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Summary Cases & Lectures minor BMS: Infection and immunity $10.94   Ajouter au panier

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Summary Cases & Lectures minor BMS: Infection and immunity

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Document detailing all cases and lectures of the minor Infection and immunity.

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  • 9 septembre 2023
  • 283
  • 2022/2023
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Cases: Infection and immunity
Case 1: Commensal microbes
Keywords:
- commensals, opportunists, strict pathogens
- role of microbiome in opportunistic infections (antibiotic-associated colitis, bacterial
vaginosis, urinary tract infection/pyelonephritis)
- skin microbiome, Staphylococcus epidermidis, Staphylococcus aureus
- respiratory tract microbiome
- eye & ear microbiome
- gastrointestinal tract microbiome (including role of pH, diet, functions of gut microbiota, and
bile acids)
- genitourinary tract microbiome
- intestinal microbial colonization (including impact of birth mode, infant diet, lifestyle)
- intestinal microbial aid in host metabolism (SCFA synthesis, carbohydrates and protein
fermentation, methanogenesis)
- colonization resistance
- intestinal microbiota and disease (metabolic syndrome, cardiovascular disease, cancer)
- prebiotics, probiotics, fecal microbiota transplantation

33.1 Humans are holobionts
 Microbiome= refers to all the genes found in one’s microbiota; all the microorganisms that
live in and on an organism
 humans cannot live a normal life without their microbial partners → we are holobionts
 Holobionts= host and microbes relying on each other and importantly, evolving together.
 Adult carries about same number of microbial cells as human somatic cells
 Commensal= organisms that are normally found on those parts of the body exposed
to the external environment, e.g. the bacteria in the gut and on the skin (normal
microbiota)
 Opportunist pathogens= an organism that can cause an infection in individuals with
abnormal host defences: commensals can be opportunistic pathogens → only infect
the host when immune system is decreased
 Pathogen= organisms that cause infections in an individual with normal host defences

33.2 The microbiome develops from birth to adulthood
Development of a stable microbiome
 The community of microbiota we host is not static → begins developing at birth, changes as
we age
 During infancy, our microbiota are most sensitive to the environment
 This early time in our lives appears to be a “win down of opportunity” for the development
of the kinds of microbes that will be beneficial for the maturation of our immune systems
 At 3 years we have adopted a more stable community of microbes

, A diverse community is linked to better health. Some factors have a clear negative influence
(antibiotics) or positive impact (breast milk), but it is the complex interaction of many factors
that determines microbial diversity.

 Newborns are colonized by microorganisms from immediate environment
➢ Babies born vaginally acquire most of their microorganisms from their mother’s birth
canal
➢ Babies born by caesarean delivery acquire microorganisms from the skin of their
initial caretakers (nurse, doctors, midwives, parents etc.)
➢ Newborn colonization is very important → swabbing the mouths of new-borns with
maternal vaginal secretions after caesarean delivery are underway
 Early in life, human milk act as a selective medium for non-pathogenic bacteria
➢ Maternal milk contains < 100 different human milk oligosaccharides (HMO)
(unique for humans)
➢ Cannot be digested by our own digestive enzymes
➢ Bifidobacterial specialized to ferment: HMOs into acetate and lactate →
abundance bifidobacterial goes up
➢ Acetate and lactate are an energy source for the baby and lower intestinal pH
➢ Lower pH prevents colonization by (opportunistic) pathogens
➢ Maternal milk also contains bacteria (incl. bifidobacterial) that can seed the
infant gut
➢ Formula-fed infants have more diverse collection of gut microbiota, including
opportunistic pathogens.
➢ Switching to cow’s milk or solid food (mostly polysaccharide) → result in loss of
bifidobacterial
- proteobacteria, firmicutes, and bacteroidetes—specifically enterobacteria,
enterococci, lactobacilli, clostridia, and Bacteroides spp.—increase and
outcompete bifidobacteria.

, With dysbiosis= lower amount of Bifidobacterium, these bacteria produce acetates
and lactates which prevents pathogens to colonized
 With dysbiosis → link to immune development. Immune system needs to learn what
good and bad bacteria are.

❖ Gut microbiota- immune maturation
 Immune development starts before birth and it continues after birth
 Most important phases is the first 6 months

,  Left side: before birth (prenatal)
• Have some developing mesenteric lymph nodes
• Some Peyer’s patches → are immune complexes, they are connected to
the outside by M cells
• M cells
• Cryptopatch → will develop into lymphoid follicle. Get stimulated by
lymphoid tissue inducing cells.

 Right side: after birth (postnatal)
• Lot of B & T cells going into lymphoid follicle → they can send out IgA
producing plasma cells
• Mature lymphoid follicle → can release IgA producing plasma cells
• IgA can be released into the lumen and binds to bacteria. IgA can neutralize
pathogens
• Peyer’s patch are only in small intestine
• Mesenteric lymph node are deeper into the tissue → can communicate with
dendritic cells


 While adult microbiota is relatively stable over time, it is highly variable from person to
person and at different sites within the same person. each human has a relatively unique
microbiota

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