The human gut microbiome is shaped by complex interspecies interactions, many of which involve metabolic competition and nutrient availability. In dysbiotic conditions, the gut microflora is significantly destabilized, and such interspecies interactions may likely lead to the prevalence of dominant microflora. Previous studies have shown that Enterococcus faecalis (Ef) and Streptococcus infantarius (Si) are enriched in the gut of patients with dysbiosis. Preliminary in vivo evidence from infant mouse colonization experiments demonstrated that Ef levels dropped significantly when co-colonized with a Δshp mutant compared to wild-type Si, suggesting that SHP contributes to enterococcal fitness in the mammalian gut. This study investigates the role of the streptococcal short hydrophobic peptide (SHP) signaling system in mediating interactions between Ef and Si. Using cell-free culture supernatants, we observed that Δshp supernatant inhibited Ef growth in a dose-dependent manner, whereas wild-type (WT) supernatant had no effect. Extraction experiments revealed that the organic fractions did not replicate the growth defect, whereas concentrating the aqueous layer resulted in broad inhibition across all samples, consistent with toxicity from concentrated media components. These results help rule out the hypothesis that Δshp produces a toxic compound and instead suggest that nutrient depletion is the underlying mechanism. To determine whether the growth defect was due to nutrient limitation, Enterococcus growth was observed in the presence of cell-free supernatant in 2X concentrated media. Nutrient restoration fully rescued Ef growth even in the presence of Δshp supernatant, suggesting that the inhibitory effect arose from nutrient depletion rather than secreted toxins. Additional tests with gut-associated Escherichia coli showed no growth impairment, suggesting a species-specific metabolic dependency between Ef and the compound(s) depleted by Δshp. These findings potentially suggest Enterococcus may utilize SHP-mediated signaling for survival in the gut during dysbiosis. More broadly, the results underscore the role of quorum-sensing pathways in shaping gut microbial ecology and provide insight into how signaling disruptions can reprogram metabolic interactions to favor dysbiosis.