Patterns of adherence to HEp-2 cells and actin polymerisation by toxigenic Corynebacterium diphtheriae strains

Hirata, Raphael; Souza, Sonia M.S.; Rocha-de-Souza, Cláudio Marcos; Andrade, Arnaldo F.B.; Monteiro-Leal, Luiz Henrique; Formiga, Luiz Carlos Duarte; Mattos‐Guaraldi, Ana Luíza

doi:10.1016/j.micpath.2003.10.002

Cited by 32 publications

(35 citation statements)

References 16 publications

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“…Both the 67 and 72 kDa polypeptide bind to erythrocyte receptors, leading to haemagglutination. Subsequently, Hirata et al (2004) demonstrated that 67-72p binds not only human erythrocytes but also the human epidermoid laryngeal carcinoma cell line HEp-2 and that binding was effectively blocked by anti-67-72p IgG antibodies. A recent MS study indicated that the 67-72p protein is encoded by a single gene, dip0733 (Sabbadini et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Characterization of DIP0733, a multi-functional virulence factor of Corynebacterium diphtheriae

et al. 2015

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Corynebacterium diphtheriae is typically recognized as an extracellular pathogen. However, a number of studies revealed its ability to invade epithelial cells, indicating a more complex pathogen-host interaction. The molecular mechanisms controlling and facilitating internalization of Cor. diphtheriae are poorly understood. In this study, we investigated the role of DIP0733 as virulence factor to elucidate how it contributes to the process of pathogen-host cell interaction. Based on in vitro experiments, it was suggested recently that the DIP0733 protein might be involved in adhesion, invasion of epithelial cells and induction of apoptosis. A corresponding Cor. diphtheriae mutant strain generated in this study was attenuated in its ability to colonize and kill the host in a Caenorhabditis elegans infection model system. Furthermore, the mutant showed an altered adhesion pattern and a drastically reduced ability to adhere and invade epithelial cells. Subsequent experiments showed an influence of DIP0733 on binding of Cor. diphtheriae to extracellular matrix proteins such as collagen and fibronectin. Furthermore, based on its fibrinogen-binding activity, DIP0733 may play a role in avoiding recognition of Cor. diphtheriae by the immune system. In summary, our findings support the idea that DIP0733 is a multi-functional virulence factor of Cor. diphtheriae.

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Section: Introductionmentioning

confidence: 99%

Characterization of DIP0733, a multi-functional virulence factor of Corynebacterium diphtheriae

et al. 2015

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“…Following a 180 min incubation, infected cells were washed three times with PBSS, fixed with methanol and stained by Giemsa (Hirata et al, 2004).…”

Section: Methodsmentioning

confidence: 99%

Invasion of endothelial cells and arthritogenic potential of endocarditis-associated Corynebacterium diphtheriae

et al. 2014

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Although infection by Corynebacterium diphtheriae is a model of extracellular mucosal pathogenesis, different clones have been also associated with invasive infections such as sepsis, endocarditis, septic arthritis and osteomyelitis. The mechanisms that promote C. diphtheriae infection and haematogenic dissemination need further investigation. In this study we evaluated the association and invasion mechanisms with human umbilical vein endothelial cells (HUVECs) and experimental arthritis in mice of endocarditis-associated strains and control non-invasive strains. C. diphtheriae strains were able to adhere to and invade HUVECs at different levels. The endocarditis-associated strains displayed an aggregative adherence pattern and a higher number of internalized viable cells in HUVECs. Transmission electron microscopy (TEM) analysis revealed intracellular bacteria free in the cytoplasm and/or contained in a host-membrane-confined compartment as single micro-organisms. Data showed bacterial internalization dependent on microfilament and microtubule stability and involvement of protein phosphorylation in the HUVEC signalling pathway. A high number of affected joints and high arthritis index in addition to the histopathological features indicated a strain-dependent ability of C. diphtheriae to cause severe polyarthritis. A correlation between the arthritis index and increased systemic levels of IL-6 and TNF-a was observed for endocarditis-associated strains. In conclusion, higher incidence of potential mechanisms by which C. diphtheriae may access the bloodstream through the endothelial barrier and stimulate the production of pro-inflammatory cytokines such as IL-6 and TNF-a, in addition to the ability to affect the joints and induce arthritis through haematogenic spread are thought to be related to the pathogenesis of endocarditis-associated strains.

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“…The blood isolate showed a higher percentage of adherence and internalization compared with throat isolates (5). Further study showed that all sucrose fermenting and non-fermenting strains isolated from throat and skin lesions exhibited localized and diffuse adherence patterns, respectively (16). However, the binding properties of C. diphtheriae strains related to invasive disease have not yet been investigated.…”

Section: Introductionmentioning

confidence: 94%

“…Adherence patterns to HEp-2 of C. diphtheriae blood isolates were assayed by methods previously described (16). Adherence assays were performed within semi-confluent HEp-2 cells grown on circular coverslips in DMEM (Sigma, USA) supplemented with 5% fetal calf serum (Gibco-BRL, USA), 50 µg/mL gentamicin, 2.5 µg/mL amphotericin B and 0.5% L-glutamine at 37°C in a 5% CO 2 atmosphere.…”

Section: Hep-2 Adherence Assaysmentioning

confidence: 99%

Potential pathogenic role of aggregative- adhering Corynebacterium diphtheriae of different clonal groups in endocarditis

Hirata

Pereira

Filardy

et al. 2008

Braz J Med Biol Res

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Patterns of adherence to HEp-2 cells and actin polymerisation by toxigenic Corynebacterium diphtheriae strains

Cited by 32 publications

References 16 publications

Characterization of DIP0733, a multi-functional virulence factor of Corynebacterium diphtheriae

Characterization of DIP0733, a multi-functional virulence factor of Corynebacterium diphtheriae

Invasion of endothelial cells and arthritogenic potential of endocarditis-associated Corynebacterium diphtheriae

Potential pathogenic role of aggregative- adhering Corynebacterium diphtheriae of different clonal groups in endocarditis

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