Anticomplementary Action of Endotoxin.

Muschel, Louis H.; Schmoker, Karen; Webb, Phyllis M.

doi:10.3181/00379727-117-29657

Cited by 19 publications

(6 citation statements)

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“…Small amounts of bound or unbound antibody ("natural" antibody) may have remained in the serum along with the LPS material. An interaction of LPS and components of C ~ without initiation by antibody, as postulated by others (33,41), could therefore not be excluded. PiUemer et al (35) had claimed an interaction between C' and certain polysaccharides without an involvement of antibody, but an antibody requirement subsequently was shown (42,43).…”

Section: General Considerationsmentioning

confidence: 92%

“…Table I clearly demonstrated a C' dependence for lesion formation on LPS, it was considered that C' could be "fixed" during the process. Indeed, numerous investigators have found that various endotoxin preparations are "anticomplementary" (30)(31)(32)(33).…”

Section: Effect Of Inhibitors Of Lesion Formation Upon Serum Bactericmentioning

confidence: 99%

“…The generalizing term most used in the past to describe the effects of endo-toxin on C' in vivo (30,32) and in vitro (30,32,33) has been "anticomplementary." The present studies have confirmed that LPS lowers C' titers in vitro, but have indicated that rather than by inhibition of C' (as suggested by the term anticomplementary), there seems to be a utilization of the entire C ~ sequence.…”

Section: General Considerationsmentioning

confidence: 99%

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Interactions of the Complement System With the Surface and Endotoxic Lipopolysaccharide of Veillonella Alcalescens

Bladen

Gewürz

Mergenhagen

1967

The Journal of Experimental Medicine

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The antibody-complement system required for immune hemolysis has been studied extensively and is being defined rapidly (1-5). The effect of antibody and complement (C t) on the red blood cell recently assumed a dramatic morphological perspective when it was demonstrated that discrete holes or lesions were produced on the erythrocyte cell membrane during immune hemolysis (6).Lysis and inhibition of growth of Gram-negative bacteria by mammalian serum can also be mediated by antibody and C' (7,8). However, little is known about the mechanism of this reaction. In general, it is thought that the actual killing and lysis of the bacterial cell results from the effect(s) of C' and lysozyme (9, 10). It was suggested that C' action upon the lipoprotein layer of the cell membrane results in perforations of the cell surface, facilitating the access of lysozyme to its mucopeptide substrate. These events were postulated to culminate in lysis of the bacterial cell. Recently one step in this reaction, the presence of perforations or lesions after action of antibody and C', was demonstrated on spheroplasts of Esckerickia coli (11). Mediation of these lesions by C' implied a possible similarity to the mechanism of action involved in the formation of lesions on erythrocytes. However, it was not established which membranes were affected by C ~, nor were the conditions necessary for this C rmediated effect determined. In this report, attention is directed toward another Gram-negative genus, Veillonella, whose cell surface layers can be clearly differentiated by electron microscopy (12). The interaction of serum C ~ and the somatic endotoxic lipopolysaccharide of Veillonella alcalescens was investigated. The results clearly demonstrate that the lipopolysaccharide complex, as contained in the outer three-layer membrane of the cell (12), serves as a substrate for the action of serum C t. The results further suggest that in their reaction with lipopolysaccharide, the C t components go through a sequence of interactions similar to that required for immune hemolysis. 767 on

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Section: General Considerationsmentioning

confidence: 92%

Section: Effect Of Inhibitors Of Lesion Formation Upon Serum Bactericmentioning

confidence: 99%

Section: General Considerationsmentioning

confidence: 99%

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Interactions of the Complement System With the Surface and Endotoxic Lipopolysaccharide of Veillonella Alcalescens

Bladen

Gewürz

Mergenhagen

1967

The Journal of Experimental Medicine

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“…Activation of the complement system results in the rapid appearance of chemotactic activity [25][26][27][28]. Bacterial lipopolysaccharides have been demonstrated to activate both the classical and the alternative pathways of complement by a mechanism that does not require antibody to the LPS molecules [29][30][31][32][33]. Upon interaction of LPS with fresh sera from various species a chemotactic factor for polymorphonuclear leukocytes is generated.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of leukocyte chemotaxis by serum factor in diabetes mellitus: Selective depression of cell responses mediated by complement-derived chemoattractants

1990

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Rat neutrophil chemotactic responses to N-formyl-methionyl-leucyl-phenylalanine (FMLP), leukotriene (LT) B4, and lipopolysaccharide-activated serum (LPS-AS) were quantitatively assessed using the micropore filter system. Cells were suspended in either normal or diabetic rat serum for testing. Diabetic donor serum did not affect migration of neutrophils in a concentration gradient of the synthetic chemotactic agents. In contrast, the migratory responses to LPS-AS were significantly less than normal in this circumstance. Summation of effects was observed when FMLP and LPS-AS, or LTB4 and LPS-AS were simultaneously added to the test chamber, with cells suspended in normal serum. Suspended in diabetic rat serum neutrophils responded normally to the synthetic chemoattractants but the response to the activated serum was blocked. Cells previously incubated in the presence of diabetic donor serum then transferred to a culture medium for testing, presented reduced migratory responses to LPS-AS. Supramaximal, inhibitory concentrations of FMLP and LTB4, did not influence the response of neutrophils to LPS-AS. In vivo, suppression of cellular emigration to an inflamed area was observed from the early stages of the diabetic state. The inhibitory activity of chemotaxis in diabetes mellitus was previously reported to be associated with a protein factor in plasma of the animals. It is suggested that the inhibitory factor of chemotaxis in diabetes mellitus interacts with neutrophil receptors for complement-derived chemoattractants to induce blockade of cell-oriented locomotion either in vitro or in vivo.

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“…A number of other polysaccharides derived from other sources have been shown in the past to activate complement. Although most of these act through the alternate pathway (115,126,142,171,194), some have been reported to activate Cl (14,15). The variant-specific glycoprotein of trypanosomes also appears to act through the classical pathway (127).…”

Section: Factors Released By Living Trypanosomesmentioning

confidence: 99%