Induces the Premature Death of Human Neutrophils through the Action of Its Lipopolysaccharide


The absence of obvious clinical symptoms during the early stages of brucellosis is linked to the Brucella stealthy strategy and its non-canonical PAMPs, which are low PRRs agonists. Still, there are clinical profiles that require explanation. For instance ‒despite the fact that neutrophils readily ingest Brucella during the onset of infection, brucellosis courses without neutrophilia, and just a low number of infected neutrophils are present in target organs. In the chronic phases, a significant proportion of the patients display absolute neutropenia and bone marrow pancytopenia linked to the myeloid cell linage. Examination of the Brucella infected bone marrow reveals granulomas and phagocytosis of myeloid cells. Based on these observations we explored the fate of native neutrophils during their interaction with Brucella. We found that the bacterium induces the premature cell death of neutrophils without inducing proinflammatory phenotypic changes. This event was reproduced by the lipid A of the Brucella LPS and depends on NADPH-oxidase activation and low ROS formation. We believe that this phenomenon explains ‒at least in part‒ the hematological and histological profiles observed during brucellosis. In addition, it may be that dying Brucella-infected neutrophils serve as “Trojan horse” vehicles for infecting phagocytic cells without promoting activation.


Vyšlo v časopise: Induces the Premature Death of Human Neutrophils through the Action of Its Lipopolysaccharide. PLoS Pathog 11(5): e32767. doi:10.1371/journal.ppat.1004853
Kategorie: Research Article
prolekare.web.journal.doi_sk: 10.1371/journal.ppat.1004853

Souhrn

The absence of obvious clinical symptoms during the early stages of brucellosis is linked to the Brucella stealthy strategy and its non-canonical PAMPs, which are low PRRs agonists. Still, there are clinical profiles that require explanation. For instance ‒despite the fact that neutrophils readily ingest Brucella during the onset of infection, brucellosis courses without neutrophilia, and just a low number of infected neutrophils are present in target organs. In the chronic phases, a significant proportion of the patients display absolute neutropenia and bone marrow pancytopenia linked to the myeloid cell linage. Examination of the Brucella infected bone marrow reveals granulomas and phagocytosis of myeloid cells. Based on these observations we explored the fate of native neutrophils during their interaction with Brucella. We found that the bacterium induces the premature cell death of neutrophils without inducing proinflammatory phenotypic changes. This event was reproduced by the lipid A of the Brucella LPS and depends on NADPH-oxidase activation and low ROS formation. We believe that this phenomenon explains ‒at least in part‒ the hematological and histological profiles observed during brucellosis. In addition, it may be that dying Brucella-infected neutrophils serve as “Trojan horse” vehicles for infecting phagocytic cells without promoting activation.


Zdroje

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