Evidence of Bacteroides fragilis Protection from Bartonella henselae-Induced Damage (original) (raw)
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Frontiers in Microbiology, 2016
Bartonella henselae is a gram-negative facultative intracellular bacterium and is the causative agent of cat-scratch disease. Our previous data have established that Bacteroides fragilis colonization is able to prevent B. henselae damages through the polysaccharide A (PSA) in an experimental murine model. In order to determine whether the PSA is essential for the protection against pathogenic effects of B. henselae in immunocompromised hosts, SCID mice were co-infected with B. fragilis wild type or its mutant B. fragilis PSA and the effects of infection on murine tissues have been observed by High-Frequency Ultrasound (HFUS), histopathological examination, and Transmission Electron Microscopy (TEM). For the first time, echostructure, hepatic lobes length, vascular alterations, and indirect signs of hepatic dysfunctions, routinely used as signs of disease in humans, have been analyzed in an immunocompromised murine model. Our findings showed echostructural alterations in all infected mice compared with the Phosphate Buffer Solution (PBS) control group; further, those infected with B. henselae and co-infected with B. henselae/B. fragilis PSA presented the major echostructural alterations. Half of the mice infected with B. henselae and all those coinfected with B. henselae/B. fragilis PSA have showed an altered hepatic echogenicity compared with the renal cortex. The echogenicity score of co-infected mice with B. henselae/B. fragilis PSA differed significantly compared with the PBS control group (p < 0.05). Moreover the inflammation score of the histopathological evaluation was fairly concordant with ultrasound findings. Ultrastructural analysis performed by TEM revealed no significant alterations in liver samples of SCID mice infected with B. fragilis wild type while those infected with B. fragilis PSA showed the presence of collagen around the main vessels compared with the PBS control group. The liver samples of mice infected with B. henselae showed macro-areas rich in collagen, stellate cells, and histiocytic cells. Interestingly, our data demonstrated that immunocompromised SCID
Annals of the New York Academy of Sciences, 2005
Bartonella are the only bacteria known to induce angioproliferative lesions of the human vasculature and liver during infection. Previous work from our lab suggests that GroEL participates in the mitogenic response observed in HUVEC cultures supplemented with the soluble fraction of Bartonella bacilliformis. Work in this study shows that exposure to high concentrations of the fraction is actually cytotoxic for HUVECs. To analyze this phenomenon, live B. bacillformis-HUVEC cocultures were employed to study the effect of excess bacterial GroEL on the host cell during active infection. Four B. bacilliformis strains were generated to produce varying levels of GroEL. HUVEC co-cultures with LSS100, a strain that synthesizes markedly greater quantities of GroEL relative to others, significantly accelerates apoptosis of the co-cultured HUVECs relative to other strains. Acceleration of apoptosis can be inhibited by Z-VAD-FMK, a pan-caspase inhibitor. Time course data show that at 18 h of infection, both LSS100 and control strains significantly inhibit spontaneous apoptosis of co-cultured HUVECs, as previously reported for other Bartonella species. However, by 48 h LSS100 significantly increases apoptosis of the host cell. We hypothesize that intracellular Bartonella GroEL functions as an HSP60 analog, a eukaryotic orthologue known to accelerate procaspase 3 activation by enhancing its vulnerability to upstream activator caspases. These data suggest another strategy whereby Bartonella may regulate host cell growth.
The Role of the Host Immune Response in Pathogenesis ofBartonella henselae
DNA and Cell Biology, 2003
Bartonella henselae can infect humans resulting in a wide range of disease syndromes including cat-scratch disease, fever with bacteremia, endocarditis, bacillary angiomatosis, and bacillary peliosis hepatis, among others. The nature and severity of the clinical presentation correlates well with the status of the hosts' immune system. Individuals with impaired immune function, including HIV infection, progress to systemic infections more often. Patients with intact immune function who become infected with B. henselae usually get cat-scratch disease, a disease that usually involves lymphadenopathy resulting from a strong cellular immune response to the bacterium. However, immunocompromised patients often progress to bacillary angiomatosis or bacillary peliosis hepatis. The reduced ability of the hosts immune response to control bacterial infection apparently results in a bacteremia of longer duration, and in some patients the presence of angiogenic lesions that are unique among bacterial infections to Bartonella. Recently, the role of immune effector cells that produce angiogenic cytokines upon stimulation with B. henselae has been proposed. Here, the current status of the role of the immune response in both controlling infection and in B. henselae-triggered immunopathogenesis is presented.
Infection and Immunity, 2001
Bartonella henselae is the causative agent of cat scratch disease (CSD), a self-limiting condition characterized by a subacute regional lymphadenopathy that may develop into disseminated bartonellosis in immunocompromised subjects. Mice experimentally infected with B. henselae display typical liver and spleen granulomas rich in T cells and macrophages. So far there are no data on the interaction between bartonellae and macrophages. In order to clarify this topic, we investigated the interaction of B. henselae with J774, a mouse macrophage cell line. Analysis of bacterial uptake by functional assays and transmission electron microscopy indicates that bartonellae can enter and survive inside J774. Entry occurred within 30 min postinfection and reached a plateau at 160 min. Infection of J774 was followed by a dose-dependent release of the proinflammatory cytokines tumor necrosis factor alpha, interleukin 1 (IL-1), and IL-6. Bartonellae persisted intracellularly without loss of viability for at least 8 h, and their number slightly decreased 24 h postinfection.
