## 10 Concluding Remarks  
Exposure to plant phenolic compounds leads to changes in the composition of plant and animal host microbiomes which can decisively contribute to host fitness and health. However, our understanding of the molecular mechanisms underlying the direct effects of PPCs on microbes, as well as on host-microbe interactions, is still largely unexplored, in terms of compounds, microbes, and hosts examined. These insights are necessary to substantiate a causal nexus between exposure to PPCs and its effects on microbes and the host. Here, molecular research into the interaction between _Lactobacillus_ spp. and individual PPCs was reviewed (Table 5). A variety of mechanisms are induced by PPCs to increase the oxidative stress response in these microorganisms which highlights the antimicrobial nature of these compounds. These responses, together with the induction of general stress responses, revealed that these compounds are perceived, but not always, as stressors by these microorganisms. To cope with this selective pressure, _Lactobacillus_ relies, in addition to known metabolic pathways for PPC detoxification, on efflux pumps to extrude, at least, hydroxycinnamic acids and stilbenes out of the cell. Furthermore, exposure to different PPCs variably adjusts the capacity of lactobacillus for carbohydrate acquisition and metabolism. The adaptation of nitrogen metabolism in to different PPCs is conserved and oriented to control the import and production of ammonia/amino-containing compounds. These metabolic adaptations, together with the induction of oxidative and general stress responses, are important ecological fitness determinants that leave _Lactobacillus_ better able to cope with the stress encountered in the host environment. \begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Locus Tags** & **Species** & **PPC Effector (Ref.) a** & **Effect** & **Phenotype Involved (Ref.) b** \\ \hline \hline \multicolumn{4}{c}{**Immunomodulation**} \\ \hline _lp\_3581a_ & _lamD:_ auto-inducing peptide (AIP) precursor & _L. plantarum_ & OLE & – & Immunomodulatory capacity [107] \\ _lp\_3581_ & _lamC:_ two-component system, LytTR & & OLE & – & Immunomodulatory capacity [107] \\ _lp\_0422_ & _plnE:_ bacteriocin precursor peptide & & OLE & – & Immunomodulatory capacity [107] \\ _lp\_0421_ & _plnF:_ bacteriocin precursor peptide & & OLE & & Immunomodulatory capacity [107] \\ _lp\_0419_ & _plnI:_ bacteriocin immunity protein & & OLE & & Immunomodulatory capacity [107] \\ _lp\_0423_ & _plnG:_ bacteriocin ABC transporter, ATP-binding and permease protein & & OLE & – & Immunomodulatory capacity [107] \\ _lp\_0424_ & _plnH:_ bacteriocin ABC transporter, accessory factor & & OLE & – & Immunomodulatory capacity [107] \\ _lp\_0428_ & _plnV:_ membrane protein & & OLE & – & Immunomodulatory capacity [107] \\ _lp\_19A:_ PTS system,_N- & & & & & \\ _lp\_2647_ & acetylglucosamine/galactosamine- & & OLE & – & Immunomodulatory capacity [108] \\ \multicolumn{4}{c}{specific EIIA} & \multicolumn{1}{c}{component} & & & \\ _lp\_2650_ & _N-_acetylglucosamine-specific EIIB & & OLE & – & Immunomodulatory capacity [108] \\ \multicolumn{4}{c}{component} \\ _lp\_2460_ & \multicolumn{1}{c}{prophege P2b protein 21} & \multicolumn{1}{c}{OLE} & – & & \\ \hline \hline \end{tabular}  
* Reference describing the regulation of the molecular actor (gene or protein) by the plant phenolic compound. _p_-CA (_p_-coumaric acid), RSV (resveratrol), OLE (oleuropein), HXT (hydroxytrosol), TA (tamic acid);
* reference describing the phenotype associated with the molecular actor (gene or protein); +, upregulation; \(-\), downregulation.  
\end{table} 
Table 4: _Cont._  
\begin{table}
\begin{tabular}{c c c c} \hline \hline
**Phenolic Compound** & **Technique** & **Species** & **References** \\ \hline
**Hydroacycinnamic acids** & & & \\ \(p\)-cumaric acid & & & \\ \(\qquad\) & Transcriptomics & _L.