Algerian Journal of Health Sciences
Volume 1, Numéro 1, Pages 44-54
2019-01-02
Intracellular Survival Of Mycobacteria Within Macrophages: Role Of Ca2+- Dependent Signal In Mycobacterium Aviumpathogenesis?
Authors : Staali Leila .
Abstract
Background: Pathogenic Mycobacterium aviumare able to survive intracellularly withinhost cells defenses after phagocytosis, whereas nonpathogenic strainssuch as M. smegmatisare efficiently killed. In the present study, we attempted to explore the molecular mechanisms by which M. avium escape the intracellular killing. We also tried to investigate the effect of changes in cytosolic Ca2+levels on M. avium survival, the phagosome-lysosome fusion and the NFκB activation. Methods: To explore the invasion mechanism by which the pathogenic bacteria survive inside phagocytic cells as confirmed by killing assays, live and dead M. avium were testedby fluorescence microscopy techniques. The hypothesis that calcium levelscould playa keyrole in regulating the immune responseduring mycobacterial infections, was verified by using Ca2+ inhibitors. Results: We have shown that following phagocytosis, virulent M. aviuminvade successfully and replicate within host cells. The intracellular survival of this bacterium was not affected by the nitric oxide production. Our results suggest that M. avium escape the intraphagosomal killingby blocking the phagosome-lysosome fusion. Furthermore, the NFκB activation was strongly inhibited by M. avium by a mechanism which might be in a part, regulated by the intracellular Ca2+-signaling. Conclusion: These findingsargue that the virulentM. avium strain might escape the intracellular killing within host phagocytes by a mechanism that inhibits the phagosome-lysosome fusion. This process seems to be a Ca2+-signaling dependent. Moreover, the NFκB is efficiently blocked in bacteria-infected macrophages. This should be regulated by a Ca2+-dependent pathway. Interestingly, we conclude that mechanisms involved in M. avium resistance, during mycobacterial infections, could be linked and/or regulated by the intracellular Ca2+pathways.
Keywords
Mycobacteria, M. avium, Macrophages, Phagocytosis, Fluorescence microscopy
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