11681232
Description
| Question | Answer |
| sterile sites of human body | bloodstream, CSF, heart, liver, kidneys |
| Human Microbiome Project | goal was to acquire a “reference” microbiome of healthy adult humans samples from 250 people, analyzed by 16S rRNA sequencing --> community metagenomes obtained, genes and biological pathways can be guessed |
| conclusions of human microbiome project | 1) NO reference microbiome exists for healthy adult humans 2) One body site is more likely to be similar to an identical body site on another person than a different body site on same person 3) No virulent pathogens just waiting around, just opportunistic pathogens 4) At a given site there are different phylogenies for each individual BUT same metabolic pathways still represented |
| How might different microbial communities perform the same functions at a given site? | --> distinct groups of microbes can provide roughly the same set of metabolites as each other |
| How to compare two colonies from two different individuals | do metagenomics, then BLAST, then predict all the different functional genes for each community |
| What areas of the skin can microbes occupy? | can occupy sweat glands, sebaceous glands, hair follicles, epidermal surface --> NOT a uniform environment depending where on the body the skin is! |
| different skin environments | surface = cool, dry, salty, acidic (gram positive S. epidermis love this) axilla, scalp, ear, genital = more humid face, chest, back = more sebaceous glands |
| P. acnes | lives in sebaceous glands, digests triglycerides in sebum --> stimulates immune system --> produce inflammatory fatty free acids --> clog pores, create ACNE! lots of diversity at the strain level = metagenome sequencing shows diversity, not 16S |
| oral cavity microenvironments: below the gum line | anoxic, microbes digest proteins secreted by host & catabolize amino acids healthy state: streptococci, actinomyces, veillonella diseased state: P. gingivalis dominates! --> gum detachment + tooth loss |
| oral cavity microenvironments: above the gum line | bacteria must be able to withstand antibacterial factors in saliva (lysozymes) streptococci are most abundant, ferment carbohydrates to acids (lactate, formate, acetate) --> sugars abundant, pH drops --> enamel dissolution when carbohydrates are exhausted, pH rises and enamel dissolution stops |
| What happens with poor oral hygiene? | acid-loving S. mutans and lactobacilli dominate and produce more acids through fermentation --> destroy enamel, more grow with increase in acids is a positive feedback loop |
| Stages of enamel decay | 1) Healthy, only a few commensals 2) Healthy, more commensals pack in 3) Damaging, acid-tolerant fermenters enter and alter environment 4) Damaging, acid-tolerant fermenters completely outcompeting commensals and taking over biofilm |
| Microbiome of vaginally born babies vs Cesarean section | vaginally born babies have higher species diversity 3 days after birth babies of CS in prospective studies found to have greater instances of asthma and allergies --> early exposure to microbes can influence immune system? |
| microbiome pH going down the human gut | stomach pH = 2 small intestine pH = 4-5 large intestine pH = 7 |
| alpha diversity | the average human's diversity in the GI (about 1000 species) |
| beta diversity | ALL GI microbiota sampled to date (about 10,000) |
| in general, what AFFECTS the GI microbiome? | host genes; birth procedure (C section vs vaginal); early diet; early microbial exposure; antibiotic perturbation |
| in general, what is the EFFECT of the GI microbiome? | --> digestion --> nutrient processing --> immune system --> nervous system |
| How do we tolerate billions of commensals? | we NEED these microbes for the development of an immune system |
| Experimental evidence of gut microbiome's important role in the immune system | Germ free mice: accumulate a lot of iNKT T-cells in GI mucosa --> more susceptible to CHEMICALS that cause IBD + asthma IF production of iNKT cells blocked --> germ free mice get less sick! Non-sterile mice: imbalance of T-cells balanced by transfusion of microbes NEONATALLY (as babies), not not as adults |
| TH17 cells vs Treg cells in segmented filamentous bacteria (SFB) | TH17 helper cells ramp up infection, while Treg dampen inflammation If balanced: healthy microbiome If imbalanced: disease (IBD, asthma, eczema OR lack of protection from pathogens) |
| Gut microbiome link to obesity/metabolic disease: antibiotics and weight gain | feed constant low level antibiotics to healthy mice with no change in diet --> gain weight faster GI microbiome changes how the body stores/metabolizes food? |
| Gut microbiome link to metabolic disease: H. pylori and hormones | test humans with or without H. pylori in stomachs after eating --> those WITH had much lower hormone ghrelin (hormone which stimulates us to eat) --> alters our behavior *H. pylori can help us to stop eating* |
| CHO diet effect on microbiome (diet --> GI) | germ free mice fed (plant carbohydrates) CHO diet --> after twelve weeks were colonized with non-sterile mice fed same diet --> half stay on CHO diet, half fatty western diet --> 16S sequencing shows GI microbiomes between diets are diff! --> more species diversity for CHO + gain less body fat |
| Microbiome effect on fat accumulation (GI --> body) | donor mice NOT sterile, half raised on CHO diet and half on Western --> both donors GI microbes transplanted to GF mice raised on CHO diet --> no change in diet for recipients!! --> GF mice who got microbes from Western donor had a larger body fat increase than from CHO diet (donors genetically obese --> same result) |
| disbiosis | sweeping changes in population of microbes that produce an imbalance in your GI microbes |
| gnotobiotic mice | germ free mice, easier to study than humans |
| Bacteriodes fragillis and Clostridiae in Human Microbiome | SFBs that grow in GI, you need a balance of these to end up with a balance of TH17 and Tregs or else disbiosis will cause disease! |
| effect of human fecal transplant on GF mice | take obese human twins, and lean human twins --> inoculate fecal samples into GF mice --> feed mice same LF-HPP diet --> measure fat mass after 35 days *microbes from obese twins led to greater fat gain than from lean twins* |
| results of cohousing mice with "lean" microbiota and "obese" microbiota (fed on same diet) | Lean + obese = obese mice gain some fat mass but not much, lean don't change Obese + obese = obese mice gain the most fat mass Lean + Lean = no change GF + Lean + Obese = GF LOSE fat mass |
| results of cohousing mice with "lean" microbiota and "obese" microbiota (fed on different diets) | "lean" microbes protect mice with "obese" microbes IF diet is low in saturated fats + high in fruits and veggies (LoSF-HiFV) NOT protected if fed opposite: HiSF-LoFV --> change in microbiome must be accompanied by change in diet to be healthy! |
| signaling pathways that most affect metabolic outcomes | --> fermenting bacteria production of short-chain fatty acids --> small intestine microbes modification of bile salts |
| What happens when you disturb the GI ecosystem? | antibiotics --> reduction in species diversity "weed" species C. difficile can survive and become dominant --> painful antibiotic-resistant diarrhea (AWFUL) occurs NOT from exposure but from killing off its competition |
| treatments for recalcitrant C. difficile | Fecal microbial transplant: harvest stool from healthy patient --> transplant to patient through colonoscopy |
| probiotics effect on health | provided in food or capsules can help people but negative side effects occur from adding dominant species to gut in high numbers |
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