Importance of the Omp25/Omp31 family in the internalization and intracellular replication of virulent B. ovis in murine macrophages and HeLa cells

Martín-Martín, Ana I.; Caro-Hernández, Paola; Orduña, Antonio; Vizcaı́no, Nieves; Fernández-Lago, Luis

doi:10.1016/j.micinf.2008.02.013

Cited by 45 publications

(52 citation statements)

References 19 publications

(18 reference statements)

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“…Three to five representatives are present in the genome of every Bartonella species, and homologs are widespread among Rhizobiales but rare beyond this taxon (reference 294 and personal observation). The Hbps show considerable sequence similarity to members of the OMP25/31 family of Brucella (75), which are apparently crucial for several aspects of pathogenesis, although their molecular function is not known (74,276). Furthermore, homologies to the well-known Neisseria Opa proteins, which are critical mediators of host cell interaction involving invasion and immunomodulation (372, 388), have been described (296).…”

Section: Other Virulence Factorsmentioning

confidence: 99%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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SUMMARY Bartonella spp. are facultative intracellular pathogens that employ a unique stealth infection strategy comprising immune evasion and modulation, intimate interaction with nucleated cells, and intraerythrocytic persistence. Infections with Bartonella are ubiquitous among mammals, and many species can infect humans either as their natural host or incidentally as zoonotic pathogens. Upon inoculation into a naive host, the bartonellae first colonize a primary niche that is widely accepted to involve the manipulation of nucleated host cells, e.g., in the microvasculature. Consistently, in vitro research showed that Bartonella harbors an ample arsenal of virulence factors to modulate the response of such cells, gain entrance, and establish an intracellular niche. Subsequently, the bacteria are seeded into the bloodstream where they invade erythrocytes and give rise to a typically asymptomatic intraerythrocytic bacteremia. While this course of infection is characteristic for natural hosts, zoonotic infections or the infection of immunocompromised patients may alter the path of Bartonella and result in considerable morbidity. In this review we compile current knowledge on the molecular processes underlying both the infection strategy and pathogenesis of Bartonella and discuss their connection to the clinical presentation of human patients, which ranges from minor complaints to life-threatening disease.

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Section: Other Virulence Factorsmentioning

confidence: 99%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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“…ovis has never been reported as a human pathogen and mainly infects rams. Little is known about the virulence of B. ovis, although some clues have been obtained from a study that deciphered the whole genome sequence (53) and from a small number of studies performed with individual genes (9,33,51). Additionally, it is known that-similarly to S Brucella and in contrast to R derivatives of S strains (45)-B. ovis enters the macrophage through cholesterol-rich lipid rafts (36).…”

Section: Melitensis B Abortus and B Suis)mentioning

confidence: 99%

“…Strains of the genus Brucella may be smooth (S) or rough (R), depending on the presence or absence, respectively, of O-polysaccharide (O-PS) chains in the LPS. O-PS masks other components of the bacterial surface (6), and since R mutant (M) strains derived from S strains are impaired in the interaction with phagocytes and are attenuated in animal models of infection (22,40,44), it is considered a key virulence factor in S Brucella species (such as B. melitensis, B. abortus, and B. suis).Nevertheless, B. ovis is a naturally R Brucella species that is virulent in its natural host and in laboratory animal models (9,33,51). This ability of B. ovis to infect the host despite the absence of O-PS in the OM, together with its tropism for the male genital tract, is indicative of virulence mechanisms differing, at least in part, from those employed by S Brucella species, which are able to colonize the placenta and typically induce abortions.…”

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confidence: 99%

“…Nevertheless, B. ovis is a naturally R Brucella species that is virulent in its natural host and in laboratory animal models (9,33,51). This ability of B. ovis to infect the host despite the absence of O-PS in the OM, together with its tropism for the male genital tract, is indicative of virulence mechanisms differing, at least in part, from those employed by S Brucella species, which are able to colonize the placenta and typically induce abortions.…”

