Elodie Ghedin: the lung microbiota in SHIV-infected macaques. (Alison Morris is clinical side of this work, Elodie is bioinformatics)
An animal model of HIV-associated lung diseases; work in ppreparation for studies of human HIV lung microbiota. Lung disease is more common in HIV people with COPD (chronic obstructive pulmonary disease) on antiretroviral therapy than on people not getting drug therapy. Independent of smoking, HIV reduces pulmonary function, increases Pneumocyctis infection which increases obstruction. Collected bronchial lavage samples monthly (15 months), also blood, CD4 counts, clinical measurements of function.
Results very different for different monkeys! (even though one cohort in a closed facility) Follow CD4 T-cell counts do decline at weeks 4-5, fairly consistently, and then rebound. If look at airway obstruction, see decline in lung function at weeks 9-25 in about half the monkeys. She says the data is 'entropic' - a slightly evasive way of saying that it's noisy.
Pneumocystis: in 10 of the 12 monkeys in this experiment, but have another set that didn't get Pneumocystis. No significant difference in microbial communities of monkeys with and without Pneumosystis, but big difference to monkeys not infected with SHIV. (Same in a different set of monkeys.)
I had thought that the lungs of healthy people were close to sterile, but my expert seatmate twells me this is now known to be wrong. She says that lots of bacteria live in healthy lungs.
Charlie Xiang: Diversity of bacterial vaginosis. (Oh dear, strong accent - luckily he's reading the text on his slides, but needing to look at the slides makes it hard to write. And so far he's just giving a boilerplate talk, telling this specialized audience what he would tell a non-expert audience.) He heads China's 973 program:
Part 1: This project: 50 women with bacterial vaginosis and 50 healthy controls. 16S rRNA-PCR-DGGE (not very informative, why bother?), 454 sequencing, qPCR. Two ecological diversity indices, one says vaginosis microbiota is more diverse, other says it's less diverse. But looking at the taxa, vaginosis communities look much more diverse. (He's showing the figures from a paper (Ling et al. 2010 BMC Genomics 11:488-503), not optimized for presentation in a talk.)
Part 2: Women with bacterial vaginosis, 22 with cervicitis, 18 with both, plus healthy controls. Total numbers of bacteria similar, but identities different. But no cervicitis-specific pattern.
Questions: Might vaginosis be simply due to a deficiency of Lactobacillus, rather than to increased numbers of other species? Or to some decrease in innate defenses of the host?
Alan Walker: Human colon vs diet. 'Non-digestible carbohydrates' (non-digestible by humans) are major sources of nutrients for colon bacteria (!10^11/gm of colon contents). e.g. plant cell-wall polysaccharides. Different bacteria do different steps. Butyrate is a major energy source for many gut species.
High bacterial growth rate in proximal colon (on CHO), in distal colon bacteria switch to protein fermentation (byproducts more toxic for human cells, may be major cause of colon cancer). We know little about effects of ~normal diet on colon bacteria (not probiotics or weird supplements). People are not very honest about reporting what they eat. So they locked overweight/obese people up and controlled everything they could eat for 10 weeks! Collected fecal samples. Hard to get people to eat a lot of bran - 'resistant starch' is easier.
Microbiota? DGGE, 16S sequencing, qPCR: Samples clustered by individual, not by diet. Saw only a few changes that correlated with diet (only significant for resistant starch). Ruminococcus up in most people with resistant starch; in other people different bacteria went up during diets high in resistant starch. Now he's analyzing whether the bacteria are in the liquid fraction or the feces or attached to the fibers, but I missed hearing why this is interesting.
Bottom line: different people's bacteria respond differently, and responses by different bacteria have different consequences. Gee, just like ecology, every ecosystem is different!
Question: Enterotypes? He's not convinced this classification is useful.
George Weinstock reporting on work with Martin Antonio: Microbial ecology of the infant nasopharynx: impact of the PCV-7 vaccination in Gambia (West Africa). MRC has labs and field study sites in Gambia - very good for field studies. (George is stepping in because Martin had visa problems - George hasn't seen these slides!)
Child pneumonia - 70% of deaths in Africa and Asia. 40% are pneumocccal (S. pneumoniae) - this is the meningitis belt. Lots of serotypes, some virulent (rarely carriage). New vaccines include the major African serotypes. Are the vaccines changing the abundances of different serotypes? Will serotype switching happen?
Aims: what is normal nasopharynx microbiome in first year of life, and does the vaccine change this?
3 groups, ~100 total. 1=Control = non-vaccinated infants from non-vaccinated villages. 2= vaccinated infants in non-vaccinated villages; 3= vaccinated infants in vaccinated villages. 17 samples from each infant in first year of life. Sequence 16S rRNA with 454.
Haemophilus (my organism) is abundant in all of them pre-vaccination (10-40%), but declines after 27 weeks and isn't changed significantly by the pneumoccal vaccination. In response to a question, he said that all the infants received the Haemophilus vaccine (Hib?).
See significant effect of vaccination on some species. Diversity measures - nothing exciting.
Why I'm Marching for Science
16 hours ago in Angry by Choice