RESUMEN
Beneficial microbes that target molecules and pathways, such as oxidative stress, which can negatively affect both host and microbiota, may hold promise as an inflammatory bowel disease therapy. Prior work showed that a five-strain fermented milk product (FMP) improved colitis in T-bet(-/-) Rag2(-/-) mice. By varying the number of strains used in the FMP, we found that Lactococcus lactis I-1631 was sufficient to ameliorate colitis. Using comparative genomic analyses, we identified genes unique to L. lactis I-1631 involved in oxygen respiration. Respiration of oxygen results in reactive oxygen species (ROS) generation. Also, ROS are produced at high levels during intestinal inflammation and cause tissue damage. L. lactis I-1631 possesses genes encoding enzymes that detoxify ROS, such as superoxide dismutase (SodA). Thus, we hypothesized that lactococcal SodA played a role in attenuating colitis. Inactivation of the sodA gene abolished L. lactis I-1631's beneficial effect in the T-bet(-/-) Rag2(-/-) model. Similar effects were obtained in two additional colonic inflammation models, Il10(-/-) mice and dextran sulfate sodium-treated mice. Efforts to understand how a lipophobic superoxide anion (O2 (-)) can be detoxified by cytoplasmic lactoccocal SodA led to the finding that host antimicrobial-mediated lysis is a prerequisite for SodA release and SodA's extracytoplasmic O2 (-) scavenging. L. lactis I-1631 may represent a promising vehicle to deliver antioxidant, colitis-attenuating SodA to the inflamed intestinal mucosa, and host antimicrobials may play a critical role in mediating SodA's bioaccessibility.
Asunto(s)
Colitis/metabolismo , Lactococcus lactis/metabolismo , Muramidasa/metabolismo , Superóxido Dismutasa/metabolismo , Animales , Colitis/enzimología , Colitis/microbiología , Mucosa Intestinal/enzimología , Mucosa Intestinal/metabolismo , Mucosa Intestinal/microbiología , Ratones , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Crustose coralline red algae (CCA) are important components of marine ecosystems thriving from tropical waters and up to the poles. They fulfill important ecological services including framework building and induction of larval settlement. Like other marine organisms, CCAs have not been spared by the increase in marine disease outbreaks. The white-band syndrome has been recently observed in corallines from the Mediterranean Sea indicating that the disease threat has extended from tropical to temperate waters. Here, we examined the microbiome and the pathobiome of healthy and diseased Neogoniolithon brassica-florida coralline algae in the Mediterranean Sea by combining culture-dependent and -independent approaches. The coralline white-band syndrome was associated with a distinct pathobiome compared to healthy tissues and showed similarities with the white-band syndrome described in the Caribbean Sea. A sequence related to the genus Hoeflea, order Rhizobiales, characterized the white-band disease pathobiome described by amplicon sequencing. No representative of this genus was isolated by culture. We, however, successfully isolated an abundant member of the healthy CCA microbiome, an Alphaproteobateria of the family Rhodobacteraceae. In conclusion, we did not identify a potential causative agent of the disease, but through the complementarity of culture dependent and independent approaches we characterized the healthy microbiome of the coralline and the possible opportunistic bacteria colonizing diseased tissues.
RESUMEN
Coral reef ecosystems worldwide are immediately threatened by the impacts of climate change. Here we report on the condition of coral reefs over 83â¯km of coastline at the island of Upolu, Samoa in the remote South West Pacific in 2016 during the Tara Pacific Expedition. Despite the distance to large urban centers, coral cover was extremely low (<1%) at approximately half of the sites and below 10% at 78% of sites. Two reef fish species, Acanthurus triostegus and Zanclus cornutus, were 10% smaller at Upolu than at neighboring islands. Importantly, coral cover was higher within marine protected areas, indicating that local management action remains a useful tool to support the resilience of local reef ecosystems to anthropogenic impacts. This study may be interpreted as cautionary sign for reef ecosystem health in remote locations on this planet, reinforcing the need to immediately reduce anthropogenic impacts on a global scale.