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confidence: 99%

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Quorum-Sensing and BvrR/BvrS Regulation, the Type IV Secretion System, Cyclic Glucans, and BacA in the Virulence of Brucella ovis: Similarities to and Differences from Smooth Brucellae

et al. 2012

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ABSTRACTBrucella ovisis a rough bacterium—lacking O-polysaccharide chains in the lipopolysaccharide—that is virulent in its natural host and whose virulence mechanisms remain almost unexplored. In a search for additional traits that distinguishB. ovisfrom smoothBrucella, which require O-polysaccharide chains for virulence, we have analyzed the significance inB. ovisof the main virulence factors described for smoothBrucella. Attempts to obtain strains of virulentB. ovisstrain PA that are mutated in the BvrR/BvrS two-component regulatory system were unsuccessful, suggesting the requirement of that system forin vitrosurvival, while the inactivation ofbacA—in contrast to the results seen with smoothBrucella—did not affect splenic colonization in mice or behavior in J774.A1 murine macrophages. Defects in the synthesis of cyclic ß-1,2 glucans reduced the uptake ofB. ovisPA in macrophages and, although the intracellular multiplication rate was unaffected, led to attenuation in mice. Growth of strains with mutations in the type IV secretion system (encoded by thevirBoperon) and the quorum-sensing-related regulator VjbR was severely attenuated in the mouse model, and although the mutant strains internalized like the parental strain in J774.A1 murine macrophages, they were impaired for intracellular replication. As described forB. melitensis, VjbR regulates the transcription of thevirBoperon positively, and theN-dodecanoyl-dl-homoserine lactone (C12-HSL) autoinducer abrogates this effect. In contrast, no apparent VjbR-mediated regulation of thefliFflagellar gene was observed inB. ovis, probably due to the two deletions detected upstream offliF. These results, together with others reported in the text, point to similarities between rough virulentB. ovisand smoothBrucellaspecies as regards virulence but also reveal distinctive traits that could be related to the particular pathogenicity and host tropism characteristics ofB. ovis.

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“…O antígeno 29-kDa é composto por duas OMPs, a Omp25 e a Omp31 (VISCAÍNO et al, 2001). Destes, a Omp25 está diretamente envolvida na invasão, replicação e sobrevivência da B. ovis no interior de células hospedeiras (CARO-HERNÁNDEZ et al, 2007;MARTÍN-MARTÍN et al, 2008). A invasão celular ocorre por receptores de moléculas contendo ácido siálico ou resíduos sulfatados, poucos minutos após a aderência nas células alvos (CASTANEDA-ROLDAN et al, 2004).…”

Section: Aderência E Penetraçãounclassified

Brucella ovis: invasão, tráfego, fatores de virulência e resposta imune

Antunes¹,

Megid²

2013

Sem. Ci. Agr.

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ResumoA brucelose permanece como problema econômico em animais e de saúde pública. Em todo o mundo a brucelose ovina ocasionada pela Brucella ovis é considerada uma das principais causas de infertilidade em ovinos. Os fatores responsáveis pela persistência do agente não são conhecidos, bem como os mecanismos imunes envolvidos na defesa e eventualmente na persistência do agente. Brucella spp. induz resposta inflamatória moderada. A natureza intracelular do agente estimula resposta imune celular do tipo linfócito T helper 1. Os estudos de patogenia da brucelose ovina são escassos. Recentes avanços demonstraram que a resposta inflamatória moderada induzida pelas brucelas representam provavelmente o resultado de tentativa de escape da resposta imune e supressão da resposta imune hospedeira. Foram revisados os mecanismos descritos pelas brucelas e pela Brucella ovis para penetração no hospedeiro, escape da resposta imune, bem como a resposta imunológica gerada pela infecção. Palavras-chave: Brucelose, patogenia, imunopatologia, Brucella ovis AbstractBrucellosis remains an economic problem in animals and public health. Worldwide ovine brucellosis caused by Brucella ovis is considered a major cause of infertility in sheep. The factors responsible for persistence of the agent are not known, as well as the mechanisms involved in immune defense and possibly the persistence of the agent. Brucella spp. induces moderate inflammatory response. The nature of the intracellular agent stimulates immune response of the type 1 helper T lymphocytes. Studies of the pathogenesis of ovine brucellosis are scarce. Recent developments have shown that the inflammatory response induced by moderate brucelas represent probably the result of an attempt to escape the immune response and suppression of host immune response. Were reviewed by the mechanisms described by brucelas and Brucella ovis for penetration into the host, escape of the immune response and the immune response generated by the infection.

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Importance of the Omp25/Omp31 family in the internalization and intracellular replication of virulent B. ovis in murine macrophages and HeLa cells

Cited by 45 publications

References 19 publications

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

Quorum-Sensing and BvrR/BvrS Regulation, the Type IV Secretion System, Cyclic Glucans, and BacA in the Virulence of Brucella ovis: Similarities to and Differences from Smooth Brucellae

Brucella ovis: invasão, tráfego, fatores de virulência e resposta imune

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