Successful pathogens must efficiently defeat or delay host immune responses, including those triggered by release or exposure of microbe-associated molecular patterns (MAMPs). Knowledge on the molecular details leading to this phenomenon in plant-pathogen interactions is still scarce. We took advantage of the well-established Arabidopsis thaliana-Pseudomonas syringae pathovar tomato DC3000 (Pst DC3000) patho-system to explore the molecular prerequisites for the suppression of MAMP-triggered host defense by the bacterial invader. Using a transgenic Arabidopsis line expressing the calcium sensor apoaequorin, we discovered that Pst DC3000 colonization results in a complete inhibition of MAMP-induced cytosolic calcium influx, a key event of immediate-early host immune signaling. A range of further plant-associated bacterial species is also able to prevent, either partially or fully, the MAMP-triggered cytosolic calcium pattern. Genetic analysis revealed that this suppressive effect partially relies on the type III secretion system (T3SS), but cannot be attributed to individual members of the currently known arsenal of Pst DC3000 effector proteins. While the phytotoxin coronatine and bacterial flagellin individually are dispensable for the effective inhibition of MAMP-induced calcium signatures, they contribute to the attenuation of calcium influx in the absence of the bacterial T3SS. Our findings suggest that the capacity to interfere with early plant immune responses is a widespread ability among plant-associated bacteria that at least in Pst DC3000 requires the combinatorial effect of multiple virulence determinants. This may also include the desensitization of host pattern recognition receptors by the prolonged exposure to MAMPs during bacterial pathogenesis.