Peptidoglycan of Actinomyces naeslundii induces inflammatory cytokine production and stimulates osteoclastogenesis in alveolar bone resorption

Sato, Takenori; Watanabe, Koichi; Kumada, Hidefumi; Toyama, Toshizo; Tani‐Ishii, Nobuyuki; Hamada, Naoki

doi:10.1016/j.archoralbio.2012.07.012

Cited by 42 publications

(33 citation statements)

References 35 publications

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“…As shown in Fig. 3, XH001 is a strong inducer of TNF-α gene expression, consistent with observations for other Actinomyces species (27). Interestingly, when TM7x was physically attached to XH001, induction of TNF-α gene expression was greatly reduced, suggesting that TM7x can either prevent detection of XH001 by macrophages or possibly suppress TNF-α gene expression in macrophages.…”

Section: Resultssupporting

confidence: 88%

Cultivation of a human-associated TM7 phylotype reveals a reduced genome and epibiotic parasitic lifestyle

He¹,

McLean

Edlund

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

413

547

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The candidate phylum TM7 is globally distributed and often associated with human inflammatory mucosal diseases. Despite its prevalence, the TM7 phylum remains recalcitrant to cultivation, making it one of the most enigmatic phyla known. In this study, we cultivated a TM7 phylotype (TM7x) from the human oral cavity. This extremely small coccus (200-300 nm) has a distinctive lifestyle not previously observed in human-associated microbes. It is an obligate epibiont of an Actinomyces odontolyticus strain (XH001) yet also has a parasitic phase, thereby killing its host. This first completed genome (705 kb) for a human-associated TM7 phylotype revealed a complete lack of amino acid biosynthetic capacity. Comparative genomics analyses with uncultivated environmental TM7 assemblies show remarkable conserved gene synteny and only minimal gene loss/gain that may have occurred as TM7x adapted to conditions within the human host. Transcriptomic and metabolomic profiles provided the first indications, to our knowledge, that there is signaling interaction between TM7x and XH001. Furthermore, the induction of TNF-α production in macrophages by XH001 was repressed in the presence of TM7x, suggesting its potential immune suppression ability. Overall, our data provide intriguing insights into the uncultivability, pathogenicity, and unique lifestyle of this previously uncharacterized oral TM7 phylotype.TM7 | human-associated | epibiont | oral microbiome | interspecies interaction

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Section: Resultssupporting

confidence: 88%

Cultivation of a human-associated TM7 phylotype reveals a reduced genome and epibiotic parasitic lifestyle

He¹,

McLean

Edlund

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

413

547

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“…During osteoclast differentiation, modulating the gene expression of Toll-like receptors (TLRs) results in the predominant expression of TLR2 and TLR4 (33). Although both macrophage-colony stimulating factor (M-CSF) and the receptor activator of the NF-кB ligand are essential for osteoclastogenesis, studies have shown that LPS and PGN affect osteoclastogenesis in a dose-dependent manner (36,37). Moreover, LPS through TLR4 recognition and PGN through TLR2 recognition initiate an inflammatory cascade (i.e., IL-1b, IL-6, and TNF-a release) via the activation of NF-кB and mitogen-activated protein kinase, resulting in bone resorption (33,36,37).…”

Section: Discussionmentioning

confidence: 99%

“…Although both macrophage-colony stimulating factor (M-CSF) and the receptor activator of the NF-кB ligand are essential for osteoclastogenesis, studies have shown that LPS and PGN affect osteoclastogenesis in a dose-dependent manner (36,37). Moreover, LPS through TLR4 recognition and PGN through TLR2 recognition initiate an inflammatory cascade (i.e., IL-1b, IL-6, and TNF-a release) via the activation of NF-кB and mitogen-activated protein kinase, resulting in bone resorption (33,36,37). In our findings of inhalational lung injury-induced bone loss, the possibility exists that these bacterial components escaped into the systemic circulation to affect skeletal health directly.…”

