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SUMMARY:Faculty Recruitment Public Seminars – GHI Position in Host-micro
 be Interactions
DTSTART:20220602T100000
DTEND:20220603T153000
DTSTAMP:20260510T022903Z
UID:228740ebd4d96e1db5501320642435c506824603faee4d7a3076deae
CATEGORIES:Conferences - Seminars
DESCRIPTION:As per programme\nAll seminars in SV 1717 except Amelia Barber
  Friday\, June 3\, 2022\, 10.15 - 11.15 ---> AI 1153\n\nThursday\, June 2\
 , 2022\, 10.00 - 11.00\, SV 1717\nDr. Camille Goemans\nEMBL\, Heidelberg\n
 The impact of antibiotics on the human gut microbiota\n\nAntibiotics are u
 sed to fight pathogens but also target commensal bacteria\, disturbing the
  composition of gut microbiota and causing dysbiosis and disease. Despite 
 this well-known collateral damage\, the activity spectrum of different ant
 ibiotic classes on gut bacteria remains poorly characterized. We tested th
 e impact of 144 antibiotics on 38 representative human gut microbiome spec
 ies and found out that antibiotics with broad inhibition spectrum but sele
 ctive microbial killing may be the most dangerous for the gut microbiota. 
 In addition\, we screened and identified drugs that specifically antagoniz
 ed the antibiotic activity against abundant Bacteroides species but not 
 against relevant pathogens. These findings highlight the activity spectra 
 of antibiotics in commensal bacteria and suggest strategies to circumvent 
 their adverse effects on the gut microbiota.\n\n***\nThursday\, June 2\, 2
 022\, 13.30 - 14.30\, SV 1717\nDr.Ilana Gabanyi\nInstitut Pasteur\, Paris\
 nThe cross-talk between gut-bacteria and neurons\n\nThe bacteria present i
 n the intestine\, both commensal and potentially pathogenic ones\, are abl
 e to influence neuronal activity. This cross-talk controls immune response
 s and host metabolism. In my talk\, I will first show how the activation o
 f enteric-associated neurons induced by potentially pathogenic bacteria tr
 iggers a tissue-protective response in gut macrophages enabling them to pr
 otect the neurons in case of an enteric infection. Next\, I will present h
 ow brain neurons sense microbiota-derived muropeptides\, components of the
  peptidoglycan present in every bacterial cell wall. This new microbe-sens
 ing mechanism regulates host metabolism and reveals that bacterial peptido
 glycan plays a major role in mediating gut–brain communication via the n
 euronal Nod2 receptor. Activation of Nod2 in hypothalamic inhibitory neuro
 ns is essential for proper appetite and body temperature control\, primari
 ly in female mice. Understanding the action of neuroactive bacterial compo
 unds helps further elucidate bacterial-host interactions and may open new 
 avenues for the development of targeted treatments for enteric and metabol
 ic diseases.\n\n***\nThursday\, June 2\, 2022\, 15.30 - 16.30\, SV 1717\nD
 r. Xin Li\nCornell University\, New York\nHost-mycobiota interactions: sen
 sing intestinal fungi regulates both local and systemic immunity\n\nThe fu
 ngal microbiota (mycobiota) is an integral part of the complex\, multi-kin
 gdom microbial community which colonizes the mammalian gastrointestinal tr
 act and plays an important role in immune regulation. Fungal dysbiosis has
  been linked to several immune-mediated diseases. In his seminar\, he wil
 l share his recent work on the exploration of host-fungal immunological in
 teractions in the gut using integrated approaches. His recent findings un
 veil the fungal strain-dependent nature of host-fungal interactions in the
  human gut. Dr. Li will also describe his work on how gut fungal dysbiosis
  activates the gut fungi-lung allergy immune axis. Dr. Li's future researc
 h focuses on how microbiota/mycobiota influence immunological interactions
  during homeostasis and inflammatory conditions\, with the ultimate goal o
 f identifying novel therapeutic targets of inflammatory origin.  \n\n***
 **************************************************\n\nFriday\, June 3\, 20
 22\, 08.15 - 09.15\, SV 1717\nDr. Ziad Al Nabhani\nUniversity of Bern\nEar
 ly life imprinting of the immune system by gut microbiota\n\nThe way we gr
 ow up and learn to interact with others affects us lifelong. Similarly\, u
 pon birth\, the immune system learns from\, and interacts with\, multiple 
 microorganisms that colonize the intestine referred as "microbiota". Emerg
 ing evidence from human and mice studies suggest that perturbation of micr
 obial-immune crosstalk early in infancy have a long-lasting consequence on
  the host immunity and on the susceptibility to develop chronic inflammato
 ry diseases such as allergy\, inflammatory bowel diseases\, cancer\, metab
 olic and neurodegenerative disorders. We recently revealed that a strong i
 mmune response is induced by the gut microbiota following milk secession a
 nd introduction of solid food at weaning. This response termed the "weanin
 g reaction"\, is induced only at this weaning time window and is required 
 to prevent the development and the exacerbation of chronic inflammatory di
 seases later in life. Antibiotic exposure and/or excessive fats intake dur
 ing this critical window dysregulate the weaning reaction and increase the
  subsequent susceptibility to develop pathology\, an immune memory phenome
 non called the "pathological imprinting".\n\n***\nFriday\, June 3\, 2022\,
  10.15 - 11.15\, ---> AI 1153\nDr. Amelia Barber\nLeibniz Institute for Na
 tural Product Research and Infection\nBiology-Hans Knöll Institute\, Jena
  Institution\nDrug resistance and the genomics of virulence in human funga
 l pathogens\n\nFungal infections represent a significant and increasing th
 reat to human health and are responsible for more deaths each year than tu
 berculosis or malaria. Treatment of these infections remains a significant
  challenge due to their eukaryotic nature and high similarity to human cel
 ls\, a problem that is further compounded by the widespread emergence of a
 ntifungal resistance. Despite this obvious importance\, much about fungal 
 pathogens remains unstudied. In one of the most problematic fungal pathoge
 ns\, A. fumigatus\, a comprehensive survey of genomic diversity and how i
 t contributes to virulence and antifungal drug resistance has been lacking
 . Through the large-scale genomic analysis of environmental and clinical i
 solates\, we identified a previously undescribed level of genetic variatio
 n in A. fumigatus. We also observed an enrichment for clinical isolates i
 n a genetic cluster whose genomes were larger and carried a distinct genom
 ic profile. Finally\, we leveraged the power of genome-wide association to
  identify genomic variation associated with clinical isolates and triazole
  resistance\, as well as characterize genetic variation in known virulence
  factors. Additional work has focused on identifying environmental drivers
  of antifungal resistance using a combination of field work\, laboratory e
 xperiments\, and bioinformatics. The work presented here provides a founda
 tion to greatly expand our understanding of an important human fungal path
 ogen.
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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