Pattern-Triggered Immunity (PTI) in plants confers broad resistance against diverse pathogens and can serve as promising tool for improving broad-spectrum, durable resistance in breeding programs. The purpose of this research is to understand the mechanism of PTI by using pathogen monitoring during PTI exposure. Through transcriptome analysis of the plant pathogen, Pseudomonas syringae pv. tomato DC3000 (DC3K) during early disease and exposure to PTI in the model plant, Arabidopsis thaliana, we found that PTI-exposed bacteria exhibit few transcriptional shifts compared to infecting bacteria. Additionally, PTI-exposed bacteria exhibited mis-regulation of key regulons including the AlgU regulon and HrpL regulons which modulate virulence, motility, and stress response. Genes involved in sulfur starvation-induced response (SSI) were also upregulated in bacteria exposed to PTI leading us to hypothesize whether sulfate sequestration is a potential unique mechanism of PTI. We identified the A. thaliana sulfate transporter, SULTR1;2, as the PTI responsive sulfate transporter. We tested and validated the sulfate binding protein gene, sbp, as a marker for sulfate starvation response in DC3K and determined that sbp is upregulated during PTI and sultr1;2 induction. However, apoplastic sulfate concentrations are unaltered during PTI and there is sufficient sulfate and cysteine for apoplastic growth of DC3K during PTI. As PTI is triggered by non-plant pathogens as well, we used human enteric pathogens such as Escherichia coli O157:H7 and Salmonella enterica as our output strains to investigate bacterial exposure to PTI through co-inoculations with DC3K with and without a functional type III secretion system to create a permissive and non-permissive environment for improved endophytic colonization. Using this co-inoculation assay in both model and crop host systems, we found that both host and strain factors contribute to opportunistic colonization by human enteric pathogens during plant disease. These strain factors include acquisition of plant-derived nutrients and response to general stressors that are modulated by the sigma factor, RpoS. Our research provides a better understanding of the molecular mechanism of PTI, which can provide plant breeders with the information needed to optimize the biotechnological potential of PTI by providing new targets for effective plant disease management.