Identification of a streptococcal octapeptide motif involved in acute rheumatic fever

被引:47
作者
Dinkla, Katrin
Nitsche-Schmitz, D. Patric
Barroso, Vanessa
Reissmann, Silvana
Johansson, Helena M.
Frick, Inga-Maria
Rohde, Manfred
Chhatwal, Gursharan S.
机构
[1] Helmholtz Ctr Infect Res, Dept Microbial Pathogenesis, D-38124 Braunschweig, Germany
[2] Lund Univ, Dept Clin Sci, S-22184 Lund, Sweden
关键词
D O I
10.1074/jbc.M701047200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Acute rheumatic fever is a serious autoimmune sequela of pharyngitis caused by certain group A streptococci. One mechanism applied by streptococcal strains capable of causing acute rheumatic fever is formation of an autoantigenic complex with human collagen IV. In some geographic regions with a high incidence of acute rheumatic fever pharyngeal carriage of group C and group G streptococci prevails. Examination of such strains revealed the presence of M-like surface proteins that bind human collagen. Using a peptide array and recombinant proteins with targeted amino acid substitutions, we could demonstrate that formation of collagen complexes during streptococcal infections depends on an octapeptide motif, which is present in collagen binding M and M-like proteins of different beta-hemolytic streptococcal species. Mice immunized with streptococcal proteins that contain the collagen binding octapeptide motif developed high serum titers of anti-collagen antibodies. In sera of rheumatic fever patients such a collagen autoimmune response was accompanied by specific reactivity against the collagen-binding proteins, linking the observed effect to clinical cases. Taken together, the data demonstrate that the identified octapeptide motif through its action on collagen plays a crucial role in the pathogenesis of rheumatic fever. Eradication of streptococci that express proteins with the collagen binding motif appears advisable for controlling rheumatic fever.
引用
收藏
页码:18686 / 18693
页数:8
相关论文
共 37 条
[1]
Increased endothelial cell expression of α3β1 integrin in cardiac valvulopathy in the primary (Hughes) and secondary antiphospholipid syndrome [J].
Afek, A ;
Shoenfeld, Y ;
Manor, R ;
Goldberg, I ;
Ziporen, L ;
George, J ;
Polak-Charcon, S ;
Amigo, MC ;
Garcia-Torres, R ;
Segal, R ;
Kopolovic, J .
LUPUS, 1999, 8 (07) :502-507
[2]
Ahmed J, 2003, Bangladesh Med Res Counc Bull, V29, P113
[3]
[Anonymous], 2004, WHO TECHN REP SER
[4]
[Anonymous], GRAM POSITIVE PATHOG
[5]
Molecular basis of group A streptococcal virulence [J].
Bisno, AL ;
Brito, MO ;
Collins, CM .
LANCET INFECTIOUS DISEASES, 2003, 3 (04) :191-200
[6]
GROUP-A STREPTOCOCCAL INFECTIONS AND ACUTE RHEUMATIC-FEVER [J].
BISNO, AL .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (11) :783-793
[7]
Acute rheumatic fever [J].
Carapetis, JR ;
McDonald, M ;
Wilson, NJ .
LANCET, 2005, 366 (9480) :155-168
[8]
Carapetis JR, 1997, ADV EXP MED BIOL, V418, P233
[9]
Pathogenesis of group A streptococcal infections [J].
Cunningham, MW .
CLINICAL MICROBIOLOGY REVIEWS, 2000, 13 (03) :470-+
[10]
CUNNINGHAM MW, 1989, J IMMUNOL, V143, P2677