Quorum sensing is how bacteria communicate in response to cell density through the uptake and release of small signaling molecules called autoinducers. Through this form of signaling, bacteria dictate biofilm formation, motility, and pathogenesis, among many other cellular responses. Gram-negative bacteria employ N-acyl homoserine lactone molecules as their signaling molecule of choice, which then initiate a signaling cascade to turn on specific promoters. Previous research looking at bacterial behavior in the bistable regime has been largely from a deterministic point of view. Our two-cell model instead takes a stochastic approach, incorporating random noise into the system. Three models were observed: one with only one positive feedback loop, one with two feedback loops and no dimerization of the transcription factor, and one all-encompassing model with both feedback loops and dimerization. Two parameter values were varied in computer-run time trials: signal movement between the two cells and autoinducer turnover, or how quickly molecules were being replaced in the extracellular environment. As signal movement increased, the cells were more likely to enter the on state, and to enter it together. As autoinducer turnover increased, the cells were less likely to enter the on state and also less likely to turn on together. These results point to the potential to suppress QS by decreasing signal movement and increasing the affinity of the autoinducer to return to its parent cell, which could hold importance for research in the field of pathogenesis and microbial food spoilage. Future research will focus on acquiring accurate parameter rates, examining the role of negative feedback loops, and suppressing QS through inhibition of dimerization and blocking the second amplifying feedback loop from being initiated.