Volkov et al. strains of and genera [3]. However, this was objected to by Norskov-Lauritsen and Kilian [4] who assigned this bacterium to a novel genus called family, after citing their 16S RNA sequencing results. Since then, is usually a Gram-negative coccobacillus that is 0.5C0.8 m 0.6C1.4 m in size [5]. is non-motile, non-spore-forming and does not form capsules [5]. Furthermore, it ferments fructose, glucose, maltose and mannose, although not sucrose, lactose, raffinose, melibiose, arabinose and trehalose [5]. is also positive for catalase, Rabbit Polyclonal to DNA Polymerase zeta oxidase, and H2S besides being unfavorable for indole and ornithine decarboxylase. The bacterium reduces nitrate, and has lysine decarboxylases, and urease [6]. To date, there are 83 genome assemblies of different strains of deposited in the NCBI database, of which only 12 are complete. The reference genome, encoding 1898 genes, is usually that of strain and has a size of 2.13 Mb (44.4% GC content). It is deposited under the accession number “type”:”entrez-nucleotide”,”attrs”:”text”:”NZ_CP012958″,”term_id”:”1008818483″,”term_text”:”NZ_CP012958″NZ_CP012958 [7]. Seven serotypes (a to g) of have been identified based on the surface antigen O-polysaccharide side chain of their lipopolysaccharide 3-Formyl rifamycin [8,9]. Whether certain serotypes are more virulent than others is usually unclear, and their distribution in individuals suffering from periodontitis appears to vary across populations of different ethnicities [10]. was once reported as the microbe that is most-commonly isolated from periodontal lesions. A total of 95% of patients with localized aggressive periodontitis were found to be infected by [11]. This was especially true of the highly pathogenic serotype b clone, JP2, which was consistently isolated from Northwest African populations [12]. In this study, 60.4% of the 217 dental plaque samples obtained from periodontitis patients cultured positive for with periodontitis is more apparent in those of African or Middle Eastern descent [14]. Therefore, more work should be done in investigating the factors of susceptibility to periodontitis and its relationship with has an arsenal of virulence factors, which allows itself to invade host tissues, evade the host immune system, and condition the host tissue environment for its survival. These virulence factors include adhesive factors, lipopolysaccharide (LPS), cytolethal distending toxins (CDT), outer membrane vesicles (OMVs), and outer membrane proteins (Omp). In this review, however, we focus on its intriguing toxin, leukotoxin A (LtxA) that specifically targets and kills leukocytes. Leukotoxin A is considered the most significant virulence factor of as it has been shown to be toxic to hematopoietic cells and therefore plays important roles in the evasion of host immunity and persistent contamination in hosts. extracts were first described as leukotoxic in a study by Tsai et al. [15]. Shortly after this discovery, the leukotoxicity was attributed to the LtxA isolated from [15]. LtxA was also found to confer -hemolysis capabilities to is particularly associated with the localized form rather than the generalized form. Among 3-Formyl rifamycin various virulence factors produced by from phagocytosis and other host immune responses. The mechanisms, by which this occurs, could vary in different leukocyte types. Neutrophils, when exposed to LtxA, will degranulate and release proteolytic enzymes and metalloproteases, which contribute to periodontal tissue destruction and create a proteolytic environment that degrades immunoglobulins [19]. LtxA can also target macrophages and activate the inflammasome complex, which then leads to the secretion of pro-inflammatory cytokines. This intensifies inflammation at infected sites in patients with localized aggressive periodontitis, causing major discomfort [20]. Additionally, it has 3-Formyl rifamycin been found that neutrophils exposed 3-Formyl rifamycin to LtxA express citrullinated proteins characteristic of RA, implying the significance of LtxA as a major virulence factor in different diseases associated with [21,22]. Due to its unique target specificity and complex actions that allow to evade host immunity, LtxA has been studied intensively. 1.3. Ltx Operon The leukotoxin operon of encodes four genes, namely.