Asunto(s)
Antozoos/crecimiento & desarrollo , Conservación de los Recursos Naturales/métodos , Arrecifes de Coral , Monitoreo del Ambiente/métodos , Animales , Cambio Climático , Ecosistema , Peces/crecimiento & desarrollo , Estado Independiente de SamoaRESUMEN
Crustose coralline algae (CCA) are major benthic calcifiers that play crucial roles in coral reef ecosystems. Two diseases affecting CCA have recently been investigated: coralline white band syndrome (CWBS) and coralline white patch disease (CWPD). These diseases can trigger major losses in CCA cover on tropical coral reefs, but their causative agents remain unknown. Here, we provide data from the first investigation of the bacterial communities associated with healthy and diseased CCA tissues. We show that Neogoniolithon mamillare diseased tissues had distinct microbial communities compared to healthy tissues and demonstrate that CWBS and CWPD were associated with different pathobiomes, indicating that they had different disease causations. CWBS tissues were composed of opportunistic bacteria, and the origin of the disease was undetermined. In contrast, a vibrio related to Vibrio tubiashii characterized the CWPD pathobiome, suggesting that it could be a putative disease agent and supporting the case of a temperature dependent disease associated with global warming.
RESUMEN
Resident gut microbes co-exist with transient bacteria to form the gut microbiota. Despite increasing evidence suggesting a role for transient microbes on gut microbiota function, the interplay between resident and transient members of this microbial community is poorly defined. We aimed to determine the extent to which a host's autochthonous gut microbiota influences niche permissivity to transient bacteria using a fermented milk product (FMP) as a vehicle for five food-borne bacterial strains. Using conventional and gnotobiotic rats and gut microbiome analyses (16S rRNA genes pyrosequencing and reverse transcription qPCR), we demonstrated that the clearance kinetics of one FMP bacterium, Lactococcus lactis CNCM I-1631, were dependent on the structure of the resident gut microbiota. Susceptibility of the resident gut microbiota to modulation by FMP intervention correlated with increased persistence of L. lactis. We also observed gut microbiome configurations that were associated with altered stability upon exposure to transient bacteria. Our study supports the concept that allochthonous bacteria have transient and subject-specific effects on the gut microbiome that can be leveraged to re-engineer the gut microbiome and improve dysbiosis-related diseases.
Asunto(s)
Bacterias/metabolismo , Productos Lácteos Cultivados/microbiología , Disbiosis/terapia , Microbioma Gastrointestinal , Lactococcus lactis/fisiología , Animales , Bacterias/genética , Disbiosis/microbiología , Ecología , Heces/microbiología , Vida Libre de Gérmenes , Masculino , Ratas , Análisis de Secuencia de ADNRESUMEN
Crustose coralline algae (CCA) are major benthic calcifiers that play crucial roles in marine ecosystems, particularly coral reefs. Over the past two decades, epizootics have been reported for several CCA species on coral reefs worldwide. However, their causes remain often unknown in part because few studies have investigated CCA pathologies at a microscopic scale. We studied the cellular changes associated with two syndromes: Coralline White Band Syndrome (CWBS) and Coralline White Patch Disease (CWPD) from samples collected in Curaçao, southern Caribbean. Healthy-looking tissue of diseased CCA did not differ from healthy tissue of healthy CCA. In diseased tissues of both pathologies, the three characteristic cell layers of CCA revealed cells completely depleted of protoplasmic content, but presenting an intact cell wall. In addition, CWBS showed a transition area between healthy and diseased tissues consisting of cells partially deprived of protoplasmic material, most likely corresponding to the white band characterizing the disease at the macroscopic level. This transition area was absent in CWPD. Regrowth at the lesion boundary were sometimes observed in both syndromes. Tissues of both healthy and diseased CCA were colonised by diverse boring organisms. Fungal infections associated with the diseased cells were not seen. However, other bioeroders were more abundant in diseased vs healthy CCA and in diseased vs healthy-looking tissues of diseased CCA. Although their role in the pathogenesis is unclear, this suggests that disease increases CCA susceptibility to bioerosion. Further investigations using an integrated approach are needed to carry out the complete diagnosis of these diseases.