Monocyte–Endothelial Cell Coculture Enhances Infection of Endothelial Cells with<i>Chlamydia pneumoniae</i>

Lin, Tsung-Han; Campbell, Lee Ann; Rosenfeld, Michael E.; Kuo, Cho‐Chou

doi:10.1086/315349

Cited by 35 publications

(24 citation statements)

References 29 publications

(30 reference statements)

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“…As discussed above, the human monocyte-like cell U937 was able to amplify chlamydial replication in smooth muscle and epithelial cells (26,28). In our experiments, the GR1 Ϫ /CD11b ϩ cell population, which may include monocytes/macrophages, also weakly amplified chlamydial replication, although the differences were not statistically significant.…”

Section: Figure 5 Depletion Of Gr1supporting

confidence: 44%

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Polymorphonuclear Neutrophils Improve Replication ofChlamydia pneumoniaeIn Vivo upon MyD88-Dependent Attraction

Rodríguez

Fend

Jennen

et al. 2005

The Journal of Immunology

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Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. In this study, we show that GR1+/CD45+ polymorphonuclear neutrophils (PMN) surprisingly increase the bacterial load of C. pneumoniae in vivo. Upon intranasal infection of wild-type mice, the lung weight is increased; the cytokines TNF, IL-12p40, and IFN-γ, as well as the chemokines keratinocyte-derived chemokine, MCP-1, and MIP-2 are secreted; and GR1+/CD45+ PMN are recruited into lungs 3 days postinfection. In contrast, in infected MyD88-deficient mice, which lack a key adaptor molecule in the signaling cascade of TLRs and IL-1R family members, the increase of the lung weight is attenuated, and from the analyzed cyto- and chemokines, only IL-12p40 is detectable. Upon infection, almost no influx of inflammatory cells into lungs of MyD88-deficient mice can be observed. Six days postinfection, however, MyD88-deficient mice were able to produce TNF, IFN-γ, keratinocyte-derived chemokine, and MCP-1 in amounts similar to wild-type mice, but failed to secrete IL-12p40 and MIP-2. At this time point, the infection increased the lung weight to a level similar to wild-type mice. Curiously, the chlamydial burden in MyD88-deficient mice 3 days postinfection is lower than in wild-type mice, a finding that can be reproduced in wild-type mice by depletion of GR1+ cells. In analyzing how PMN influence the chlamydial burden in vivo, we find that PMN are infected and enhance the replication of C. pneumoniae in epithelial cells. Thus, the lower chlamydial burden in MyD88-deficient mice can be explained by the failure to recruit PMN.

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Section: Figure 5 Depletion Of Gr1supporting

confidence: 44%

“…A similar function has been reported for the monocyte-like cell U937. Thus, coculture of U937 cells with human endothelial cells enhanced the infection of the latter cells by C. pneumoniae (26). Subsequently, it was suggested that the infectivity-enhancing factor is identical with human insulin-like growth factor 2 (27).…”

Section: Figure 5 Depletion Of Gr1mentioning

confidence: 99%

Polymorphonuclear Neutrophils Improve Replication ofChlamydia pneumoniaeIn Vivo upon MyD88-Dependent Attraction

Rodríguez

Fend

Jennen

et al. 2005

The Journal of Immunology

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“…Pathology studies have detected the organism within atherosclerotic lesions but not in adjacent normal tissue by immunohistochemistry, PCR, and electron microscopy (19), and the pathogen has been isolated from atherosclerotic lesions and propagated in vitro (4,19,27). Cell biology studies have suggested that the organism can be detected in circulating leukocytes, has the capacity to infect all atheroma cell types (13,28,34), and can induce the expression of inflammatory cytokines, procoagulants, matrix metalloproteinase, and adhesion molecules (8,9,12). Animal model studies have shown that C. pneumoniae can cause arterial inflammation in normolipidemic mice and rabbits and initiate lesion development or contribute to exacerbation of lesions in rabbits or mice, respectively (29,33).…”

