Cell‐to‐Cell Contact of Human Monocytes with Infected Arterial Smooth‐Muscle Cells Enhances Growth of<i>Chlamydia pneumoniae</i>

Puolakkainen, Mirja; Campbell, Lee Ann; Lin, Tsung-Han; Richards, Theresa S.; Patton, Dorothy L.; Kuo, Cho‐Chou

doi:10.1086/368267

Cited by 12 publications

(7 citation statements)

References 23 publications

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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: 45%

“…Subsequently, it was suggested that the infectivity-enhancing factor is identical with human insulin-like growth factor 2 (27). Using a different cellular system, a recent study demonstrated that human monocytes also enhance the growth of C. pneumoniae in arterial smooth muscle cells (28). In this case, cell to cell contact was required, and it was suggested that mannose 6-phosphate receptor expressed on monocytes is implicated in this process.…”

Section: Figure 5 Depletion Of Gr1mentioning

confidence: 99%

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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: 45%

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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“…This depletes the pathogen of viable host cells in the vicinity and, in turn, reduces microbial dissemination (84). Most interestingly, cell-to-cell contact increases Chlamydia spread during infection (85), suggesting that chlamydiae indeed use physical cell contacts for direct pathogen transmission. This is in line with our own observations that in epithelial cell cultures a significant amount of Chlamydia infection/spread (up to 25%) is mediated via physical cell-to-cell contact (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Chlamydia psittaci -Infected Dendritic Cells Communicate with NK Cells via Exosomes To Activate Antibacterial Immunity

et al. 2019

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Dendritic cells (DCs) and natural killer (NK) cells are critically involved in the early response against various bacterial microbes. Functional activation of infected DCs and NK cell-mediated gamma interferon (IFN-γ) secretion essentially contribute to the protective immunity against Chlamydia. How DCs and NK cells cooperate during the antichlamydial response is not fully understood. Therefore, in the present study, we investigated the functional interplay between Chlamydia-infected DCs and NK cells. Our biochemical and cell biological experiments show that Chlamydia psittaci-infected DCs display enhanced exosome release. We find that such extracellular vesicles (referred to as dexosomes) do not contain infectious bacterial material but strongly induce IFN-γ production by NK cells. This directly affects C. psittaci growth in infected target cells. Furthermore, NK cell-released IFN-γ in cooperation with tumor necrosis factor alpha (TNF-α) and/or dexosomes augments apoptosis of both noninfected and infected epithelial cells. Thus, the combined effect of dexosomes and proinflammatory cytokines restricts C. psittaci growth and attenuates bacterial subversion of apoptotic host cell death. In conclusion, this provides new insights into the functional cooperation between DCs, dexosomes, and NK cells in the early steps of antichlamydial defense.

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“…53,54,55 Thus, both IL-6 and MCP-1 through autocrine or paracrine actions may additionally stimulate the Cpn effects beyond that which was observed in the present set of experiments. The addition of monocytes to the system could further enhance this effect, as coculturing of monocytes and vascular smooth muscle cells alone cannot only enhance the growth of C. pneumoniae 56 but also stimulate the production of IL-6 and MCP-1. 57 These data do not dispute the importance of a host immune response as an essential contributor to the overall atherosclerotic plaque development process.…”

Section: Discussionmentioning

confidence: 99%

Chlamydophila pneumoniae Infection Leads to Smooth Muscle Cell Proliferation and Thickening in the Coronary Artery without Contributions from a Host Immune Response

Deniset

Cheung

Dibrov

et al. 2010

The American Journal of Pathology

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Chlamydophila pneumonia (C. pneumonia) infection has been associated with the progression of atherosclerosis. It remains unclear, however, whether C. pneumoniae in the absence of an immune response can alone initiate atherogenic events within a complex vessel environment. Left anterior descending coronary arteries isolated from porcine hearts were dissected and placed in culture medium for 72 hours before infection with C. pneumoniae. C. pneumoniae replicated within the arterial wall for the duration of the experiment (up to 10 days). A significant increase in chlamydial-HSP60 protein expression from day 2 to 10 post-infection (pi) indicated the presence of metabolically active C. pneumonia within infected vessels. Significant arterial thickening in infected coronary segments was observed by a considerable decrease in the ratio of lumen to total vessel area (48 ؎ 3% at day 4 pi versus 23 ؎ 3% at day 10 pi) and a significant increase in the ratio of media to luminal area (113 ؎ 16% at day 4 pi versus 365 ؎ 65% at day 10 pi). Structural changes were accompanied by an up-regulation of host HSP60 and proliferating cell nuclear antigen expression levels. Immunohistochemical staining confirmed proliferating cell nuclear antigen expression to be primarily localized within smooth muscle cells of the medial area. These results demonstrate that C. pneumoniae infection can stimulate arterial thickening in a complex vessel environment without the presence of a host immune response and further supports the involvement of HSP60 in this action.

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Cell‐to‐Cell Contact of Human Monocytes with Infected Arterial Smooth‐Muscle Cells Enhances Growth ofChlamydia pneumoniae

Cited by 12 publications

References 23 publications

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

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

Chlamydia psittaci -Infected Dendritic Cells Communicate with NK Cells via Exosomes To Activate Antibacterial Immunity

Chlamydophila pneumoniae Infection Leads to Smooth Muscle Cell Proliferation and Thickening in the Coronary Artery without Contributions from a Host Immune Response

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