Thomas R et al. (2013) J Med Microbiol "Stenotrophomonas maltophilia: pathogenesis model using Caenorhabditis elegans."

Neela V, Thomas R, Hamat RA

[J Med Microbiol, 2013]

Stenotrophomonas maltophilia plays an important role as an opportunistic pathogen in immunocompromised individuals. Despite its clinical implication, the true knowledge regarding the pathogenicity of these bacteria remains unclear. Various methods have been employed to prove this bacterium to be pathogenic. However, the debate whether S. maltophilia is a true pathogen or a colonizer still remains unanswered as effective killing was not seen in earlier experiments with different animal models of infection (Denton et al., 1998; Adamak et al., 2011; Pompilo et al., 2011). Study by Rouf et al. (2011) on murine lung infection model illustrated that different strains of mice exhibited different outcome for S. maltophilia infection. Strains such as A/J and DBA/2 were permissive for clinical isolates of S. maltophilia and showed higher levels of pro-inflammatory cytokines. In contrast, BALB/c and C57BL/6 strains were non-permissive for S. maltophilia. While Huang et al. (2009) showed nematotoxic activity by environmental S. maltophilia strain against free-living nematode, Panagrellus redivivus, and plant-parasitic nematode, Bursaphelenchus xylophilus.

Gibert L et al. (2014) FEMS Microbiol Lett "The major autolysin of Staphylococcus lugdunensis, AtlL, is involved in cell separation, stress-induced autolysis and contributes to bacterial pathogenesis."

Legris S, Gibert L, Lesouhaitier O, Marlinghaus L, Pons JL, Szabados F, Didi J, Pestel-Caron M

[FEMS Microbiol Lett, 2014]

Staphylococcus lugdunensis is a human skin commensal organism, but it is considered as a virulent Staphylococcus species. In a previous study, we described the first S.lugdunensis autolysin, AtlL. This enzyme displays two enzymatic domains and generates two peptidoglycan hydrolases, an N-acetylmuramoyl-l-alanine amidase and an N-acetylglucosaminidase. In this study, to further investigate the functions of this autolysin, a atlL mutant was constructed. The microscopic examination of the mutant showed cell aggregates and revealed a rough outer cell surface demonstrating, respectively, the roles of AtlL in cell separation and peptidoglycan turnover. This atlL mutant exhibited a lower susceptibility to Triton X-100-induced autolysis assays and appears to be more resistant to cell wall antibiotic-induced lysis and death compared with its parental strain. The atlL mutation affected the biofilm formation capacity of S.lugdunensis. Furthermore, the atlL mutant showed trends toward reduced virulence using the Caenorhabditis elegans model. Overall, AtlL appears as a major cell wall autolysin of S.lugdunensis implicated in cell separation, in stress-induced autolysis and in bacterial pathogenesis.