Chlamydia trachomatis and chlamydia pneumoniae bind specifically to phosphatidylethanolamine in HeLa cells and to galnacβ1-4galβ1-4glc sequences found in asialo-GM1 and asialo-GM2

1991 ◽  
Vol 175 (3) ◽  
pp. 1082-1089 ◽  
Author(s):  
H.C. Krivan ◽  
B. Nilsson ◽  
C.A. Lingwood ◽  
H. Ryu
1998 ◽  
Vol 66 (4) ◽  
pp. 1607-1612 ◽  
Author(s):  
Albertina F. Swanson ◽  
R. Alan B. Ezekowitz ◽  
Amy Lee ◽  
Cho-chou Kuo

ABSTRACT The role that collectin (mannose-binding protein) may play in the host’s defense against chlamydial infection was investigated. Recombinant human mannose-binding protein was used in the inhibition of cell culture infection by Chlamydia trachomatis(C/TW-3/OT, E/UW-5/Cx, and L2/434/Bu), Chlamydia pneumoniae (AR-39), and Chlamydia psittaci (6BC). Mannose-binding protein (MBP) inhibited infection of all chlamydial strains by at least 50% at 0.098 μg/ml for TW-3 and UW-5, and at 6.25 μg/ml for 434, AR-39, and 6BC. The ability of MBP to inhibit infection with strain L2 was not affected by supplementation with complement or addition of an L2-specific neutralizing monoclonal antibody. Enzyme-linked immunosorbent assay and dot blot analyses showed MBP bound to the surface of the organism to exert inhibition, which appeared to block the attachment of radiolabeled organisms to HeLa cells. Immunoblotting and affinity chromatography indicated that MBP binds to the 40-kDa glycoprotein (the major outer membrane protein) on the outer surface of the chlamydial elementary body. Hapten inhibition assays with monosaccharides and defined oligosaccharides showed that the inhibitory effects of MBP were abrogated by mannose or high-mannose type oligomannose-oligosaccharide. The latter carbohydrate is the ligand of the 40-kDa glycoprotein ofC. trachomatis L2, which is known to mediate attachment, suggesting that the MBP binds to high mannose moieties on the surface of chlamydial organisms. These results suggest that MBP plays a role in first-line host defense against chlamydial infection in humans.


2019 ◽  
Vol 21 (4) ◽  
Author(s):  
Michaela Ohmer ◽  
Tina Tzivelekidis ◽  
Nora Niedenführ ◽  
Larisa Volceanov‐Hahn ◽  
Svenja Barth ◽  
...  

2012 ◽  
Vol 12 (1) ◽  
pp. 176 ◽  
Author(s):  
Cassandra J Wasson ◽  
Jessica L Zourelias ◽  
Nathan A Aardsma ◽  
Janis T Eells ◽  
Mike T Ganger ◽  
...  

2001 ◽  
Vol 69 (11) ◽  
pp. 7121-7129 ◽  
Author(s):  
Silke F. Fischer ◽  
Claudia Schwarz ◽  
Juliane Vier ◽  
Georg Häcker

ABSTRACT Chlamydia pneumoniae is an obligate intracellular bacterium which frequently causes airway infection in humans and has been implicated in atherosclerosis. Here we show that infection withC. pneumoniae protects HeLa human epithelioid cells against apoptosis induced by external stimuli. In infected HeLa cells, apoptosis induced by staurosporine and CD95-death-receptor signaling was strongly reduced. Upon treatment with staurosporine, generation of effector caspase activity, processing of caspase-3 and caspase-9 and cytochrome c redistribution were all profoundly inhibited in cells infected with C. pneumoniae. Bacterial protein synthesis during early infection was required for this inhibition. Furthermore, cytochrome c-induced processing and activation of caspases were inhibited in cytosolic extracts from infected cells, suggesting that a C. pneumoniae-dependent antiapoptotic factor was generated in the cytosol upon infection. Infection with C. pneumoniaefailed to induce significant NF-κB activation in HeLa cells, indicating that no NF-κB-dependent cellular factors were involved in the protection against apoptosis. These results show that C. pneumoniae is capable of interfering with the host cell's apoptotic apparatus at probably at least two steps in signal transduction and might explain the propensity of these bacteria to cause chronic infections in humans.


2019 ◽  
Vol 77 (7) ◽  
Author(s):  
Yuanjun Liu ◽  
Chunmin Hu ◽  
Yina Sun ◽  
Haoqing Wu ◽  
Xiaojun Chen ◽  
...  

ABSTRACT Non-coding circular RNAs (circRNAs) have been shown to have important roles in many diseases; however, no study has indicated circRNAs are involved in Chlamydia trachomatis infection. In this study, we used circRNA microarray to measure the global circRNA expression profiles in HeLa cells with or without C. trachomatis serovar E (Ct.E) infection. CircRNA/miRNA/mRNA interactions were predicted and bioinformatics analyses were performed. The differentially expressed circRNAs were selected according to our criterion for validation by reverse-transcription and quantitative polymerase chain reaction (RT-qPCR). The mRNA microarray was used to detect the mRNA expression profiles after Ct.E infection. Among 853 differentially expressed circRNAs, 453 were upregulated and 400 were downregulated after Ct.E infection. Target miRNAs and miRNA-targeted mRNAs of these circRNAs were predicted. RT-qPCR analysis indicated hsa_circRNA_001226, hsa_circRNA_007046 and hsa_circRNA_400027 were elevated similar to those determined in the circRNA microarray analysis. The mRNA microarray results showed 915 genes were upregulated and 619 genes were downregulated after Ct.E infection. Thirty-four differentially expressed genes overlapped in the bioinformatics and mRNA microarray results. KEGG pathway analysis revealed several signaling pathways, including endocytosis, MAPK and PI3P-Akt signaling pathways, that were targeted by circRNAs may play important roles in Chlamydia infection. This study provides evidence that circRNAs in host cells are involved in the process of Chlamydia infection.


Pathology ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 76-78
Author(s):  
Cecilia C.L. Ngan ◽  
Ai-Ee Ling ◽  
Roy K.W. Chan

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Fangzhen Luo ◽  
Mingyi Shu ◽  
Silu Gong ◽  
Yating Wen ◽  
Bei He ◽  
...  

ABSTRACT Chlamydia trachomatis has evolved strategies to prevent host cell apoptosis to evade the host immune defense. However, the precise mechanisms of antiapoptotic activity of C. trachomatis still need to be clarified. Pgp3, one of eight plasmid proteins of C. trachomatis, has been identified to be closely associated with chlamydial virulence. In this study, we attempted to explore the effects and the mechanisms of Pgp3 protein on apoptosis in HeLa cells; the results showed that Pgp3 increased Bcl-2/Bax ratio and prevented caspase-3 activation to suppress apoptosis induced by TNF-α and cycloheximide (CHX) through ERK1/2 pathway activation. Downregulation of DJ-1 with siRNA-DJ-1(si-DJ-1) reduced ERK1/2 phosphorylation and elevated apoptotic rate significantly in Pgp3-HeLa cells. However, inhibition of ERK1/2 signal pathway with ERK inhibitor PD98059 had little effect on DJ-1 expression. These findings confirm that plasmid protein Pgp3 contributes to apoptosis resistance through ERK1/2 signal pathway mediated by upregulation of DJ-1 expression. Therefore, the present study provided novel insights into the role of Pgp3 in apoptosis and suggested that manipulation of the host apoptosis response could be a new approach for the prevention and treatment of C. trachomatis infection.


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