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  • In this study Rb increased the


    In this study, Rb1 increased the phosphorylation of p38 MAPK and Akt and macrophage phagocytosis of bacteria in mouse lung cells, consistent with the in vitro results. A recent study showed that Rb1 diminished the severity of lung injury in rats exposed to LPS. Rb1 inhibited the LPS-induced increase in inflammatory mediators, including tumor necrosis factor-α, monocyte chemoattractant protein-1, and interleukin-8 [37]. In addition, Rb1 ameliorated pathologic changes in the liver and lung, decreased mortality, and stabilized arterial oxygenation and blood pressure in a polymicrobial septic shock model [16]. Therefore, Rb1 may be a good adjuvant for the treatment of bacterial infection and the resolution of acute inflammatory conditions, such as sepsis and acute lung injury.
    Conflicts of interest
    Acknowledgments This study was supported by a grant (HCRI15015-22) from the Chonnam National University Hwasun Hospital Institute for Biomedical Science and Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2015R1D1A3A01016932).
    Introduction The defensive strategies by which a host eliminates Treponema pallidum (T. pallidum), the etiologic agent of syphilis, are poorly understood. The host develops and resolves lesions, which are a direct manifestation of the inflammatory processes triggered by T. pallidum within compromised tissues [1]. Macrophages, a family of dynamic cells, are on the first line of defense against invading T. pallidum in compromised tissues, where they act as effectors of the immune response [1,2]. Macrophages internalize and kill T. pallidum [3] and coordinate their responses to clear spirochete from the infected tissues [4] and increase cytokine (such as tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β)) secretion in primary syphilis [5]. Macrophages exert various biological functions and undergo highly reversible and transient polarization processes in a broad spectrum of inflammatory conditions. For the sake of simplicity and efficiency, a model system has been established to identify macrophages on a continuum, with pro-inflammatory M1 macrophages representing one extreme and anti-inflammatory M2 macrophages representing the opposite extreme. M1 and M2 macrophages can serve distinct functions in regulating the ap4 [[6], [7], [8]]. Recent evidence has suggested that protein kinase B, also known as the Akt signaling pathway, plays crucial roles in macrophage activation and gene expression [9]. Additionally, Akt activation can initiate the downstream mammalian target of rapamycin (mTOR) pathway and regulate the macrophage polarization process [10]. Moreover, mTOR can activate IκB kinase and its downstream nuclear factor κB (NF-κB) to promote inflammatory factor secretion [11]. Evidence suggests that this activation occurs in a variety of inflammatory diseases, such as rheumatoid arthritis [12], atherosclerosis [13], and cancer [14]. However, the function of the Akt, mTOR and ap4 NF-κB signaling pathway in macrophages during the syphilis infection process is poorly understood. In this context, identifying macrophage polarization and the underlying molecular mechanisms involved in this process may offer novel potential treatment options for controlling the inflammatory response in syphilis patients.
    Materials and methods
    Discussion Conceptually, syphilis is a spirochete-driven type of inflammation [16]. The cells in primary seropositive syphilis have the greatest ability to produce cytokines. Immunohistochemistry and molecular studies in humans have confirmed that primary lesions are enriched with natural killer cells, plasma cells, and macrophages capable of expressing mRNA for the cytokines IFN-γ, IL-2 and IL-12 [4,17]. Cytokines stimulate macrophages to destroy bacteria, suggesting that activated macrophages are responsible for the clearance of treponemes from infected tissue. The mode of macrophage activation determines the success or failure of the host response to T. pallidum aggression [3]. The role of macrophages is also emphasized by the concept of macrophage polarization, and macrophage polarization in early syphilis has not been thoroughly investigated. In this study, when macrophages were stimulated with T. pallidum in vitro, the expression of the M1 surface marker iNOS was up-regulated with incubation time, and the expression of the M2 surface marker CD206 was low and unchanged during the 12 h incubation. Moreover, the expression levels of the M1-associated cytokines IL-1β and TNF-α were increased, but the expression of the M2-associated cytokine IL-10 was reduced at both the mRNA and protein levels. The results revealed that T. pallidum induced M0 macrophage polarization to M1 macrophages in vitro during the early phase. The relative capacities of M1 and M2 macrophages to serve as reservoirs or to spread spirochete need to thoroughly study in the future.