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SUMMARY:Dissecting the immunopathogenesis of Mycobacterium abscessus infec
 tion in zebrafish embryos
DTSTART:20171212T121500
DTSTAMP:20260513T185017Z
UID:fe54041ad956a1c2bb009a2968329b0a46da5c2a728611c159d869fa
CATEGORIES:Conferences - Seminars
DESCRIPTION:Laurent Kremer\, Institut de Recherche en Infectiologie de Mon
 tpellier (IRIM)\, Université de Montpellier\, France\nMycobacterium absce
 ssus is a rapidly growing\, nontuberculous\, multidrug resistant mycobacte
 rium\, which can cause severe lung infections. This mycobacterium\, like o
 ther mycobacteria\, has a lipid-rich hydrophobic cell wall containing uniq
 ue lipids\, of which glycopeptidolipids (GPL) have emerged in recent years
  as major immunomodulators. M. abscessus presents smooth (S) and rough (R)
  morphotypes and the difference is determined by the presence or absence\,
  respectively\, of GPL. Epidemiological studies suggested that the R varia
 nt is involved in more severe clinical forms\, with a hyper-proinflammator
 y response. However\, the underlying physiopathological mechanisms remain 
 largely unknown. A zebrafish embryo model was developed to investigate the
  pathogenesis of M. abscessus infection. In contrast to the S variant\, th
 e R variant induces a more robust and lethal infection in embryos\, charac
 terized by the formation of extracellular cords and abscesses\, often foun
 d in the Central Nervous System. The high propensity of M. abscessus R to 
 form cords in vivo prevents the bacilli from being phagocytosed by macroph
 ages and neutrophils and promotes the induction of a strong inflammatory r
 esponse that leads to rapid tissue damage and to larval death. We conducte
 d a comparative stepwise dissection of the inflammatory response in S and 
 R pathogenesis. Our results highlight the importance of both macrophages a
 nd neutrophils in controlling cord formation and production/maintenance of
  protective granulomas. Moreover\, this experimental model emphasizes the 
 requirement of a functional CFTR protein in innate immunity and resistance
  to M. abscessus infection\, which is particularly relevant to infections 
 in cystic fibrosis patients who are vulnerable to M. abscessus infections.
 \n \nReferences: \nA. Bernut\, M. Nguyen-Chi\, I. Halloum\, J.L. Herrmann
 \, G. Lutfalla\, and L. Kremer. 2016. Mycobacterium abscessus-induced gran
 uloma formation is strictly dependent on TNF signaling and neutrophil traf
 ficking. PLOS Pathog. 12: e1005986.\n \nI. Halloum\, S. Carrère-Kremer\,
  M. Blaise\, A. Viljoen\, A. Bernut\, V. Le Moigne\, C. Vilchèze\, Y. Gu
 érardel\, G. Lutfalla\, J.L. Herrmann\, W.R. Jacobs\, Jr.\, and L. Kremer
 . 2016. Deletion of a dehydratase important for intracellular growth and c
 ording renders rough Mycobacterium abscessus avirulent. Proc. Natl. Acad. 
 Sci USA. 113: E4228-4237.\n \nA. Bernut\, J.L. Herrmann\, K. Kissa\, J.F 
 Dubremetz\, J.L. Gaillard\, G. Lutfalla\, and L. Kremer. 2014. Mycobacteri
 um abscessus cording prevents phagocytosis and promotes abscess formation.
  Proc. Natl. Acad. Sci USA. 111: E943-952.
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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