_Brucella_ infection did not induce cytotoxicity and did not alter the decidualization status of cells, but elicited the secretion of IL-8 and MCP-1 in either decidualized or non-decidualized T-HESC. The proinflammatory responses induced by _Brucella_ infection in T-HESC may contribute to the gestational complications and abortion during brucellosis. Brucellae reside mostly within phagocytes and other cells, including trophoblasts, where they establish a preferred replicative niche inside the endoplasmic reticulum. [PERSON] et al. (2018) propose that _Brucella_ takes advantage of the environment provided by the cellular niches in which it resides to generate reservoirs and disseminate to other organs, such as spleen, lymph nodes, liver, bone marrow, epididymis, and placenta. They discuss in this review how the favored cellular niches for _Brucella_ infection in the host give rise to anatomical reservoirs that may lead to chronic infections or persistence in asymptomatic subjects, and which may be considered a threat for further contamination. The natural infection by _Brucella_ occurs mainly by oral and nasal routes through the consumption of raw milk and unpasteurized dairy products from infected animals, the inhalation of aerosols containing the pathogen, and/or contact with infected animals and their secretions. Considering that the oral route is the main route of natural infection in humans and animals, there is a need to understand the mechanisms of the establishment of oral infection so that new therapeutic strategies can be developed in order to control this disease. [PERSON] et al. (2018) report the role of ST2 receptor in a murine model of oral infection with _Brucella abortus_ and its influence on gut homeostasis and control of bacterial replication. Their results suggest that ST2\({}^{-/-}\) are more resistant to _B. abortus_ infection, as lower bacterial CFUs were detected in the livers and spleens of knockout mice when compared to wild-type Additionally, they observed an increase in intestinal permeability in WT infected mice compared to ST2\({}^{-/-}\) animals. Finally, their findings suggest that ST2 receptor is involved in the invasion process of _B. abortus_ by the mucosa in the oral infection model. Regarding pathology, the most frequent clinical characteristics of brucellosis besides abortion are hepatomegaly, splenomegaly, and peripheral lymphadenopathy, revealing the preference of _Brucella_ for the reticulendothelial system. The research article by [PERSON] et al. (2018) describes how _Brucella abortus_ infection induces the upregulation of class II transactivator protein (CIITA) with concomitant MHC-I and -II expression in immortalized human hepatic stellate cell line (LX-2) in a manner that is independent from the expression of the type 4 secretion system (T4 SS). Since hepatocytes constitute the most abundant epithelial cell in the liver, experiments were conducted to determine the contribution of these cells in antigen presentation in the context of _B. abortus_ infection. The results indicated that _B. abortus_-infected hepatocytes have an increased MHC-I expression, but MHC-II levels remain at basal levels. Overall, the authors revealed that _B. abortus_ infection of hepatic stellate cells and hepatocytes is able to differentially regulate the MHC expression, thus stimulating the T-cell specific-immune response in the liver. The central nervous system (CNS) invasion by bacteria of the genus _Brucella_ results in an inflammatory disorder termed neurobrucellosis. The precise mechanism whereby the bacterium leaves the bloodstream and gains access to the CNS remains unclear. Regardless of the mechanism, it is clear that once the bacterium reaches the CNS it induces a pathological pro-inflammatory response. The study of [PERSON] et al. (2018) investigated the role of _Brucella abortus_-stimulated platelets on human brain microvascular endothelial cell (HBMEC) activation. Platelets enhanced HBMEC activation in response to _B. abortus_ infection. Additionally, supernatants from _B.