4.4 Article

Alterations in Caenorhabditis elegans and Cronobacter sakazakii lipopolysaccharide during interaction

Journal

ARCHIVES OF MICROBIOLOGY
Volume 197, Issue 2, Pages 327-337

Publisher

SPRINGER
DOI: 10.1007/s00203-014-1064-1

Keywords

Caenorhabditis elegans; Cronobacter sakazakii; Innate immune system; Lipopolysaccharide; p38 MAPK pathway

Categories

Funding

  1. National Institutes of Health, National Center for Research Resources
  2. Department of Biotechnology (DBT)
  3. University Grand Commission (UGC)
  4. Indian Council of Medical Research (ICMR)
  5. Council of Scientific and Industrial Research (CSIR)
  6. Department of Science and Technology (DST), Government of India, New Delhi, India
  7. DBT
  8. CSIR, India
  9. Department of Biotechnology, Ministry of Science and Technology, Government of India [BT/BI/25/001/2006]

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Lipopolysaccharide is one of the pathogen-associated molecular patterns of Gram-negative bacteria which are essential for its pathogenicity. Cronobacter sakazakii is an opportunistic, emergent pathogen, which infects and cause mortality in Caenorhabditis elegans. In this study, modifications in host and C. sakazakii LPS during infections were evaluated. The physiological assays revealed that LPS alone is sufficient to affect the host pharyngeal pumping rate, brood size and cause lethality. FTIR spectra of LPS revealed that C. sakazakii modifies its LPS to escape from the recognition of host immune system. These results indicate that LPS plays a key role in C. sakazakii pathogenicity. qPCR studies revealed that LPS modulated the expression of selected host immune (clec-60, clec-87, lys-7, ilys-3, F08G5.6, atf-7, scl-2, cpr-2) and aging-related genes (skn-1, clk-2, bra-2, age-1, bec-1, daf-16, daf-2). Moreover, it was confirmed that p38 MAPK pathway has a major role in host immune response against LPS-mediated challenges.

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