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Periodontal Disease and Osteomyelitis
Published in Wilson Harvey, Alan Bennett, Prostaglandins in Bone Resorption, 2020
Although LPS has received more attention than other bacterial components, these should not be overlooked. Lipoteichoic acids, which are polymers containing carbohydrates and fatty acids, are found in the cell wall of Gram-positive organisms which include some plaque-forming bacteria.56 Hausmann et al.33 showed that they were capable of stimulating bone resorption in culture, but were independent of endogenous PG synthesis. When the lipids were removed by hydrolysis, the remaining teichoic acid did not stimulate resorption. Similar properties were reported57 for an amphipathic antigen (αcA) from Actinomyces viscosus, a Gram-positive bacteria also found in dental plaque. It caused bone resorption dependent on the presence of its lipid moiety, but independent of PG synthesis in the bone.
Infective endocarditis by Actinomyces species: a systematic review
Published in Journal of Chemotherapy, 2023
Petros Ioannou, Stella Baliou, Ioanna Papakitsou, Diamantis P. Kofteridis
Actinomyces species are Gram-positive bacteria that colonize the mouth, colon, and vagina and are the causes of actinomycosis, which is a slowly progressive infection that may mimic malignancy due to the invasiveness of tissues and the ability to form sinus tracts [1]. The most common encountered species associated with actinomycosis is A. israeilii [2]. Other species that may also cause actinomycosis, even though they are less frequently encountered are Actinomyces naeslundii, Actinomyces viscosus, Actinomyces odontolyticus, Actinomyces gerencseriae, Actinomyces graevenitzii, and Actinomyces meyeri [3–9]. With development of newer methods for pathogen identification, such as MALDI-TOF and genotypic methods such as comparative 16S ribosomal RNA (rRNA), new Actinomyces species have been identified from both human and animal specimens [6,10,11]. On the other hand, some Actinomyces species have been reclassified as Trueperella, Actinotignum, or Cellulomonas due to the same pathogen identification methods [6,10–14].
Synergistic effects of D-arginine, D-methionine and D-histidine against Porphyromonas gingivalis biofilms
Published in Biofouling, 2021
Zhenyang Zhang, Baosheng Li, Qing Cai, Shuwei Qiao, Dan Wang, Heling Wang, Huiyan Zhang, Yalan Yang, Weiyan Meng
Single P. gingivalis colonies were inoculated into BHI liquid medium, and the inoculum was adjusted to 107 colony-forming units (CFU) ml−1 of medium (CFU ml−1) (Qi et al. 2018). The bacterial suspension was then added to 96-well plates (Nest, Wuxi, China), mixed with a series of concentrations of D-AAs, and subsequently incubated for 72 h at 37 °C under anaerobic conditions. Simultaneously, the OD 600 value was measured every 4 h with a microplate reader (Synergy HT, BioTek, USA) (Wang et al. 2019). For each D-AA, the concentration of the sample first showing no turbidity at 72 h was recorded as the MIC. Streptococcus sanguinis ATCC 10556 and Actinomyces viscosus ATCC 27044 were used for supplementary experiments. Briefly, S. sanguinis, and A. viscosus were both subcultured and incubated at 37 °C under anaerobic conditions. After adjusting the bacterial concentrations for both suspensions to 107 CFU ml−1, gradient concentrations of R, M, or H (4 mM, 8 mM, 12 mM, and 16 mM) individually, and equimolar solutions of RMH (4 mM, 8 mM, 12 mM, 16 mM, 20 mM) were added to the suspensions. Subsequently, S. sanguinis and A. viscosus were incubated for 24 and 48 h, respectively, after which the OD 600 value was measured.
COVID-19;-The origin, genetics,and management of the infection of mothers and babies
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hassan Ih El-Sayyad, Yousef Ka Abdalhafid
If the body, s immune does not overcome viral infection, the SARS-CoV-2 multiply. Then, there is a massive degree of lung injury associated with the increased secretion of the substantial amount of cytokines (IFN-α, IFN-γ, IL-1β, IL-6, IL-12, IL-18, IL-33, and TNF-α) and chemokines (CCL2, CCL3, CCL5, CXCL8, CXCL9, and CXCL10) in the body (Li et al., 2020). This leads to the formation of a cytokine storm or COVID-19 acute respiratory syndrome leading to death [51]. In addition, SARS-CoV-2 infection damages the pulmonary lining cells interfering with the growth of pathogenic bacteria to develop secondary pneumonia [52]. The viral infection decreased gut microbiota and Veillonella, and Actinomyces [53], Clostridium hathewayi, Actinomyces viscosus, and Bacteroides nordii) . It depleted beneficial commensals as Eubacterium ventriosum, Faecalibacterium prausnitzii, Roseburia, Lachnospiraceae and it increased the pathogenic ones such as Streptococcus and Rothia [54]. however the alteration of lung microbiota and increase in Staphylococcus, Streptococcus and Enterobacteriaceae predicted the production of cytokine storm and inflammation [55] .