Lipid rafts, caveolae, caveolin-1, and entry by Chlamydiae into host cells

Stuart, Elizabeth S.; Webley, Wilmore C.; Norkin, Leonard C.

doi:10.1016/s0014-4827(03)00059-4

Cited by 96 publications

(95 citation statements)

References 34 publications

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“…1A and D) while serovar E EB attachment/entry was rather patchy and clustered throughout both HEC-1B and HeLa cell monolayers [13], a pattern reminiscent of chlamydial attachment to apical surfaces of polarized primary human and pig genital epithelial cells cultured ex vivo [15,18]. This intriguing difference between strains may possibly be due to the recognition of and binding to different receptor molecules on host cell surfaces that, for serovar E, may be enriched or clustered in some regions or microdomains of polarized epithelial cell apical membranes, such as lipid rafts or caveolae, proposed to be involved in serovar E but not in serovar L2 entry [19,20]. Although their role in chlamydial entry is still controversial [21][22][23], it is an interesting possibility, as many pathogens are known to interact with these membrane microdomains and that receptor molecules, such as membrane-associated estrogen receptors that locate to caveolae, have been implicated in serovar E attachment/entry [11,24].…”

Section: Discussionmentioning

confidence: 99%

Comparison of Chlamydia trachomatis serovar L2 growth in polarized genital epithelial cells grown in three-dimensional culture with non-polarized cells

Dessus-Babus

Moore

Whittimore

et al. 2008

Microbes and Infection

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A common model for studying Chlamydia trachomatis and growing chlamydial stocks uses Lymphogranuloma venereum serovar L2 and non-polarized HeLa cells. However, recent publications indicate that the growth rate and progeny yields can vary considerably for a particular strain depending on the cell line/type used, and seem to be partially related to cell tropism. In the present study, the growth of invasive serovar L2 was compared in endometrial HEC-1B and endocervical HeLa cells polarized on collagen-coated microcarrier beads, as well as in HeLa cells grown in tissue culture flasks. Microscopy analysis revealed no difference in chlamydial attachment/ entry patterns or in inclusion development throughout the developmental cycle between cell lines. Very comparable growth curves in both cell lines were also found using real-time PCR analysis, with increases in chlamydial DNA content of 400-500-fold between 2 and 36 h post-inoculation. Similar progeny yields with comparable infectivity were recovered from HEC-1B and HeLa cell bead cultures, and no difference in chlamydial growth was found in polarized vs. non-polarized HeLa cells. In conclusion, unlike other C. trachomatis strains such as urogenital serovar E, invasive serovar L2 grows equally well in physiologically different endometrial and endocervical environments, regardless of the host cell polarization state.

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Section: Discussionmentioning

confidence: 99%

Comparison of Chlamydia trachomatis serovar L2 growth in polarized genital epithelial cells grown in three-dimensional culture with non-polarized cells

Dessus-Babus

Moore

Whittimore

et al. 2008

Microbes and Infection

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“…MRI is emerging as a powerful tool for cell tracking via paramagnetic and superparamagnetic cell labeling (27)(28)(29)(30)(31)(32)(33)(34). Superparamagnetic iron oxide (SPIO) particles have been used both clinically (28) and in research studies of various biological processes, such as the detection of stem cells, tumor cells, and tumor-associated macrophages; migration and homing of stem cells to bone marrow, lymphocytes in the liver, spleen, and pancreas; and detection of T-cells and THP-1 phagocytes (29 -33).…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism of contrast material internalization into fibroblasts was evaluated by the addition of nystatin to the labeling media. Nystatin, a general inhibitor of caveolaemediated endocytosis, is known to precipitate cholesterol in the plasma membrane of the cell, thereby disrupting caveolae function (27). Fibroblasts were labeled with biotin-BSA-GdDTPA (48 hr, 10 mg/ml) with or without the addition of nystatin (50 M).…”

Section: Caveolae-mediated Internalization Of Biotin-bsa-gddtpamentioning

confidence: 99%

Labeling fibroblasts with biotin‐BSA‐GdDTPA‐FAM for tracking of tumor‐associated stroma by fluorescence and MR imaging

Granot¹,

Kunz-Schughart

Neeman

2005

Magnetic Resonance in Med

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Fibroblasts at the tumor-host interface can differentiate into myofibroblasts and pericytes, and contribute to the guidance and stabilization of endothelial sprouts. After intravenous administration of biotin-BSA-GdDTPA-FAM in mice with subcutaneous MLS human ovarian carcinoma tumors, the distribution of the macromolecular MRI/optical contrast material was confined to blood vessels in normal tissues, while it co-registered with ␣SMA-positive stroma tracks within the tumor. These ␣SMA-positive tumor-associated myofibroblasts and pericytes showed uptake of the contrast material into intracellular granules. We evaluated the use of this contrast material for in vitro labeling of tumor fibroblasts as an approach for tracking their involvement in angiogenesis. Fluorescence microscopy demonstrated internalization of the contrast material, and MRI revealed a significant increase in the R 1 relaxation rate of labeled fibroblasts. R 1 not only remained elevated for 2 weeks in culture, it also increased with cell proliferation, indicating prolonged retention of the contrast material and subsequent intracellular processing and redistribution of the material, and thereby enhancing MR contrast. Moreover, cells that were labeled ex vivo with MR contrast material and co-inoculated with tumor cells in mice were detected in vivo by MRI. Uptake of the contrast material was suppressed by nystatin, suggesting internalization by caveolae-mediated endocytosis. This study shows that labeling of fibroblasts with biotin-BSA-GdDTPA-FAM is feasible and would allow noninvasive in vivo tracking of fibroblasts during tumor angiogenesis and vessel maturation. Magn Reson Med 54:789 -797, 2005.

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“…The actin rearrangements that occur during entry are transient and may be terminated by secreted chlamydial effectors such as CT166, which glucosylates Rac1 (Thalmann et al 2010), or CT694, which interacts and colocalizes with AHNAK, an actin-binding protein (Hower et al 2009). Additional host factors that contribute to uptake into nonphagocytic cells include clathrin (Boleti et al 1999;Hybiske and Stephens 2007a) and cholesterol-rich microdomains (Norkin et al 2001;Jutras et al 2003;Stuart et al 2003;Gabel et al 2004). …”

Section: Mechanisms Of Chlamydia Invasion Of Epithelial Cellsmentioning

confidence: 99%

Chlamydial Intracellular Survival Strategies

Bastidas

Elwell

Engel

et al. 2013

Cold Spring Harbor Perspectives in Medicine

202

197

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Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen and the causative agent of blinding trachoma. Although Chlamydia is protected from humoral immune responses by residing within remodeled intracellular vacuoles, it still must contend with multilayered intracellular innate immune defenses deployed by its host while scavenging for nutrients. Here we provide an overview of Chlamydia biology and highlight recent findings detailing how this vacuole-bound pathogen manipulates host -cellular functions to invade host cells and maintain a replicative niche.

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Lipid rafts, caveolae, caveolin-1, and entry by Chlamydiae into host cells

Cited by 96 publications

References 34 publications

Comparison of Chlamydia trachomatis serovar L2 growth in polarized genital epithelial cells grown in three-dimensional culture with non-polarized cells

Comparison of Chlamydia trachomatis serovar L2 growth in polarized genital epithelial cells grown in three-dimensional culture with non-polarized cells

Labeling fibroblasts with biotin‐BSA‐GdDTPA‐FAM for tracking of tumor‐associated stroma by fluorescence and MR imaging

Chlamydial Intracellular Survival Strategies

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