Enhanced Susceptibility to Brucella abortus Infection in Dextran Sodium Sulfate Treated Human Cervical Cancer HeLa Cells
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Treatment of dextran sodium sulfate(DSS) on HeLa cells results to an enhanced susceptibilityto Brucella(B.) abortus infection. An increase in the adherence, invasion and intracellularreplication of B. abortus was observed in DSS-treated cells. Furthermore, a marked elevation inthe intensity of F-actin fluorescence was also observed in DSS-treated cells compared withuntreated B. abortus-infected cells. An upregulation of phagocytic signaling proteins by Westernblot analysis demonstrated an apparent activation of ERK, p38α and JNK phosphorylationlevels in B. abortus-infected DSS-treated cells compared with the control. Colocalization withLAMP-1 proteins was attenuated in DSS-treated cells upon intracellular trafficking of thepathogen compared with control cells. The results of this study demonstrated consistency withother pathogens. The uptake and intracellular replication of B. abortus is hypothesized to bestimulated by various dextran receptors such as C-type lectins that are involved in phagocytosiswhich can either be direct phagocytic receptors, modulators of the expression of other receptorsor as opsonins leading to an enhanced internalization of B. abortus. The complexity of theseinteractions thus would warrant further investigation into the role of DSS in the pathogenesis ofbrucellosis. In summary, we conclude that DSS enhanced adhesion, phagocytosis and intracellularreplication of B. abortus in epithelial cells which could lead to suppression of the innateimmune system in chronic Brucella infection.
Abstract
Treatment of dextran sodium sulfate(DSS) on HeLa cells results to an enhanced susceptibilityto Brucella(B.) abortus infection. An increase in the adherence, invasion and intracellularreplication of B. abortus was observed in DSS-treated cells. Furthermore, a marked elevation inthe intensity of F-actin fluorescence was also observed in DSS-treated cells compared withuntreated B. abortus-infected cells. An upregulation of phagocytic signaling proteins by Westernblot analysis demonstrated an apparent activation of ERK, p38α and JNK phosphorylationlevels in B. abortus-infected DSS-treated cells compared with the control. Colocalization withLAMP-1 proteins was attenuated in DSS-treated cells upon intracellular trafficking of thepathogen compared with control cells. The results of this study demonstrated consistency withother pathogens. The uptake and intracellular replication of B. abortus is hypothesized to bestimulated by various dextran receptors such as C-type lectins that are involved in phagocytosiswhich can either be direct phagocytic receptors, modulators of the expression of other receptorsor as opsonins leading to an enhanced internalization of B. abortus. The complexity of theseinteractions thus would warrant further investigation into the role of DSS in the pathogenesis ofbrucellosis. In summary, we conclude that DSS enhanced adhesion, phagocytosis and intracellularreplication of B. abortus in epithelial cells which could lead to suppression of the innateimmune system in chronic Brucella infection.
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