Serum complement, bactericidal

As noted above many Gram-negative bacteria are sensitive to the direct killing action of serum complement. This bactericidal activity depends... 

Evidence that exogenous LPS can protect organisms from the bactericidal activity of serum complement has been reported. Purified LPS from a strain of E. coli (ML 308 225) was found to bind to that strain, and relatively large quantities protected it from complement killing. Subsequently investigations found that only the purified LPS from the strain under examination could protect the cells LPS from other sources showing little or no activity. The mechanism of resistance by the bound LPS was not understood, nor was the reason for the observed specificity of the reaction. The possibility that this phenomenon may have some importance during bacterial infection remains open. 

The importance of the 08 antigen of E. coli((xl 3 linked trisaccharides of al- 2 linked D-mannose) was investigated in relation to serum complement resistance, by introducing the 08-polysaccharide determinants of a smooth form Hfr donor strain into its rough mutant recipient. The presence of the 08 antigen caused a delay in the bactericidal reaction, but did not fully protect the cell. It is clear that while the O-specific polysaccharides of E. coli and other Gram-negative bacteria can be important virulence factors, other determinants are necessary for the expression of full virulence. 

B cell bh4 bp BPI BSA C domain C1-C9 cAMP CAP CD cDNA CFU CFU-GEMM bone-marrow-derived lymphocyte tetrahydrobiopterin base pairs bactericidal/permeability-inducing protein bovine serum albumin constant domain complement components cyclic adenosine monophosphate cationic antimicrobial protein cluster of differentiation complementary deoxynucleic acid colony-forming unit granulocyte-erythroid-monocyte-megakaryocyte CFU... 

John Hunter noted in 1792 that blood resisted putrefaction for a longer period if serum was present, that is another bactericidal factor complemented the effect of other factors. It was later identified and called complement. 

Uropathogenic E. coli cause 90% of the urinary tract infections. The bacteria colonize from the feces or perineal region and ascend the urinary tract to the bladder. With the aid of specific adhesins (pyelonephritis-associated pili) they are able to colonize the bladder. Another factor involved in the pathogenicity of the uropathogenic strains of E. coli is their resistance to complement-dependent bactericidal effect of serum. This phenomenon is associated with the presence of a capsule, which decrease the ability of antibodies and/or complement to bind to the bacterial surface, which in turn prevents the phagocytes from recognizing and engulfing the bacterial cells. 

Another mechanism ofcomplement regulation at the level of the terminal complement pathway involves extrusion of the membrane attack complex as occurs with Salmonella minnesota. C5b-7 complexes that are assembled on the bacterium are released upon the incorporation of C8 into the complex. The molecular configuration of C5b-9 in the bacterial membrane also appears to be an important ctor in determining the fete of the bacterium Joiner et al showed that C5b-9 complexes (bactericidal and nonbactericidal MAC) were associated with different outer membrane proteins in serum sensitive and serum resistant N. gonorrhoeae, respectively. ... 

The quantity of capsular polysaccharide is apparently of importance in a variety of pathogens. Klebsiella pneumoniae. Salmonella typhi, 5. typhi-murium, E. coli. Streptococcus pneumoniae and Staphylococcus aureus have all been reported to show a relationship between the amount of capsular material and virulence, resistance to phagocytosis, or resistance to humoral host defences. It has been suggested in the case of E. coli that the amount of K-antigen, as measured by its ability to coat red blood cells and inhibit their aggregation by haemagglutinating antiserum, is the most important factor determining resistance to the complement-mediated bactericidal activity of serum. Other studies have found evidence that the type of capsular polysaccharide may be more important. 

Introduction - Cranplement was discovered in the late nineteenth century %fhen it was recognized that the bactericidal activity of fresh serum required the participation of at least two factors a heat-stable factor, specific for the particular organism (antibody) and a second, non-specific, heat-labile factor designated complement. During the two decades following the discovery of complement, it became apparent that complement did, in fact, consist of several components which act in a definite sequence to effect lysis and death of the bacteria. In the 1950 s, the development of sophisticated methods in protein chemistry and suited>le functional assays for Individual complement components facilitated the elucidation of the chemical, physical, and functional properties of the complement system. 

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