Abstract
In Brucellosis, the role of hepatic stellate cells (HSCs) in the induction of liver fibrosis has been elucidated recently. Here, we study how the infection modulates the antigen-presenting capacity of LX-2 cells. Brucella abortus infection induces the upregulation of class II transactivator protein (CIITA) with concomitant MHC-I and -II expression in LX-2 cells in a manner that is independent from the expression of the type 4 secretion system (T4SS). In concordance, B. abortus infection increases the phagocytic ability of LX-2 cells and induces MHC-II-restricted antigen processing and presentation. In view of the ability of B. abortus-infected LX-2 cells to produce monocyte-attracting factors, we tested the capacity of culture supernatants from B. abortus-infected monocytes on MHC-I and –II expression in LX-2 cells. Culture supernatants from B. abortus-infected monocytes do not induce MHC-I and -II expression. However, these supernatants inhibit MHC-II expression induced by IFN-γ in an IL-10 dependent mechanism. 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. Our results indicated that B. abortus-infected hepatocytes have an increased MHC-I expression, but MHC-II levels remain at basal levels. Overall, B. abortus infection induces MHC-I and -II expression in LX-2 cells, increasing the antigen presentation. Nevertheless, this response could be modulated by resident or infiltrating monocytes/macrophages.
Highlights
Brucella spp. are Gram-negative intracellular bacteria that infect domestic and natural animals and produce an incapacitating chronic disease when transmitted to humans
Our results indicate that B. abortus infection stimulated major histocompatibility complex (MHC)-I and -II expression in LX-2 cells, yielding a level comparable to that of IFN-γ-stimulated cells used as a positive control (Figure 1)
The type 4 secretion system (T4SS) encoded by the virB operon participates in the establishment of the intracellular replication niche of Brucella in different cell types [13], as well as contributing to the induction of a fibrotic phenotype in hepatic stellate cells (HSCs) during B. abortus infection
Summary
Brucella spp. are Gram-negative intracellular bacteria that infect domestic and natural animals and produce an incapacitating chronic disease when transmitted to humans. As a frequent niche of infections, the liver provides a tolerogenic environment. Such immunotolerant capacity is based on the presence of a resident immune cell repertoire in constant stimulation and the hepatic blood source that spread a unique growth factor and cytokine milieu [3]. The immune system of the liver is capable of inducing a prompt-response to tumor cells and pathogenic microorganisms [4]. The majority of the microorganisms that arrive in the liver are eradicated. Even though these several mechanisms can remove infectious agents, Brucella spp. can escape the immune response and persist in the liver.
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