?
- phagocytes activate T cells
- T helper cells activate B cells
what are cytokines?
chemicals that T helper cells release
to stimulate ÷ and differentiation of B cells
describe the process of activation of T helper cells
is this exactly what i need to know?
- bacterium engulfed by macrophage
- macrophage presents antigens -> becomes APC
- APC binds to T helper cell with complementary CD4 receptors
- T helper cell is activated and divides via mitosis to form …
-
-> T memory cells
-> active T helper cells
compare and contrast the humoral response and the cell mediated response
check if right
- humoral response produces antibodies whereas the cell mediated response produces T killer cells
- cell mediated works against intracellular pathogens while humoral works against extracellular pathogens
- both are specific to an antigen
- both require formation of APCs and presence of MHCs
explain why a person newly infected with TB may not show any symptoms
immune system ‘seals off’ infected phagocyte in structures (in lungs) called tubercles
-> bacteria become dormant in there so person shows no symptoms
describe how Mycobacterium tuberculosis causes TB
- infection occurs when tiny droplets (cough / sneeze) containing bacteria inhaled
- in lungs, bacteria taken up by phagocyte -> survives and replicates inside phagocyte
- immune system seals off infected phagocyte using tubercles => bacteria now dormant
- later, dormant bacteria may become reactivated and overcome immune system -> likely in ppl with weak immune system eg. AIDS patients
- length of time between infection and development of TB varies (weeks to years)
M. tuberculosis has waxy cell wall-> so not killed by immune system
explain the role of APCs
just ask about this whole card -> is it right??
- macrophage displays antigen from pathogen on surface (after hydrolysis in phagocytosis)
- enhances recognition in T helper cells which cannot directly interface with pathogens in body fluid
check
name the 2 types of specific immune response
- humoral
- cell mediated
how do antibodies help to clear an infection?
- agglutinating pathogens so phagocytosis enhanced
- neutralising toxins
- preventing pathogens binding to human cells
-> antibodies bind to antigens on pathogen, blocking receptors needed to bind to host cell
differences between structure of membrane-bound and secreted antibodies
membrane bound have extra section of protein on heavy chain that anchors them to B cell membrane
membrane bound antibody
attached to membrane of B cell
secreted antibody
free from attachment
why is non-specific / primary response slow?
aren’t many B cells that make antibody needed to bind to antigen
HIV evasion mechanisms
- high rate of mutation
- mutations change antigen structures -> forming new strains of virus (a.k.a antigenic variation)
- memory cells won’t recognise new strains
- disrupts antigen presentation in infected cells -> prevents immune system recognising + killing them
why are infections caused by antibiotic-resistant bacteria more common in hospitals?
- more antibiotics used there
- so bacteria in hospitals more likely to have evolved resistance against them
how do hospitals prevent and control HAIs caused by antibiotic-resistant bacteria?
- doctors shouldn’t prescribe antibiotics for minor bacterial / viral infections OR to prevent infections
- doctors should use narrow-spectrum antibiotics if possible eg. when strain of bacteria person is infected with is identified
- doctors should rotate use of diff antibiotics
- patients should take all antibiotics prescribed so infection fully cleared
describe what ribsosomes do in bacterial cells
produce proteins from mRNA
devise an experiment to determine the effect of diff antibiotics on bacteria
- use sterile forceps to place mast ring (5+ diff a.b) OR paper discs soaked in distilled H₂O(-ve control) onto 2 diff petri dishes (where agar seeded with E.coli bacteria, spread evenly)
- close dishes and seal BUT leave small gap so O₂ can enter = no buildup anaerobic bacteria
- leave cultures to incubate at 25℃ for 24hrs
- open petri dish + use ruler to measure clear zone for each paper disc/ mast ring section (for diff a.b) -> use ∏r²
NOTES:
- aseptic tech throughout
- controls:
-> same conc a.b used
-> type and vol bacteria (E.coli)
Mycobacterium tuberculosis evasion mechanisms
- produce substances that prevent lysosome fusing with phagocytic vacuole …
- so bacteria not broken down = multiply undetected inside phagocytes
- disrupts antigen presentation -> prevents immune system recognising + killing infected cells
introns
sections of gene that don’t code for a.a
exons
sections of gene that do code for a.a
explain how one gene can give rise to more than one protein through post-transcriptional changes to mRNA
(4 marks)
- during transcription, introns + exons copied into mRNA -> mRNA strands containing both introns + exons = pre-mRNA
- introns removed by “splicing” -> + exons joined, forming mRNA strands (takes place in nucleus -> is a post-transcriptional change)
- smt certain exons + introns removed = alt. splicing -> forms diff mRNA strands
- so more than 1 a.a seq = more than 1 protein produced from 1 gene
describe some codes of practice hospitals use to prevent and control HAIs
- staff + visitors wash hands before + after seeing patient
- equipment/surfaces disinfected + sterilised
- ppl with HAIs moved to isolation ward -> less liekly to transmit infection to other patients
HIV requires a host cell to replicate.
suggest why it needs a host cell
doesn’t have stuff eg. enzymes + ribosomes to replicate on its own
