| Literature DB >> 26116716 |
Jiyeun Kate Kim1, Dae Woo Son1, Chan-Hee Kim1, Jae Hyun Cho1, Roberta Marchetti2, Alba Silipo2, Luisa Sturiale3, Ha Young Park1, Ye Rang Huh1, Hiroshi Nakayama4, Takema Fukatsu5, Antonio Molinaro2, Bok Luel Lee6.
Abstract
The molecular characterization of symbionts is pivotal for understanding the cross-talk between symbionts and hosts. In addition to valuable knowledge obtained from symbiont genomic studies, the biochemical characterization of symbionts is important to fully understand symbiotic interactions. The bean bug (Riptortus pedestris) has been recognized as a useful experimental insect gut symbiosis model system because of its cultivatable Burkholderia symbionts. This system is greatly advantageous because it allows the acquisition of a large quantity of homogeneous symbionts from the host midgut. Using these naïve gut symbionts, it is possible to directly compare in vivo symbiotic cells with in vitro cultured cells using biochemical approaches. With the goal of understanding molecular changes that occur in Burkholderia cells as they adapt to the Riptortus gut environment, we first elucidated that symbiotic Burkholderia cells are highly susceptible to purified Riptortus antimicrobial peptides. In search of the mechanisms of the increased immunosusceptibility of symbionts, we found striking differences in cell envelope structures between cultured and symbiotic Burkholderia cells. The bacterial lipopolysaccharide O antigen was absent from symbiotic cells examined by gel electrophoretic and mass spectrometric analyses, and their membranes were more sensitive to detergent lysis. These changes in the cell envelope were responsible for the increased susceptibility of the Burkholderia symbionts to host innate immunity. Our results suggest that the symbiotic interactions between the Riptortus host and Burkholderia gut symbionts induce bacterial cell envelope changes to achieve successful gut symbiosis.Entities:
Keywords: Burkholderia; LPS; bean bug; gut symbionts; host defense; host-pathogen interaction; innate immunity; symbiosis
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Year: 2015 PMID: 26116716 PMCID: PMC4543662 DOI: 10.1074/jbc.M115.651158
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157