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Immunology > Microbial cross talk with the immune system > Flashcards

Microbial cross talk with the immune system Flashcards

1
Q

how does the microbiota develop

A
  • you are born sterile and colonized by microbes from the moment you are born
  • vaginal microbes and skin microbes (C-section)
  • community develops with facultative microbes, then transitions to anaerobes
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2
Q

characteristics of the microbiota in the adult colon

A
  • dense colonization
  • varies in composition between people but same function
  • varies between body sites
  • anaerobic
  • dominated by Firmicutes and Bacteroidetes
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3
Q

what are beneficial functions of the microbiota

A
  • digestion complex carbs to produce SCFA’s in anaerobic fermentation
  • produce diverse metabolites that influence locally and systemically
  • provide colonization resistance
  • processes host compounds, mucus and bile acids
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4
Q

what is homeostatic immunity

A

when a response occurs without inducing overt inflammation

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5
Q

relative abundance of different types of bacteria during microbiota development

A
  • initial surge in proteobacteria expansion
  • after 1 week, actinobacteria expansion increases
  • firmicutes and bacteroidetes have a more constant growth pattern
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6
Q

what is the window of opportunity in the microbiota

A
  • a privileged period of development where the influences of the microbiota on the immune system are durable
  • restoring microbial interactions after the window does not rescue the impact on the immune system
  • adult-like stability in the gut microbiota takes place by 2-3 years of age
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7
Q

key factors which affect development of the microbiota

A
  • route of delivery
  • antibiotics
  • environmental exposure to different microbes and antigens
  • feeding (breast milk or formula)
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8
Q

early development of the microbiota - mouse example

A
  • a mothers microbiota influences their offsprings immune system before birth
  • SCFA’s reach the fetus
  • experiments using transient colonization of germ-free mice show alterations of innate lymphoid cell populations in pups (all germ-free but have different immune populations)
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9
Q

development of the microbiota - LPS and Type I diabetes example

A
  • showed difference inHMO utilizing bacteria of microbiome composition between people living in Finland, Russia and Estonia
  • regions with more bacteroides (Finland) have higher susceptibility to T1D
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10
Q

what happens when there is failure to induce endotoxin tolerance

A

increased autoimmune activity

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11
Q

what are the interactions between the gut microbiota and the immune system that help to promote health as we mature

A
  • antibodies and B cells
  • T cell differentiation
  • innate immune signalling
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12
Q

interactions between the microbiota and B cells

A
  • microbiota members coated by IgA and some by IgG
  • lost in germ-free mice
  • follow T-dependent and independent pathways
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13
Q

what is IgA-Seq

A

how we study which bacteria are coated by IgA under different conditions

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14
Q

interactions between the microbiota and T cells

A
  • SFB in the microbiota controls differentiation of T-cells
  • germ free mice have low TH17 cells
  • mono-colonizing mice rescues TH17
  • can protect mice from pathogen
  • close attachment delivers Ag that drive TH17
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15
Q

how do interactions between the microbiota and bile acids effect T cell function here

A
  • the microbiota converts bile acid to secondary bile acids (DCA, LCA)
  • these are then further modified and they o on to alter T cell differetntiation
  • colonize mice with mix of bacteria that produce isoDCA - more Tregs
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16
Q

interactions between the microbiota and the innate immune system

A
  • NOD1 and NOD2 detect peptidoglycan (activate NFkB) from microbiota
  • PG ends up In serum
  • altered immune system development on NOD1/2 knockouts
  • mutation of NOD2 is the strongest risk factor for Crohn’s disease
17
Q

what happens to the microbiota during disease

A

changes in microbiota cause dysbiosis in interactions with T cells, B cells and the innate immune system

18
Q

cancer and the immune system

A
  • cancerous cells are supposed to get eliminated by our immune system
  • T-cells recognize cancer Neo-antigens
  • NK cells kill by altered expression of cell surface markers
  • in cancer immunotherapy, we try to harness and accelerate this function - focused on T cells
19
Q

How do T-cells kill cancer infected cells

A
  • TCR recognizes antigen by MHC
  • need co-stimulation (2 signals)
  • after T cell activation inhibitory receptors (CTLA4 and PD1) are indeed as a checkpoint
  • these checkpoints prevent hyperactivation - lack of T cell response allows proliferation of cancerous cells
20
Q

true or false: Dysbiosis during disease or antibiotic use is associated with lack of PD-1 blockade response?

A

true

21
Q

what is a fecal microbiota transplant

A
  • transfer fees from a healthy donor because they contain an incompletely defined community of microorganisms
  • goal is rapid re-establishment of community
  • 90% effective
  • concert with FMT include transferring harmful bacteria
22
Q

classes of microbiome-bases therapeutics and what they treat

A
  • FMT: used to treat recurrent C. difficile infections
  • diets and prebiotics: supplementation of dietary fibres to promote desired compositional change in the microbiota
  • symbiotic microbial consortia: transfer a group of isolates to promote function
  • engineered symbiotic bacteria: transfer engineered bacteria at the target site that have a desired function
  • microbiota-derived proteins and metabolites: direct supplementation with proteins of metabolites (SCFA)
23
Q

cancer immunotherapy associated with the microbiota

A
  • microbiota influences response to caner treatments
  • antibiotic use can reduce immunotherapy response
  • specific microbes in the microbiota (Akk muciniphila) are associated with better treatment outcomes
  • effictiveness of CLTA4 and PD1 inhibition linked to microbiota
24
Q

most potent T cell immune checkpoints - how they are relevant in cancer

A
  • CTLA4 and PD1 inhibitory receptors
  • put the breaks on T cell hyper activation
  • in cancer T cell exhaustion is high - lack of this immune response allows proliferation of cancer cells
  • anti-CD28, anti-CTLA4 and control antibiotics cause tumour size to shrink (b/c more immune cells present)
25
Q

PD-1 based immunotherapy against tumours

A
  • influenced by gut microbiome - disrupting it with antibiotics = less response
  • survival and response to cancer immunotherapy
26
Q

what are some beneficial functions of the Microbiome in Immune Development and Regulation

A
  • IgA production
  • Treg induction
  • pathogen competition
  • barrier protection
  • immune system maturation through innate immunity
27
Q

what are some consequences of Dysbiosis (Microbial Imbalance)

A
  • increased inflammation
  • autoimmune diseases
  • allergic disorders
  • infection
  • metabolic disorders
  • specific diseases = cancer, Crohn’s, extra-intestinal conditions
28
Q

how can the Mother’s Microbiota Shape the Offspring’s Microbiome

A
  • During pregnancy: Maternal microbiota transfers microbial metabolites SCFAs
  • During birth: Vaginal birth exposes the infant to the mother’s vaginal and gut microbiota, C-sections may limit microbial diversity and lead to a microbiome dominated by skin-associated bacteria.
  • Breastfeeding: Breast milk contains carbs and beneficial bacteria

Immunology (22 decks)

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