Proinflammatory Response of Human Osteoblastic Cell Lines and Osteoblast-Monocyte Interaction upon Infection with<i>Brucella</i>spp

Delpino, M. Victoria; Fossati, Carlos A.; Baldi, Pablo C.

doi:10.1128/iai.01259-08

Cited by 66 publications

(93 citation statements)

References 45 publications

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“…16,17 Likewise other intracellular bacteria that infect cells of the CNS, such as Listeria and Mycobacterium, have a preferential tropism for microglia rather than astrocytes. 32,33 The fact that B. abortus is also able to infect astrocytes adds new evidence to the ability of this baterium to survive within nonphagocityc cell types, such as osteoblast 34 and epithelial cells. 35 There is growing evidence regarding the role of inflammation as a potential pathogenic factor in many diseases of the CNS.…”

Section: Discussionmentioning

confidence: 99%

Brucella abortus Induces the Secretion of Proinflammatory Mediators from Glial Cells Leading to Astrocyte Apoptosis

Samartino

Delpino

Godoy

et al. 2010

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

Brucella abortus Induces the Secretion of Proinflammatory Mediators from Glial Cells Leading to Astrocyte Apoptosis

Samartino

Delpino

Godoy

et al. 2010

The American Journal of Pathology

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“…17 Once adapted to the intramacrophage environment, Brucella extends its intracellular persistence indefinitely, which contributes to systemic metastasis and infection of preferred targeted cells or tissues, such as placental trophoblasts, fetal lung, male genitalia, skeletal tissues, reticuloendothelial system, and endothelium. Currently, there is minimal information available to describe the interaction of Brucella with these target cells and tissue 18,19 to provide a more holistic systems biology analysis of the pathogenesis of brucellosis at the level of the whole host organism.…”

Section: Biology Of Brucellamentioning

confidence: 99%

Pathogenesis and Immunobiology of Brucellosis

Figueiredo

Ficht

Rice‐Ficht

et al. 2015

The American Journal of Pathology

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This review of Brucellaehost interactions and immunobiology discusses recent discoveries as the basis for pathogenesis-informed rationales to prevent or treat brucellosis. Brucella spp., as animal pathogens, cause human brucellosis, a zoonosis that results in worldwide economic losses, human morbidity, and poverty. Although Brucella spp. infect humans as an incidental host, 500,000 new human infections occur annually, and no patient-friendly treatments or approved human vaccines are reported. Brucellae display strong tissue tropism for lymphoreticular and reproductive systems with an intracellular lifestyle that limits exposure to innate and adaptive immune responses, sequesters the organism from the effects of antibiotics, and drives clinical disease manifestations and pathology. Stealthy brucellae exploit strategies to establish infection, including i) evasion of intracellular destruction by restricting fusion of type IV secretion systemdependent Brucella-containing vacuoles with lysosomal compartments, ii) inhibition of apoptosis of infected mononuclear cells, and iii) prevention of dendritic cell maturation, antigen presentation, and activation of naive T cells, pathogenesis lessons that may be informative for other intracellular pathogens. Data sets of next-generation sequences of Brucella and host time-series global expression fused with proteomics and metabolomics data from in vitro and in vivo experiments now inform interactive cellular pathways and gene regulatory networks enabling full-scale systems biology analysis. The newly identified effector proteins of Brucella may represent targets for improved, safer brucellosis vaccines and therapeutics. It is noteworthy that long ago in his publication Epidemics, Hippocrates described brucellosis-type syndromes in humans living in the Mediterranean littoral. Many centuries later, British physician, David Bruce, and Greek physician, Themistokles Zammit, in 1886 would discover the causative agent, Micrococcus melitensis, of brucellosis and would identify milk products of goats as the source of infection for military troops on the island of Malta. Even after more than a century of extensive research, Brucella spp. are still serious animal pathogens that cause brucellosis, a zoonosis that results in substantial economic losses, human morbidity, and perpetuates poverty worldwide.1 These Gram-negative bacteria infect a diverse array of land and aquatic mammals,

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“…Histological examination of a dog's infected placenta has sug-gested that B. canis replicates intracellularly (18). In addition, large numbers of B. canis bacteria attach to the cell surface; however, studies of cells have failed to demonstrate unambiguously that this bacterium actually replicates intracellularly (19)(20)(21)(22)(23)(24)(25). This is significant, since B. canis harbors most of the virulence determinants defined for the genus, and the genome of this bacterium is 98 to 99% identical to the genomes of other virulent Brucella species.…”

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Brucella canis Is an Intracellular Pathogen That Induces a Lower Proinflammatory Response than Smooth Zoonotic Counterparts

et al. 2015

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e Canine brucellosis caused by Brucella canis is a disease of dogs and a zoonotic risk. B. canis harbors most of the virulence determinants defined for the genus, but its pathogenic strategy remains unclear since it has not been demonstrated that this natural rough bacterium is an intracellular pathogen. Studies of B. canis outbreaks in kennel facilities indicated that infected dogs displaying clinical signs did not present hematological alterations. A virulent B. canis strain isolated from those outbreaks readily replicated in different organs of mice for a protracted period. However, the levels of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-12 in serum were close to background levels. Furthermore, B. canis induced lower levels of gamma interferon, less inflammation of the spleen, and a reduced number of granulomas in the liver in mice than did B. abortus. When the interaction of B. canis with cells was studied ex vivo, two patterns were observed, a predominant scattered cell-associated pattern of nonviable bacteria and an infrequent intracellular replicative pattern of viable bacteria in a perinuclear location. The second pattern, responsible for the increase in intracellular multiplication, was dependent on the type IV secretion system VirB and was seen only if the inoculum used for cell infections was in early exponential phase. Intracellular replicative B. canis followed an intracellular trafficking route undistinguishable from that of B. abortus. Although B. canis induces a lower proinflammatory response and has a stealthier replication cycle, it still displays the pathogenic properties of the genus and the ability to persist in infected organs based on the ability to multiply intracellularly. Brucellosis is a disease of animals and humans caused by members of the genus Brucella. Zoonotic species such as Brucella melitensis, Brucella abortus, and Brucella suis are facultative extracellular-intracellular stealthy pathogens that are able to overcome innate immunity at early times of infection (1-3) and at specific stages of adaptive immunity (4, 5). In addition to influencing the immune response, these Brucella species are able to circumvent the killing action of professional and nonprofessional phagocytes, transit within phagocytic vacuoles, and replicate extensively within the endoplasmic reticulum of cells (6). These properties allow the bacterium to spread throughout the reticuloendothelial system and promote chronic infection (3).There are other Brucella species that are also relevant pathogens; however, their infective strategies remain unclear and are not in tune with the solid results accepted for the previously mentioned zoonotic brucellae. Among these are Brucella canis, the etiological agent of brucellosis in dogs and a zoonotic pathogen (7). This pathogen induces a subclinical infection that may remain undiagnosed for protracted periods (8-10). B. canis invades the conjunctiva or the oronasal system or penetrates through the venereal route. Then it is distributed to different organs...

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Proinflammatory Response of Human Osteoblastic Cell Lines and Osteoblast-Monocyte Interaction upon Infection withBrucellaspp

Cited by 66 publications

References 45 publications

Brucella abortus Induces the Secretion of Proinflammatory Mediators from Glial Cells Leading to Astrocyte Apoptosis

Brucella abortus Induces the Secretion of Proinflammatory Mediators from Glial Cells Leading to Astrocyte Apoptosis

Pathogenesis and Immunobiology of Brucellosis

Brucella canis Is an Intracellular Pathogen That Induces a Lower Proinflammatory Response than Smooth Zoonotic Counterparts

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