The obligate intracellular bacterial pathogen Chlamydia trachomatis injects numerous effector proteins into the epithelial cell cytoplasm to manipulate host functions important for bacterial survival.
These effectors then manipulate host cellular function to enhance the invasiveness and survival of Salmonella.
Within the cell, T3S effectors manipulate host cell function in a bacterial specific manner to facilitate bacterial growth and survival.
This Workshop gathered leading scientists from around the world to discuss their latest findings related to the mechanisms that intracellular pathogens use to subvert and manipulate host cell functions.
These 'molecular syringes' inject effectors directly into the host cell, whereupon they manipulate host cell functions [13], [14], [15], [16].
Central to plant – oomycete pathosystems is a complex signaling process in which multiple effector proteins are delivered either into the host cell or to the free diffusional space outside the plasma membrane (the host apoplast) to manipulate host cell structure and function [6].
Candidate effector molecules are believed to manipulate host cell structure and function, thereby facilitating infection and suppression of the host immune responses [ 13, 14].
Plant pathogenic fungi secrete small proteinaceous and non-proteinaceous molecules in their hosts to manipulate host cell structure and function, thereby facilitating infection (virulence factors and toxins) or triggering host plant defense responses (avirulence factors and elicitors) or both [ 8– 10].
For example, plant pathogenic Pseudomonas syringae deliver bacterial virulence factor proteins into the host cell, where they function to manipulate host defense and metabolism to benefit the extracellular bacterial colony [45], [46].
Bacterial virulence effectors use various strategies to manipulate host cell responses, often by mimicking structures or functions of eukaryotic signaling machinery.
