Periodontal Disease and Osteomyelitis
Wilson Harvey, Alan Bennett in Prostaglandins in Bone Resorption, 2020
LPS occur in the outer membrane of Gram-negative bacteria cell walls. They are heter-opolymers consisting of polysaccharides (α “core” polysaccharide and an O-specific chain) attached to a phospholipid (lipid A) by 2-keto-3-deoxyoctonate residues. The bone-resorbing activity appears to reside in the lipid A part of the molecule33 with no apparent contribution from the polysaccharide chains except for one report of activity in the polysaccharide of Fusobacterium LPS by Sveen and Skaug.34 This observation, together with bone-resorbing activity of lipoteichoic acid (LTA), a cell wall component of Gram-positive bacteria, and of several fatty acids (oleic, palmitic, stearic acid)35 prompted Hausmann et al.33 to postulate that LPS, LTA, and PGs all stimulate bone resorption via a common “lipid-sensitive” receptor on bone cells.
Recognition of microbe-associated molecular patterns by pattern recognition receptors
Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald in Principles of Mucosal Immunology, 2020
Different classes of PAMPs activate different TLRs; that is, each TLR recognizes a limited number of specific molecular signatures in different classes of microorganisms (Table 18.2). Although the diversity of pattern recognition is limited, TLRs collectively recognize most pathogenic or commensal microorganisms that may invade the mucosa. For example, TLR2 signals the presence of bacterial lipopeptides and lipoteichoic acid, which are cell-wall constituents of gram-positive bacteria. Select combinations of TLRs may act in concert to expand the repertoire of these PRRs; thus, TLR2 cooperates with TLR1 or TLR6. TLR4 is the major receptor for LPS signal activation but requires the presence of the accessory molecules MD-2 and CD14. Flagellins of flagellated bacteria are ligands for TLR5. Unmethylated CpG DNA present in prokaryotic genomes and DNA viruses is detected by TLR9. In addition, TLRs may recognize endogenous damage-associated molecular patterns such as heat-shock proteins, which are released by dying cells and function as alarm signals during inflammation.
Staphylococcus
Dongyou Liu in Handbook of Foodborne Diseases, 2018
Although S. aureus is phylogenetically identical to coagulase negative staphylococci (CoNS), it appears to be more virulent than CoNS. S. aureus colonies often produce golden color on solid media. S. aureus cell wall is a tough protective coat of about 20–40 nm in thickness. Peptidoglycan is composed of 50% of cell mass [23]. The peptidoglycan of S. aureus may act like endotoxin that is involved in the release of cytokines via complement activation, macrophages, and platelets aggregation [4]. A group of phosphate-containing polymers known as teichoic acids (cell wall techoic acid and cell membrane–associated lipoteichoic acid), bound covalently to the peptidoglycan or inserted in the lipid membrane, constitute 40% of S. aureus cell mass, and the remaining 10% is composed of surface proteins, exoproteins, and autolysins [23]. Teichoic acid carries a negative charge and plays a part in the process of biofilm formation [25] as well as acquisition and localization of metal ions and activation of autolytic enzymes. The capsular polysaccharide is possessed by more than 90% of clinical S. aureus strains [23].
Photodynamic and peptide-based strategy to inhibit Gram-positive bacterial biofilm formation
Published in Biofouling, 2019
Laura Marise de Freitas, Esteban Nicolás Lorenzón, Eduardo Maffud Cilli, Kleber Thiago de Oliveira, Carla Raquel Fontana, Thomas S. Mang
Lipoteichoic acid is composed of a polymer of glycerol phosphate or ribitol phosphate attached to a diacylglycerol residue, responsible for the insertion of the polymer into the plasma membrane (Percy and Gründling 2014). Gram-positive bacteria incorporate teichoic acid polymers of varying lengths (15–50 residues, varying according to species) in their envelope, which directly influence the density of negative charges of the bacterial surface by the amount of phosphate groups present (Malanovic and Lohner 2015). Antimicrobial peptides with their overall positive charge are attracted by the negative charges of LTA and their binding to that molecule in the cell wall does not affect their bactericidal activity. This led to the postulation that the binding of the AMP to the LTA is the starting point for action on the membrane: AMPs anchor to the LTA and use it as a “ladder”, which leads them to the plasma membrane (Malanovic and Lohner 2015).
Role of Enterococcus faecalis in refractory apical periodontitis: from pathogenicity to host cell response
Published in Journal of Oral Microbiology, 2023
Zilong Deng, Binbin Lin, Fan Liu, Wanghong Zhao
Enterococcus faecalis, a gram-positive facultative anaerobic bacterium, is an opportunistic pathogen that is commonly found in the human oral cavity and gastrointestinal tract. Evidence has shown that E. faecalis is one of the most common pathogenic microorganisms in root canals with RAP, as it is frequently isolated from root canals with endodontic failure [5–10]. E. faecalis survives for a long time in root canals, because it can tolerate a highly alkaline and oligotrophic environment to form biofilms [11,12], invade deep into the dentin tubules [13], and easily evade phagocytosis by host cells [14]. Moreover, E. faecalis can also be detected in the periradicular lesions and extraradicular biofilms in patients with RAP [15]. Lipoteichoic acid (LTA), a cell wall component of gram-positive bacteria that acts as an important virulence factor, can trigger cascades resulting in pro-inflammatory cytokine release and periapical tissue damage by binding to targets, either specifically, to CD14 and to Toll-like receptors (TLRs), or non-specifically, to membrane phospholipids [16]. E. faecalis LTA participates in biofilm formation and adhesion to eukaryotic cells due to its alanylation that modulates the net surface charge of the bacteria [17]. Significant statistical correlations were found between levels of LTA and clinical features (periapical lesion areas and symptoms) [4,6]. Collectively, the contribution of E. faecalis and its virulence factor, LTA, in the pathogenesis of RAP is pivotal.
New and emerging drugs for the treatment of acne vulgaris in adolescents
Published in Expert Opinion on Pharmacotherapy, 2019
Isabel Cristina Valente Duarte De Sousa
Antimicrobial cationic peptides (ACPs), such as cathelicidins, defensins, and bacteriocins [113], are small molecules produced by the innate immune system to defend against invading pathogens [154–156]. They possess potent antimicrobial activity and low tendency to induce resistance [156–160] due to their ability to selectively disrupt microbial membranes [113,157]. Furthermore, they exhibit anti-inflammatory effects due to their ability to bind pro-inflammatory bacterial factors, such as lipoteichoic acid, and to inhibit the secretion of pro-inflammatory cytokines, such as TNF-α and IL-1 by host cells [161]. They also possess in vitro activity against P. acnes [162], suggesting a possible future role of ACPs in the treatment of acne vulgaris. Omiganan pentahydrochloride (also known as MBI226 or CLS001), a bovine cathelicidin indolicidin derivative, is a topical ACP with rapid antimicrobial action against Gram-positive and Gram-negative bacteria, as well as fungi [163,164]. Three phase II, randomized, double-blind, vehicle-controlled, multicenter trials have evaluated the effects of omiganan pentahydrochloride gel in patients with acne, however official results have not been published [165–167]. Several other ACPs are currently under in vitro investigation for their potential use against P. acnes [113,168,169]
Related Knowledge Centers
- Autolysis
- Cell Wall
- Diglyceride
- Enzyme
- Glycerol
- Lysozyme
- Peptidoglycan
- Phospholipid
- Gram-Positive Bacteria
- Ribitol