Activation of the alternative complement pathway by L-phase variants of gram-positive bacteria. 1979

F T Saulsbury, and J A Winkelstein

The present studies were performed to investigate the potential role of the alternative complement pathway in the host's defense against bacterial L-phase variants and to gain insight into the subcellular component of gram-positive bacteria responsible for activation of the alternative pathway. L-phase variants of Staphylococcus aureus and Streptococcus faecalis were able to activate the alternative pathway and consume C3 in C4-deficient guinea pig serum in amounts comparable to their respective bacterial-phase parent organisms. Activation of the complement system via the alternative pathway resulted in death of the L-phase variants. Membranes prepared from S. faecalis L-phase variants, by either osmotic lysis or mechanical disruption, retained their ability to activate the alternative pathway. Treatment of the membranes by three different methods (water washes, hot trichloroacetic acid, and cold trichloroacetic acid) resulted in a greatly diminished ability of the membranes to activate the alternative pathway. In addition, the extracts derived from the membranes by water washes and by cold-trichloroacetic acid treatment were able to activate the alternative pathway. These studies indicate that these L-phase variants can activate the alternative pathway and suggest that membrane-associated factors play a role in the alternative pathway activation by S. faecalis L-phase variants.

UI MeSH Term Description Entries
D007740 L Forms Bacterial variants, unable to form a complete cell wall, which are formed in cultures by various bacteria; granules (L bodies) appear, unite, and grow into amorphous bodies which multiply and give rise to bacterial cells morphologically indistinguishable from the parent strain.
D001770 Blood Bactericidal Activity The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST. Activities, Blood Bactericidal,Activity, Blood Bactericidal,Bactericidal Activities, Blood,Bactericidal Activity, Blood,Blood Bactericidal Activities
D002462 Cell Membrane The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells. Plasma Membrane,Cytoplasmic Membrane,Cell Membranes,Cytoplasmic Membranes,Membrane, Cell,Membrane, Cytoplasmic,Membrane, Plasma,Membranes, Cell,Membranes, Cytoplasmic,Membranes, Plasma,Plasma Membranes
D003167 Complement Activation The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES. Activation, Complement,Activations, Complement,Complement Activations
D003170 Complement Pathway, Alternative Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX. Alternative Complement Pathway,Properdin Pathway,Alternative Complement Activation Pathway,Complement Activation Pathway, Alternative
D003176 Complement C3 A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase. C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D006168 Guinea Pigs A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. Cavia,Cavia porcellus,Guinea Pig,Pig, Guinea,Pigs, Guinea
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013210 Staphylococcus A genus of gram-positive, facultatively anaerobic, coccoid bacteria. Its organisms occur singly, in pairs, and in tetrads and characteristically divide in more than one plane to form irregular clusters. Natural populations of Staphylococcus are found on the skin and mucous membranes of warm-blooded animals. Some species are opportunistic pathogens of humans and animals.
D013211 Staphylococcus aureus Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.

Related Publications

F T Saulsbury, and J A Winkelstein
January 1977, Archives of oral biology,
F T Saulsbury, and J A Winkelstein
July 1976, Journal of bacteriology,
F T Saulsbury, and J A Winkelstein
May 1982, Critical care medicine,
F T Saulsbury, and J A Winkelstein
November 1988, Medicina clinica,
F T Saulsbury, and J A Winkelstein
January 1976, Advances in immunology,
F T Saulsbury, and J A Winkelstein
November 1979, CRC Critical reviews in immunology,
F T Saulsbury, and J A Winkelstein
April 1986, Journal of immunology (Baltimore, Md. : 1950),
F T Saulsbury, and J A Winkelstein
October 1980, Infection and immunity,
F T Saulsbury, and J A Winkelstein
October 1980, Infection and immunity,
F T Saulsbury, and J A Winkelstein
January 2002, Clinical and diagnostic laboratory immunology,
Copied contents to your clipboard!