6. inflammation and microbio summary session

Question 1

what cells are involved in granuloma formation

Answer 1

• macrophages
• epitheloid cells –> giant cells (langhans cells)
• T helper cells
• fibroblasts

Question 2

what cytokines are involved in granuloma formation and where do they come from

Answer 2

• TNFalpha from macrophages
• INFgamma from T helper cells

Question 3

outline the steps of granuloma formation

Answer 3

1. macrophages try to clean pathogen but cant and become infected and actiavted
2. activated macrophages secrete TNF alpha and other which promote the influx of T helper cells
3. T helper 1 cells secrete IFNy which further activates macrophages
4. stimulated macrophages can mature into epitheloid cells
5. if stimulatio continues epitheloid cells can fuse together and form multinucleated giants cells (langhans cells)
6. T cells and macrophages stimulate fibroblasts leading to fibrosis

Question 4

how do M cells work to sample pathogens and stimulate immune response

Answer 4

• antigen binds to adhesin molecules on M cell
• Ag is transported to basolateral pocket via transcytosis
• dendritic cells capture Ag and process
• dendritic cells present Ag to lymphocytes in situ or local lymph nodes

Question 5

discuss immune tolerance

Answer 5

Question 6

What are Type three secretion systems and what roles do they play in Salmonella infection?

Answer 6

• TTSS are protein transporters in salmonella (and other bacteria) that transport protein effectors from the bacteria into the host
• the effectors alter host cell functions such as remodelling and cytokine response
• salmonella has two TTSS
• TTSS1 promotes invastion of host cells into a salmonella containing vacuole
• TTSS2 is triggered in the vacuole and stops maturation of the vacuoles and so protects intracellular salmonella

Question 7

Describe with examples some key features that differentiate different E. coli pathotypes.

Answer 7

Three key features help define the E. coli pathotypes.

Presence and absence of Adhesion factors such as fimbriae [1]
Prescence or absence of the LEE locus [1]
Pathotype specific toxins.

For example, ETEC (Enterotoxigenic E. coli) [1] use fimbrial adhesions, do not have a LEE but have enterotoxins [1] two types LT and ST [1] that trigger hyper secretion [1]

EHECS (Enterohaemorrhagic E. coli) [1] are part of the STECS have Shiga toxin [1] and intimin [1] .

Question 8

what are CpG sites

Answer 8

the regions in the DNA sequence which comprises cytosine followed by guanine from the 5’ to 7’ direction
CpG sites are low frequency in eukaryotes but if present in eukaryotes they are METHYLATED
in bacteria high frequency CpG sites but they are NOT METHYLATED

Question 9

what are the differences between specialised and general transduction

Answer 9

transduction = Where bacteriophage capsids I is miss packed with bacterial DNA so can transfer bacterial geens ot a new host.
Generalised
- Lytic bacteriophage (phage)
- Random packing low frequency of bacterial DNA that is fragmented during viral replication and packing.

Specialised
- Lysogenic bacteriophage (phage)
The viral nucleic acid inserts in bacterial chromosome.
- It will be maintained in bacteria until activated.
- When activated replication packs of genome so risks packing adjacent bacterial DNA this is higher frequency than generalised.

Question 10

what is MLST

Answer 10

MLST typing is used to compare bacteria form same species for understanding epidemiology of spread / outbreaks.

MLST Multi locus sequence typing
seven genes compared
Clusters the bacteria
Can split into groups or show that same ones involved

WG-MLST (Whole Genome Multi locus sequence typing)
Same principle as MSLT but rather than sequence 7 genes individually sequence whole genomes and compares for relationship.