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Survival of an Aggregatibacter actinomycetemcomitans quorum sensing lux S mutant in the mouths of Rhesus monkeys: insights into ecological adaptation
Author(s) -
Velusamy Senthil K.,
Sampathkumar Vandana,
Godboley Dipti,
Fine Daniel H.
Publication year - 2017
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12184
Subject(s) - biofilm , aggregatibacter actinomycetemcomitans , microbiology and biotechnology , quorum sensing , biology , mutant , strain (injury) , in vivo , virulence , gene , downregulation and upregulation , bacteria , porphyromonas gingivalis , genetics , anatomy
Summary Experiments were designed to explore a prominent autoinducer‐2 ( AI ‐2) producing gene ( lux S) related to colonization and survival of Aggregatibacter actinomycetemcomitans , a low abundance member of the indigenous flora, that forms a key component of the dysbiotic flora in localized aggressive periodontitis. The lux S gene was disrupted in a primate strain of A. actinomycetemcomitans before implantation into the oral cavity of Rhesus monkeys (Rh). The colonization efficiency of the lux S mutant (RhAa‐ VS 4) was compared with the parental wild‐type strain (RhAa3) (positive control) and a ltx A mutant (RhAa‐ VS 2) (negative control). The in vivo results showed that the lux S mutation had minimal impact on A. actinomycetemcomitans colonization compared with the wild‐type RhAa3 strain. In vitro studies revealed that there was a significant upregulation of attachment‐related genes aae , api A, and flp in the RhAa‐ VS 4 strain compared with RhAa3. Biofilm forming ability was also significantly increased in the RhAa‐ VS 4 strain compared with RhAa3, whereas the AI ‐2 signal was ablated. The exogenous addition of the AI ‐2 precursor dihydroxy pentanedione allowed the RhAa‐ VS 4 strain to achieve RhAa3 biofilm levels. This is the first primate study to test the relevance of LuxS in vivo . In vitro assessment suggests that in vivo survival of the RhAa‐ VS 4 strain was due to the production of signaling AI‐2 molecules derived from other members of the flora as well as the upregulation of genes related to attachment and biofilm formation.