_pathogens_  
Editorial  
Host Immune Responses and Pathogenesis to  
_Brucella_ spp. Infection  
[PERSON]  
Department of Biochemistry and Immunology, Institute of Biological Sciences,  
Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil; [EMAIL_ADDRESS]  
Brucellosis, caused by the facultative intracellular bacteria _Brucella_ species, is one the most prevalent zoonoses worldwide. _Brucella_ causes >500,000 human infections per year, and brucellosis is underreported in endemic areas [1]. Between livestock losses and human morbidity, brucellosis imposes significant economic impacts, perpetuating poverty in endemic regions [2]. There is a considerable amount of evidence that indicates the capacity of _Brucella_ sp. to avoid or interfere with components of the host immune responses, which plays a critical role in their virulence. It has been suggested that _Brucella_ has developed a stealth strategy through pathogen-associated molecular patterns reduction, modification, and hiding to ensure low stimulatory activity and toxicity for cells [3]. This strategy allows _Brucella_ to reach its replication niche before activating antimicrobial mechanisms by host immune responses. However, inside the host cells, _Brucella_ releases vital molecules for the bacteria that trigger the activation of host cytosolic receptors [4, 5]. In the paper by [PERSON] et al. [6], in vivo studies using \(Asc^{-/-}\) mice infected with _Brucella_ revealed an increased bacteria load and decreased immune cell recruitment. The findings of the study suggest that the protective role of ASC may result from the induction of pyprotosis through a gasdermin D-dependent mechanism in macrophages. However, further studies are required to elucidate this complex circuit by which the host immune system recognizes _Brucella_-derived molecules. This editorial summarizes the data described in the Special Issue entitled \"Host Immune Response and Pathogenesis to _Brucella_ spp. Infection\" consisting of seven research articles and two reviews. These contributions report several aspects of host-_Brucella_ interactions, and these findings will help to advance the comprehension of bacterial pathogenesis and contribute to the future development of drugs or vaccines to control brucellosis. For a successful infection process, a pathogen has to invade, survive, and replicate in host cells. During the first steps of _Brucella_ trafficking, the bacteria is able to block the progression of its cell cycle, remaining at the G1 stage for several hours, before it reaches its replication niche. The work of [PERSON] et al. [7] demonstrated that starvation mediated by guanosine tetra- or penta-phosphate, (p)ppGpp, is one of the factors contributing to G1 arrest observed in _B. abortus_ infection in macrophages. Adhesion to target cells is another major step forward for bacterial invasion and replication. [PERSON] et al. [8] reviewed the _Brucella_ adhesins and their role in mediating adhesion to cells. These molecules include the sialic acid-binding proteins SP29 and SP41 (binding to erythrocytes and epithelial cells, respectively), the BigA and BigB proteins that contain an Ig-like domain (binding to cell adhesion molecules in epithelial cells), the monomeric autotransporters BmaA, BmaB, and BmaC (binding to extracellular matrix components, epithelial cells, osteoblasts, synovocytes, and trophoblasts), the trimeric autotransporters BtaE and BtaF (binding to ECM components and epithelial cells), and BP26 (binding to ECM components). After binding, replication in phagocytic and non-phagocytic cells is required to establish infection. One of the main clinical signs of brucellosis is abortion in domestic animals. [PERSON] et al. [9] demonstrate that _Brucella abortus_ was able to infect and survive in both non-decidualized and decidualized human endometrial stromal cells (T-HESC cell line).