2000
results in intraerythrocytic presence of B henselae Infection of human CD34+ progenitor cells with Bartonella henselae http://bloodjournal.hematologylibrary.org/content/106/4/1215.full.html Updated information and services can be found at: (1174 articles) Red Cells (3132 articles) Hematopoiesis and Stem Cells Articles on similar topics can be found in the following Blood collections http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub\_requests
Diagnostic Microbiology and Infectious Disease, 2003
Bartonella quintana is an epicellular bacterium, which in vivo as well as in vitro, invades endothelial cells and develops within them inducing proliferative effects that play a pivotal role in neovascular manifestation of this disease. We investigated the effect of live Bartonella quintana and its LPS on apoptosis and inflammatory response in HUVEC-C, an endothelial cell line. The kinetics of the programmed cell death of Bartonella quintana-infected HUVEC-C showed a peculiar course. Even if early during infection apoptosis reached a peak after 6 h, later on apoptosis was inhibited. Such apoptosis inhibition was not observed during Bartonella quintana lipopolysaccharide treatment because LPS-stimulated HUVEC-C did progress to cell death. Evaluation of multiple cell signal transduction pathways revealed an overexpression of Apaf 1 and caspase 8 in HUVEC-C after 2 h of infection, and of bcl-2 starting from 10 h post Bartonella quintana infection. Moreover, Bartonella quintana and its LPS showed a different effect on the activation of genes involved in inflammatory response as revealed by molecular analysis of host cells. Bartonella quintana appears to be able to inhibit programmed cell death, inducing intracellular signals leading to survival and proliferation through the bcl-2 gene, despite the early increase of inflammatory status induced in endothelial cells. This mechanism, together with a poor endotoxin ability to stimulate strong inflammatory response, could contribute to the capability of the bacteria to persist intracellularly, causing chronic disease and producing neovascular manifestations.
BALB/c Mice resist infection with Bartonella bacilliformis
BMC Research Notes, 2008
Background: Bartonellosis due to Bartonella bacilliformis is a highly lethal endemic and sometimes epidemic infectious disease in South America, and a serious public health concern in Perú. There is limited information on the immunologic response to B. bacilliformis infection. The objective of this research was to produce experimental infection of BALB/c mice to B. bacilliformis inoculation.
Infection and …, 2005
Bacillary angiomatosis (BA), one of the many clinical manifestations resulting from infection with the facultative intracellular bacterium Bartonella henselae, is characterized by angiogenic lesions. Macrophages have been identified as important effector cells contributing to the angiogenic process during B. henselae infection by infiltrating BA lesions and secreting vascular endothelial growth factor. Monocyte-macrophage chemoattractant protein 1 (MCP-1) recruits macrophages to sites of inflammation. In this study, we investigated the ability of B. henselae to upregulate MCP-1 gene expression and protein production in the human microvascular endothelial cell line HMEC-1. MCP-1 mRNA was induced at 6 and 24 h after treatment with bacteria, whereas protein production was elevated at 6, 24, and 48 h. This induction was not dependent on the presence of bacterial lipopolysaccharide or endothelial cell toll-like receptor 4. However, MCP-1 production was dependent on NF-B activity. Outer membrane proteins of low molecular weight were able to upregulate MCP-1 production. Furthermore, supernatants from B. henselae-infected HMEC-1 were able to induce chemotaxis of THP-1 monocytes. These data suggest a mechanism by which the macrophage effector cell is recruited to the endothelium during B. henselae infection and then contributes to bacterial-induced angiogenesis.
Infection and Immunity, 2001
The endothelium is a specific target for Bartonella henselae, and endothelial cell infection represents an important step in the pathogenesis of cat scratch disease and bacillary angiomatosis. Mechanisms of Bartonella-endothelial cell interaction as well as signaling pathways involved in target cell activation were analyzed. B. henselae strain Berlin-1, isolated from bacillary angiomatosis lesions of a human immunodeficiency virus-infected patient, potently stimulated human umbilical cord vein endothelial cells (HUVEC), as determined by NF-B activation and enhanced adhesion molecule expression. These effects were accompanied by increased PMN rolling on and adhesion to infected endothelial cell monolayers, as measured in a parallel-plate flow chamber assay. Monoclonal antibodies against E-selectin significantly reduced PMN rolling and adhesion. In our hands, B. henselae Berlin-1 was substantially more active than the typing strain B. henselae ATCC 49882.
Analysis of Bartonella Adhesin A Expression Reveals Differences between Various B. henselae Strains
Infection and Immunity, 2007
Bartonella henselae causes cat scratch disease and the vasculoproliferative disorders bacillary angiomatosis and peliosis hepatis in humans. One of the best known pathogenicity factors of B. henselae is Bartonella adhesin A (BadA), which is modularly constructed, consisting of head, neck/stalk, and membrane anchor domains. BadA is important for the adhesion of B. henselae to extracellular-matrix proteins and endothelial cells (ECs).