Abstract
Human oral microbiome and dysbiotic infections have been recently evidently identified. One of the major reasons for such dysbiosis is impairment of the immune system. Periodontitis is a chronic inflammatory disease affecting the tissues that surround and support the teeth. In the United States., approximately 65 million people are affected by this condition. Its occurrence is also associated with many important systemic diseases such as cardiovascular disease, rheumatoid arthritis, and Alzheimer’s disease. Among the most important etiologies of periodontitis is Porphyromonas gingivalis, a keystone bacterial pathogen. Keystone pathogens can orchestrate inflammatory disease by remodeling a normally benign microbiota causing imbalance between normal and pathogenic microbiota (dysbiosis). The important characteristics of P. gingivalis causing dysbiosis are its virulence factors which cause effective subversion of host defenses to its advantage allowing other pathogens to grow. Some of the mechanisms involved in these processes are still not well-understood. However, various microbial strategies target host sialoglycoproteins for immune dysregulation. In addition, the enzymes that break down sialoglycoproteins and sialoglycans are the “sialoglycoproteases”, resulting in exposed terminal sialic acid. This process could lead to pathogen-toll like receptor (TLR) interactions mediated through sialic acid receptor ligand mechanisms. Assessing the function of P. gingivalis sialoglycoproteases, could pave the way to designing carbohydrate analogues and sialic acid mimetics to serve as drug targets.
Highlights
Human microbiota consist of about 100 trilion microbial cell that constantly interact with the host counterpart through various mechanisms [1,2]
While the role of sialidase in sialic acid metabolism has been known in other oral pathogens like Tannerella forsythia [16], it is yet to be explored in P. gingivalis
The sialidases breaks down the residues of sialic acid and sialoglycoproteins that could mask or expose that receptors for enzymatic interactions and ligand binding by contributing to biological functions, such as cellular interaction and conformational stabilization of glycoproteins in the cell membranes [15]
Summary
Human microbiota consist of about 100 trilion microbial cell that constantly interact with the host counterpart through various mechanisms [1,2]. The major enzyme that facilitate this interaction between the host and pathogen is bacterial “sialoglycosidases”, the enzymes that cleave the sialic acid from sialoglycoproteins. Bacterial sialidases have been considered virulence factors in many pathogenic organisms, such as Corynebacterium diphtheriae, Vibrio cholerae, Streptococcus pneumoniae, and group B streptococci, which colonize mucosal surfaces [8] They have been shown to be involved in infection and tissue destruction [9], peroxide scavenging during oxidative stress [10], and the modulation of host innate immunity [5]. While the role of sialidase in sialic acid metabolism has been known in other oral pathogens like Tannerella forsythia [16], it is yet to be explored in P. gingivalis
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