Essential oils (EOs) are natural products composed of a mixture of volatile and aromatic compounds extracted from different parts of plants that have shown antimicrobial activities against pathogens. In this study, EOs extracted from Pimenta dioica (Myrtaceae) and Rosmarinus officinalis (Lamiaceae) were assessed for their antimicrobial activities using a panel of pathogenic Gram-positive, Gram-negative, and fungal strains. The antimicrobial activity was measured by the minimal inhibitory concentration required for the growth inhibition of the microorganisms. The cytotoxicity of the EOs was tested ex vivo using the model of human-derived macrophage THP-1 cells. In addition, an inflammatory response was evaluated using the anti-inflammatory cytokine IL-10 and the proinflammatory cytokines IL-6 and TNF-α. Results showed that both EOs had antimicrobial activity and different pathogens were exposed to concentrations ranging between 600 and 2000 μg/mL. In addition, the EOs showed no inflammatory activity when exposed to human macrophages, but a potent anti-inflammatory activity was measured when the oil from Rosmarinus officinalis was exposed to macrophages. This study demonstrates that the use of EOs is an effective alternative for pathogenic bacterial and fungal control, alone or in combination with antibiotic therapy. Moreover, the oil extracted from Rosmarinus officinalis could be used as potent anti-inflammatory agent.

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Background: Mycobacterium avium subspecies paratuberculosis (MAP), a member of the mycobacteriaceae family, causes Johne’s disease in ruminants, which resembles Crohn’s disease (CD) in humans. MAP was proposed to be one of the causes of human CD, but the evidence remains elusive. Macrophages were reported to be the only cell where MAP proliferates in ruminants and humans and is likely the major producer of TNFα-associated inflammation. However, whether human dendritic cells (DCs), another major antigen-presenting cell (APC), have the ability to harbor MAP and disseminate infection, remains unknown. Methods: Human monocyte-derived dendritic cells (moDCs) were infected with MAP and phagocytosis and intracellular survival were quantified by immunofluorescence (IF) and colony counts, respectively. MoDC cytokine expression was measured via ELISA and their activation state was measured via flow cytometry. Results: We showed that MAP can infect and replicate in human moDCs as means to evade the immune system for successful infection, through inhibition of the phago-lysosome fusion via the secretion of protein tyrosine phosphatase PtpA. This mechanism initially led to a state of tolerance in moDCs and then subsequently caused a pro-inflammatory response as infection persisted, characterized by the upregulation of IL-6 and TNFα, and downregulation of IL-10. Moreover, we showed that moDCs have the ability to phagocytose up to 18% of MAP, when exposed at a multiplicity of infection of 1:1. Conclusion: Infection and subsequent proliferation of MAP within moDCs could provide a unique means for the dissemination of MAP to lymphoid tissue, while altering immune responses to facilitate the persistence of infection of host tissues in CD.