scholarly journals Identification of the Gene Encoding the FhbB Protein of Treponema denticola, a Highly Unique Factor H-Like Protein 1 Binding Protein

2006 ◽  
Vol 75 (2) ◽  
pp. 1050-1054 ◽  
Author(s):  
John V. McDowell ◽  
Jesse Frederick ◽  
Lola Stamm ◽  
Richard T. Marconi

ABSTRACT The gene encoding the Treponema denticola factor H-like protein 1 (FHL-1) binding protein, FhbB, was recovered and characterized. Sequence conservation, expression, and properties of FhbB were analyzed. The identification of FhbB represents an important step in understanding the contribution of FHL-1 binding in T. denticola pathogenesis and in development of periodontal disease.

2004 ◽  
Vol 186 (9) ◽  
pp. 2612-2618 ◽  
Author(s):  
Kelley M. Hovis ◽  
John V. McDowell ◽  
LaToya Griffin ◽  
Richard T. Marconi

ABSTRACT In North America, tick-borne relapsing fever (TBRF) is caused by the spirochete species Borrelia hermsii, Borrelia parkeri, and Borrelia turicatae. We previously demonstrated that some isolates of B. hermsii and B. parkeri are capable of binding factor H and that cell-bound factor H can participate in the factor I-mediated cleavage of C3b. Isolates that bound factor H expressed a factor H-binding protein (FHBP) that we estimated to be approximately 19 to 20 kDa in size and thus, pending further characterization, temporarily designated FHBP19. Until this report, none of the FHBPs of the TBRF spirochetes had been characterized. Here we have recovered the gene encoding the FHBP of B. hermsii YOR from a lambda ZAP II library and determined its sequence. The gene encodes a full-length protein of 22.7 kDa, which after processing is predicted to be 20.5 kDa. This protein, which we redesignate factor H-binding protein A (FhbA), is unique to B. hermsii. Two-dimensional pulsed-field gel electrophoresis and hybridization analyses revealed that the B. hermsii gene encoding FhbA is a single genetic locus that maps to a linear plasmid of approximately 220 kb. The general properties of FhbA were also assessed. The protein was found to be surface exposed and lipidated. Analysis of the antibody response to FhbA in infected mice revealed that it is antigenic during infection, indicating expression during infection. The identification and characterization of FhbA provides further insight into the molecular mechanisms of pathogenesis of the relapsing fever spirochetes.


2007 ◽  
Vol 44 (1-3) ◽  
pp. 214
Author(s):  
John V. McDowell ◽  
Tania Saldon ◽  
David L. Gordon ◽  
Lola Stamm ◽  
Richard T. Marconi

2005 ◽  
Vol 73 (11) ◽  
pp. 7126-7132 ◽  
Author(s):  
John V. McDowell ◽  
Justin Lankford ◽  
Lola Stamm ◽  
Tania Sadlon ◽  
David L. Gordon ◽  
...  

ABSTRACT Treponema denticola is an important contributor to periodontal disease. In this study we investigated the ability of T. denticola to bind the complement regulatory proteins factor H and factor H-like protein 1 (FHL-1). The binding of these proteins has been demonstrated to facilitate evasion of the alternative complement cascade and/or to play a role in adherence and invasion. Here we demonstrate that T. denticola specifically binds FHL-1 via a 14-kDa, surface-exposed protein that we designated FhbB. Consistent with its FHL-1 binding specificity, FhbB binds only to factor H recombinant fragments spanning short consensus repeats (SCRs) 1 to 7 (H7 construct) and not to SCR constructs spanning SCRs 8 to 15 and 16 to 20. Binding of H7 to FhbB was inhibited by heparin. The specific involvement of SCR 7 in the interaction was demonstrated using an H7 mutant (H7AB) in which specific charged residues in SCR 7 were replaced by alanine. This construct lost FhbB binding ability. Analyses of the ability of FHL-1 bound to the surface of T. denticola to serve as a cofactor for factor I-mediated cleavage of C3b revealed that C3b is cleaved in an FHL-1/factor I-independent manner, perhaps by an unidentified protease. Based on the data presented here, we hypothesize that the primary function of FHL-1 binding by T. denticola might be to facilitate adherence to FHL-1 present on anchorage-dependent cells and in the extracellular matrix.


2012 ◽  
Vol 287 (16) ◽  
pp. 12715-12722 ◽  
Author(s):  
Daniel P. Miller ◽  
Jessica K. Bell ◽  
John V. McDowell ◽  
Daniel H. Conrad ◽  
John W. Burgner ◽  
...  

2018 ◽  
Vol 68 (12) ◽  
pp. 2853-2856 ◽  
Author(s):  
Igor Jelihovschi ◽  
Cristian Drochioi ◽  
Aida Corina Badescu ◽  
Raoul Vasile Lupusoru ◽  
Alexandra Elena Munteanu ◽  
...  

The diagnosis of periodontal disease is mainly based on use of clinical and radiographic evidence. In this study we employed a quantitative PCR analysis of Aggregatibacter actinomycetemcomitans and Treponema denticola as species strongly involved in periodontal diseases, burden in periodontal pockets to detect the main sampling factors that interfere with qPCR results. From 22 patients with advanced periodontal disease, subgingival plaque was comparatively collected by paper points and periodontal Gracey curettes. Samples were collected from the same situs in presence of gingival bleeding and absence of bleeding. The concordance and agreement of results between samples were assessed. The present study demonstrates that subgingival plaque sampling with sterile absorbable paper points is often accompanied by gingival bleeding resulting in quantification biases of periodontal pathogens.


1994 ◽  
Vol 269 (41) ◽  
pp. 25411-25418
Author(s):  
R Intres ◽  
S Goldflam ◽  
J R Cook ◽  
J W Crabb

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