Bacterial Virulence Factors: Secreted for Survival

Abstract

Virulence is described as an ability of an organism to infect the host and cause a disease. Virulence factors are the molecules that assist the bacterium colonize the host at the cellular level. These factors are either secretory, membrane associated or cytosolic in nature. The cytosolic factors facilitate the bacterium to undergo quick adaptive-metabolic, physiological and morphological shifts. The membrane associated virulence factors aid the bacterium in adhesion and evasion of the host cell. The secretory factors are important components of bacterial armoury which help the bacterium wade through the innate and adaptive immune response mounted within the host. In extracellular pathogens, the secretory virulence factors act synergistically to kill the host cells. In this review, we revisit the role of some of the secreted virulence factors of two human pathogens: Mycobacterium tuberculosis-an intracellular pathogen and Bacillus anthracis-an extracellular pathogen. The advances in research on the role of secretory factors of these pathogens during infection are discussed.

Keywords: Anthrax; Bacillus; Mycobacterium; Phosphatases; Tuberculosis; Virulence.

Fig. 1

Secretory phosphatase- SapM and SerB2 of Mycobacterium tuberculosis. a SapM is secreted by Mtb and enters host cells by an unknown mechanism. SapM dephosphorylates PI3P causing reduction of PI3P concentration on the phagosomal membrane. This in turn inhibits the recruitment of EEA1 protein, preventing phagosomal maturation. Additionally, SapM has been shown to block Rab7 through its CT domain, resulting in the inhibition of phagosomal maturation into a phagolysosome. b SerB2 dephosphorylates MAPK-p38 and NFκB p65 to suppress IL-8 synthesis in macrophages. SerB2 also dephosphorylates cofilin leading to its activation causing cytoskeleton remodelling

Fig. 1

Secretory phosphatase- SapM and SerB2 of Mycobacterium tuberculosis. a SapM is secreted by Mtb and enters host cells by an unknown mechanism. SapM dephosphorylates PI3P causing reduction of PI3P concentration on the phagosomal membrane. This in turn inhibits the recruitment of EEA1 protein, preventing phagosomal maturation. Additionally, SapM has been shown to block Rab7 through its CT domain, resulting in the inhibition of phagosomal maturation into a phagolysosome. b SerB2 dephosphorylates MAPK-p38 and NFκB p65 to suppress IL-8 synthesis in macrophages. SerB2 also dephosphorylates cofilin leading to its activation causing cytoskeleton remodelling

Fig. 2

Schematic diagram explaining the physiological imbalances observed in the host cells by anthrax major secreted virulence factors, which are lethal toxin (LT), edema toxin (ET), and anthrolysin O (AL)