| Full text | |
| Author(s): |
Silva, Aldacilene Souza
[1]
;
Castiblanco Valencia, Monica Marcela
[1]
;
Cianciarullo, Aurora Marques
[2]
;
Vasconcellos, Silvio Arruda
[3]
;
Barbosa, Angela Silva
[4]
;
Isaac, Lourdes
[1]
Total Authors: 6
|
| Affiliation: | [1] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, BR-05508900 Sao Paulo - Brazil
[2] Inst Butantan, Lab Genet, Sao Paulo - Brazil
[3] Univ Sao Paulo, Fac Med Vet & Zootecnia, BR-05508900 Sao Paulo - Brazil
[4] Inst Butantan, Lab Bacteriol, Sao Paulo - Brazil
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | FRONTIERS IN IMMUNOLOGY; v. 2, 2011. |
| Web of Science Citations: | 0 |
| Abstract | |
Leptospirosis is a zoonosis caused by pathogenic bacteria from the genus Leptospira. The disease represents a serious public health problem in underdeveloped tropical countries. Leptospires infect hosts through small abrasions in the skin or mucous membranes and they rapidly disseminate to target organs. The capacity of some pathogenic leptospiral strains to acquire the negative complement regulators factor H (FH) and C4b binding protein correlates with their ability to survive in human serum. In this study we assessed the functional consequences of the age macular degeneration-associated polymorphism FH His(402) or FH Tyr(402) on FH Leptospira interactions. In binding assays using sub-saturating amounts of FH, the FH Tyr(402) variant interacted with all the strains tested more strongly than the FH His(402) variant. At higher concentrations, differences tended to disappear. We then compared cofactor activities displayed by FH His(402) and FHTyr(402) bound to the surface of L. mterrogans. Both variants exhibit similar activity as cofactors for Factor I-mediated cleavage of C3b, thus indicating that they do not differ in their capacity to regulate the complement cascade. (AU) | |
| FAPESP's process: | 10/50043-0 - Complement system and pathogenicity of Leptospires: mechanisms of activation and evasion, identification of bacterial ligands, characterization of proteases and establishment of an in vivo murine model |
| Grantee: | Lourdes Isaac |
| Support Opportunities: | Research Projects - Thematic Grants |
| FAPESP's process: | 09/05979-0 - Inflammatory response and C5 dependent genetic expression in mouse liver injury |
| Grantee: | Lourdes Isaac |
| Support Opportunities: | Regular Research Grants |