Section: Discussionmentioning

confidence: 99%

Organic Dust, Lipopolysaccharide, and Peptidoglycan Inhalant Exposures Result in Bone Loss/Disease

Dusad

Thiele

Klassen

et al. 2013

Am J Respir Cell Mol Biol

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4Veterans Administration Nebraska Western Iowa Healthcare System, Omaha, NebraskaSkeletal health consequences associated with chronic inflammatory respiratory disease, and particularly chronic obstructive pulmonary disease (COPD), contribute to overall disease morbidity. Agricultural environmental exposures induce significant airway diseases, including COPD. However, animal models to understand inhalant exposureinduced lung injury and bone disease have not been described. Using micro-computed tomography (micro-CT) imaging technology and histology, bone quantity and quality measurements were investigated in mice after repetitive intranasal inhalation exposures to complex organic dust extracts (ODEs) from swine confinement facilities. Comparison experiments with LPS and peptidoglycan (PGN) alone were also performed. After 3 weeks of repetitive ODE inhalation exposure, significant loss of bone mineral density and trabecular bone volume fraction was evident, with altered morphological microarchitecture changes in the trabecular bone, compared with saline-treated control animals. Torsional resistance was also significantly reduced. Compared with saline treatment, ODE-treated mice demonstrated decreased collagen and proteoglycan content in their articular cartilage, according to histopathology. Significant bone deterioration was also evident after repetitive intranasal inhalant treatment with LPS and PGN. These findings were not secondary to animal distress, and not entirely dependent on the degree of induced lung parenchymal inflammation. Repetitive LPS treatment demonstrated the most pronounced changes in bone parameters, and PGN treatment resulted in the greatest lung parenchymal inflammatory changes. Collectively, repetitive inhalation exposures to noninfectious inflammatory agents such as complex organic dust, LPS, and PGN resulted in bone loss. This animal model may contribute to efforts toward understanding the mechanisms and evaluating the therapeutics associated with adverse skeletal health consequences after subchronic airway injury.

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“…It is believed that this bacterium can induce the destruction of soft and hard tissues through root canals and the gingival sulcus, playing a key role in the onset of periodontal disease or in the transition from gingivitis to periodontitis. 23 Treatment of the present case consisted of the oral administration of penicillin as recommended in the literature, 7,11,15 and the patient presented complete regression of the lesion.…”

Section: De Andrade Et Almentioning

confidence: 92%

Acute Primary Actinomycosis Involving the Hard Palate of a Diabetic Patient

Andrade¹,

Novaes²,

Germano³

et al. 2014

Journal of Oral and Maxillofacial Surgery

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Actinomycosis is a relatively rare infection caused by saprophytic bacteria of the oral cavity and gastrointestinal tract that can become pathogenic. The chronic hyperglycemia of diabetes mellitus induces events that promote structural changes in various tissues and are associated with problems in wound healing. This infection remains largely unknown to most clinicians because of its different presentations, and palatal involvement is extremely rare. This report describes the case of a 46-year-old woman who was diagnosed with actinomycosis involving the hard palate. The main clinical, histopathologic, and therapeutic characteristics and differential diagnosis of actinomycosis are reviewed. To date, 3 cases of actinomycosis involving the hard palate have been reported.

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Peptidoglycan of Actinomyces naeslundii induces inflammatory cytokine production and stimulates osteoclastogenesis in alveolar bone resorption

Cited by 42 publications

References 35 publications

Cultivation of a human-associated TM7 phylotype reveals a reduced genome and epibiotic parasitic lifestyle

Cultivation of a human-associated TM7 phylotype reveals a reduced genome and epibiotic parasitic lifestyle

Organic Dust, Lipopolysaccharide, and Peptidoglycan Inhalant Exposures Result in Bone Loss/Disease

Acute Primary Actinomycosis Involving the Hard Palate of a Diabetic Patient

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