The key roles of toll-like receptor (TLR) for intracellular survival of Brucella

Abstract

Brucella spp. are facultative intracellular pathogens that have the ability to survive and multiply in professional and nonprofessional phagocytes and cause abortion in domestic animals and undulant fever in humans. Brucella species can survive in a variety of cells, including macrophages and their virulence and chronic infections are thought to be due to their ability to avoid the killing mechanisms within macrophages. Inhibition of phagosome-lysosome fusion has been proposed as a mechanism for intracellular survival of Brucella in professional and nonprofessional phagocytes. Toll-like receptors (TLRs) are part of a skillful system for detection of invasion by microbial pathogens. Recognition of microbial components by TLRs triggers signaling pathways that promote expression of genes and regulate innate immune responses. Recent studies for the interaction between TLRs-Brucella have indicated the importance of control of Brucella infection. Here, we review selected aspects of TLRs-Brucella interaction, which may be helpful to understanding the mechanism of Brucella pathogenesis.

Inhibitory effect of red ginseng acidic polysaccharide from Korean red ginseng on phagocytic activity and intracellular replication ofBrucella abortusin RAW 264.7 cells

“…Therefore, RGAP could account for the inhibitory effects of Korean red ginseng against Brucella infection. Mitogen-activated protein kinase (MAPK) has also been shown to play an important role in bacterial phagocytosis and actin cytoskeleton remodeling [ 9 ]. The treatment of peritoneal macrophages with acidic polysaccharides after subsequent exposure to heat-killed S. aureus reduced the expression of phospho-JNK1/2 and p38 MAPK [ 1 ].…”

Strategies for the development of an effective vaccine against Brucellosis

“…The Brucella species comprises gram-negative, aerobic, and facultative intracellular bacteria (coccobacilli) that invade phagocytic cells including macrophages, placental trophoblasts, and epithelial cells [28,34]. A key factor in the pathogenicity of the Brucella species is its surreptitious invasion of the professional and non-professional phagocytes; a process not easily detected by the primary host immune defenses, This invasion is made possible by the presence of pathogen-associated molecular patterns in the cell envelopes (particularly in the lipopolysaccharides and lipoproteins), which circumvent phagocytosis and bactericidal effects, thereby establishing a niche conducive to pathogen survival and replication [29,30].…”