Pathogens infecting mammalian cells have developed various strategies to suppress and evade their hosts’ defensive mechanisms. In this line, the intracellular bacteria that are able to survive and propagate within their host cells must have developed strategies to avert their host’s killing attitude. Studying the interface of host-pathogen confrontation can provide valuable information for defining therapeutic approaches. In THP-1 macrophage infected with either Brucella melitensis or Listeria monocytogenes we studied the expression levels of four host genes i.e. EMP2, ST8SIA4, HCP and FRMD5 known to be involved in pathogenesis of Mycobacterium tuberculosis. Brucella melitensis and Listeria monocytogenes take different approaches to survive and propagate within their host cells. Our data showed that at this molecular level, except for FRMD5 that showed similar expression changes in both cases, the other three genes were upregulated by Brucella melitensis while they were downregulated in cells infected with Listeria monocytogenes. Brucella melitensis and Mycobacterium tuberculosis go through similar intracellular processes and interestingly two of the investigated genes i.e. EMP2 and ST4SIA8 were upregulated in THP-1 cell infected with Brucella melitensis similar to that reported for THP-1 cells infected with Mycobacterium tuberculosis. At the host-pathogen interaction interface, this study depicts rather distinct molecular events for intracellular bacteria with different intracellular fate while indicating overlapping changes for different bacteria with common survival strategies; a fact that implies designing therapeutic approaches based on common targets may be possible.

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