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confidence: 99%

Chlamydia pneumoniae -Induced Macrophage Foam Cell Formation Is Mediated by Toll-Like Receptor 2

et al. 2007

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“…Previous studies from our laboratory have shown that Chlamydia trachomatis MOMP is glycosylated and contains N-linked high-mannose-type oligosaccharides (16). Also, the mannose residues in the glycan have been shown to mediate internalization, as C. trachomatis can utilize the mannose receptor to enter and establish productive infection in mouse macrophages, while C. pneumoniae appears to use a receptors(s) other than the mannose receptor (15).Recently, a monocyte-derived soluble factor, insulin-like growth factor 2 (IGF2), was shown to enhance infection of endothelial cells by C. pneumoniae, but not C. trachomatis, suggesting involvement of an IGF2 receptor in C. pneumoniae infection (18,19). The IGF2 receptor also binds mannose 6-phosphate (M6P) and is called the M6P/IGF2 receptor (23).…”

mentioning

confidence: 99%

“…Recently, a monocyte-derived soluble factor, insulin-like growth factor 2 (IGF2), was shown to enhance infection of endothelial cells by C. pneumoniae, but not C. trachomatis, suggesting involvement of an IGF2 receptor in C. pneumoniae infection (18,19). The IGF2 receptor also binds mannose 6-phosphate (M6P) and is called the M6P/IGF2 receptor (23).…”

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confidence: 99%

Chlamydia pneumoniae Uses the Mannose 6-Phosphate/Insulin-Like Growth Factor 2 Receptor for Infection of Endothelial Cells

2005

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Several mechanisms for attachment and entry of Chlamydia have been proposed. We previously determined that the major outer membrane protein of Chlamydia trachomatis is glycosylated with a high-mannose oligosaccharide, and a similar structure inhibited the attachment and infectivity of C. trachomatis in epithelial cells. Because insulin-like growth factor 2 (IGF2) was shown to enhance the infectivity of Chlamydia pneumoniae but not C. trachomatis in endothelial cells, a hapten inhibition assay was used to analyze whether the mannose 6-phosphate (M6P)/IGF2 receptor that also binds M6P could be involved in infection of endothelial cells (HMEC-1) by Chlamydia. M6P and mannose 6-phosphate-poly[N-(2-hydroxyethyl)-acrylamide] (M6P-PAA) inhibited the infectivity of C. pneumoniae AR-39, but not C. trachomatis serovar UW5 or L2, while mannan inhibited the growth of C. trachomatis, but not C. pneumoniae. Using metabolically labeled organisms incubated with cells at 4°C (organisms attach but do not enter) or at 37°C (organisms attach and are internalized), M6P-PAA was shown to inhibit attachment and internalization of C. pneumoniae in endothelial cells but did not inhibit attachment or internalization of C. trachomatis serovar E or L2. These findings indicate that C. pneumoniae can utilize the M6P/IGF2 receptor and that the use of this receptor for attachment and entry differs between C. pneumoniae and C. trachomatis.Chlamydia pneumoniae is an intracellular bacterium that causes respiratory infections. C. pneumoniae infections can also become chronic, and chronic infections of the vasculature have been suggested to initiate and/or promote atherogenesis (4). Because chlamydiae multiply only within eukaryotic cells, internalization of the infectious chlamydial elementary bodies (EBs) and the avoidance of fusion of EB-containing phagosomes with cellular lysosomes are critical steps for establishment of infection. Chlamydiae appear to use several mechanisms to enter host cells, including receptor-mediated endocytosis in clathrin-coated pits, pinocytosis in non-clathrincoated pits, and phagocytosis (reviewed in reference 28). In general, EBs are rapidly internalized by eukaryotic cells, even nonprofessional phagocytes (3). Most likely there are multiple mechanisms for attachment and internalization, which may differ depending on the host cell type. However, the specific chlamydial structures and receptor molecules on eukaryotic cells that mediate chlamydial entry remain undefined.Several chlamydial ligands have been suggested to mediate attachment, including heparan sulfate, chlamydial hsp70, OmcB, and the major outer membrane protein (MOMP) (28). Previous studies from our laboratory have shown that Chlamydia trachomatis MOMP is glycosylated and contains N-linked high-mannose-type oligosaccharides (16). Also, the mannose residues in the glycan have been shown to mediate internalization, as C. trachomatis can utilize the mannose receptor to enter and establish productive infection in mouse macrophages, while C. pneumoniae appears...

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Monocyte–Endothelial Cell Coculture Enhances Infection of Endothelial Cells withChlamydia pneumoniae

Cited by 35 publications

References 29 publications

Polymorphonuclear Neutrophils Improve Replication ofChlamydia pneumoniaeIn Vivo upon MyD88-Dependent Attraction

Polymorphonuclear Neutrophils Improve Replication ofChlamydia pneumoniaeIn Vivo upon MyD88-Dependent Attraction

Chlamydia pneumoniae -Induced Macrophage Foam Cell Formation Is Mediated by Toll-Like Receptor 2

Chlamydia pneumoniae Uses the Mannose 6-Phosphate/Insulin-Like Growth Factor 2 Receptor for Infection of Endothelial Cells

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