scholarly journals Streptococcal cell wall arthritis. Passive transfer of disease with a T cell line and crossreactivity of streptococcal cell wall antigens with Mycobacterium tuberculosis.

1989 ◽  
Vol 170 (2) ◽  
pp. 369-382 ◽  
Author(s):  
S Q DeJoy ◽  
K M Ferguson ◽  
T M Sapp ◽  
J B Zabriskie ◽  
A L Oronsky ◽  
...  

Primary lymph node cells derived from streptococcal cell wall arthritic rats or those derived from adjuvant arthritic rats proliferated in response to cell wall antigens derived from either streptococcal cell walls or those from M. tuberculosis. In addition, two T cell lines have been isolated from lymph nodes of rats during the chronic phase of streptococcal cell wall arthritis. These T cell lines transfered clinical disease to naive syngeneic irradiated recipients, and they proliferated in the presence of cell wall antigens derived from streptococci or antigens derived from Mycobacterium but failed to proliferate in the presence of the 65-kD antigen (containing the sequence TFGLQLELT) derived from Mycobacterium. These observations indicate that T cells play a crucial role in the pathogenesis of streptococcal cell wall arthritis and suggest that antigenic crossreactivity exists between cell walls of group A streptococci and antigens derived from Mycobacterium. The 65-kD Mycobacterium protein is not involved in the observed antigenic crossreactivity.

1965 ◽  
Vol 122 (5) ◽  
pp. 877-890 ◽  
Author(s):  
Jiri Rotta ◽  
Thomas J. Prendergast ◽  
Walter W. Karakawa ◽  
Charles K. Harmon ◽  
Richard M. Krause

The streptococcal cell wall mucopeptide when injected into mice either intraperitoneally or intravenously enhances the resitance to subsequent challenge with virulent Group A streptococci. Rabbits which are injected intravenously with solubilized mucopeptide develop a fever response which has a resemblance to that achieved with endotoxin. Mice which survive 6 to 7 weeks after challenge with virulent Group A streptococci yield at autopsy search Group A streptococci serologically identical to the challenge organisms. A preparative dose of cell walls injected into mice prior to challenge diminished this late recovery of streptococci. Group A-variant streptococci were recovered from mice which survived challenge and carried the organisms for several weeks. Filterable bacterial forms, which grew on L form media, were recovered from infected mice. The serologic type of the L forms was identical to that of the challenge organisms.


1961 ◽  
Vol 114 (1) ◽  
pp. 127-140 ◽  
Author(s):  
Richard M. Krause ◽  
Maclyn McCarty

Lysis of trypsinized Group A streptococcal cell walls with phage-associated lysin releases into solution dialyzable and non-dialyzable mucopeptide fractions composed of N-acetylglucosamine, N-acetylmuramic acid and alanine, glutamic acid, lysine, and glycine in addition to the characteristic group-specific carbohydrate. The latter substance contains appreciable amounts of N-acetylmuramic acid and the amino acids as well as N-acetylglucosamine and rhamnose. Hot formamide extraction of the cell walls results in a soluble fraction of group-specific carbohydrate and an insoluble residue. The Group A carbohydrate in this instance is composed of rhamnose and N-acetylglucosamine. The composition of the insoluble residue is similar to that of the mucopeptide fractions released from the cell wall by phage-associated lysin. This residue was shown by electron microscopy to be composed of discrete discs which appear similar in structure to the intact cell wall. The specific carbohydrate obtained by hot formamide extraction of Group A-variant cell walls was composed almost exclusively of rhamnose. The residue fraction was similar to that of Group A. The residue of cell walls extracted with hot formamide is extensively solubilized not only by phage-associated lysin and S. albus enzyme, but also by lysozyme, which has no measurable effect on the intact streptococcal cell wall.


1968 ◽  
Vol 127 (3) ◽  
pp. 489-505 ◽  
Author(s):  
Vincent A. Fischetti ◽  
John B. Zabriskie

Evidence has been presented that Group C bacteriophages differ as to their inactivating site on the streptococcal cell wall. While all three phages adsorb to isolated cell walls, only the C1 phage was inactivated by enzymatically prepared group-specific carbohydrate. None of the Group C phages were inactivated by chemically extracted group-specific carbohydrate. In contrast, all virulent Group A streptococcal bacteriophages adsorbed only to living Group A streptococci. However, Group A temperate phages were able to adsorb to isolated cell walls but not to group-specific carbohydrate. While it has not been possible to identify the specific inactivating substance for the Group A virulent phages, certain pieces of evidence indirectly implicate the group-specific carbohydrate, specifically the N-acetylglucosamine moiety. The fact that Group A virulent phages failed to adsorb to heat-killed Group A streptococcal cells suggests that additional factors produced by the living cell are needed for complete viral inactivation.


1969 ◽  
Vol 129 (1) ◽  
pp. 37-49 ◽  
Author(s):  
S. H. Ohanian ◽  
J. H. Schwab ◽  
W. J. Cromartie

Mice injected intraperitoneally with isolated cell wall fragments of Group A streptococci develop a carditis similar to that previously observed in mice injected with crude extracts of this organism. Neither the soluble cytoplasmic components of Group A streptococcal cells nor the nonfragmented cell walls produced carditis in this experimental model. Fluorescein and 125I-labeled antibodies specific for Group A streptococcal cell wall antigens were used to demonstrate that, for 5 wk after injection, cell wall material is localized around the sites of active lesions in the heart. In addition, the cell wall antigen accumulates in the liver, spleen, mediastinal lymph nodes, and the adjacent loose connective tissue, where it persists for at least 10 wk.


1992 ◽  
Vol 139 (2) ◽  
pp. 455-467 ◽  
Author(s):  
Ina S. Klasen ◽  
Jeanette Kool ◽  
Marie José Melief ◽  
Ina Loeve ◽  
Wim B. van den Berg ◽  
...  

1992 ◽  
Vol 66 (11) ◽  
pp. 6788-6793 ◽  
Author(s):  
D Ou ◽  
P Chong ◽  
Y Choi ◽  
P McVeigh ◽  
W A Jefferies ◽  
...  

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