Immunostimulation by LPS and Its Derivatives

Behling, Ulrich H.; Nowotny, Alois

doi:10.1007/978-1-4684-4115-4_11

Cited by 10 publications

(3 citation statements)

References 37 publications

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“…Furthermore, no LPS has been described among the components of myxospore cells (Sutherland, 1976). LPS and LPS-containing cells have been recognized as potent inducers of rapid inflammatory responses (Snyderman & Verghese, 1980) and bone marrow cell depletion in mice (Behling & Nowotny, 1981). This was not observed in our assays with M .…”

Section: Discussionmentioning

confidence: 67%

Immunomodulation by Myxospores of Myxococcus xanthus

et al. 1985

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Glycerol-induced myxospores of Myxococcus xanthus caused non-specific modulation of humoral and cellular immune responses in laboratory animals. The number of cells which formed specific haemolysins in spleens of mice immunized with sheep erythrocytes was increased when 0.5 X 10(8) myxospores were inoculated 2 d after the erythrocytes, and decreased when myxospores were injected 2 d before or at the same time as the erythrocytes. Both the IgG primary response and the secondary response to erythrocytes were decreased in rabbits after pretreatment with 2 X 10(8) myxospores per rabbit. Delayed-type hypersensitivity to sheep erythrocytes was also suppressed in mice after intraperitoneal (i.p.) injection of 0.3 X 10(8) myxospores. One day after i.p. injection of myxospores, neither an inflammatory response nor bone marrow cell depletion was observed in mice. These results support the idea that M. xanthus myxospores possess diverse immunomodulation properties apparently due to factors different from the classical LPS of Gram-negative bacteria.

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Section: Discussionmentioning

confidence: 67%

Immunomodulation by Myxospores of Myxococcus xanthus

et al. 1985

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“…Although bacterial lipopolysaccharides (LPSs) or endotoxins are considered to be potent immunopotentiating agents (14,29; for a review, see reference 38), their use as immunological adjuvants is precluded by the fact that they are extremely toxic and pyrogenic for most animal species, even when given in small amounts (38). These effects have been attributed to the diphosphoryl lipid A portion of the LPS molecule (38,39,41); however, removal of a phosphate group from the reducing end of diphosphoryl lipid A yields monophosphoryl lipid A (MPL).…”

mentioning

confidence: 99%

Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A

et al. 1988

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Treatment with nontoxic monophosphoryl lipid A (MPL), which was derived from a polysaccharidedeficient, heptoseless Re mutant of Salmonella typhimurium, was found to inactivate suppressor T-cell activity, as evidenced by a decrease in the degree of low-dose immunological paralysis expressed and an increase in the magnitude of the antibody response to type III pneumococcal polysaccharide. The effects produced, which could not be attributed to the polyclonal activation of immune B cells by MPL, were dependent upon the dose of MPL used, as well as the time when MPL was given relative to low-dose priming or immunization with type III pneumococcal polysaccharide. Neither amplifier nor helper T-cell activity was decreased by treatment with the same, or larger, doses of MPL. The significance of these findings to the use of MPL as an immunological adjuvant or an immunomodulating agent is discussed.

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“…These findings have been reviewed in detail elsewhere (2,3,7). Since the endotoxins or lipopolysaccharides (LPSs) of gramnegative bacteria are potent immunological adjuvants (13,16,22,25,43), we sought to determine whether some, though certainly not all, of their immunomodulatory properties might be attributed to a modification in regulatory T cell * Corresponding author. function, i.e., to an increase or decrease in Ta or Ts activity, respectively.…”

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confidence: 99%

Structural features that influence the ability of lipid A and its analogs to abolish expression of suppressor T cell activity

et al. 1992

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Lipid A preparations derived from the lipopolysaccharides of several gram-negative bacteria, as well as chemically defined synthetic lipid A's and their analogs (both glucosamine mono-and disaccharides), were used to establish the chemical structures required for (i) abolishing the expression of suppressor T cell (Ts) function and (ii) inducing polyclonal activation of B cells. Salmonella minnesota R595 lipid A (diphosphoryl lipid A) possesses both of these activities. Decreasing the number of phosphate groups in lipid A from two to one (monophosphoryl lipid A) as well as decreasing the fatty acyl content, primarily by removing the residue at the 3 position, resulted in a progressive reduction in toxicity; however, these structural modifications did not influence its ability to abolish the expression ofTs function. Reducing the fatty acyl content from five to four (lipid A precursor IVA or Ia) eliminated the capacity to influence Ts function but not to induce polyclonal activation of B cells. None of the monosaccharide analogs of lipid A examined influenced the expression of Ts activity, although some were able to activate B cells polyclonally. Thus, in order to be able to abolish the expression of Ts function, lipid A (i) must be a glucosamine disaccharide, (ii) may have either one or two phosphate groups, and (iii) must have at least five fatty acyl groups. Also, the chain length of the nonhydroxylated fatty acid, as well as the location of acyloxyacyl groups (2' versus 3' position), may play an important role. These findings indicate that the chemical structures responsible for the toxicity of lipid A differ from those that influence its capacity to abolish the expression of Ts function and to induce polyclonal activation of B cells.

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Immunostimulation by LPS and Its Derivatives

Cited by 10 publications

References 37 publications

Immunomodulation by Myxospores of Myxococcus xanthus

Immunomodulation by Myxospores of Myxococcus xanthus

Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A

Structural features that influence the ability of lipid A and its analogs to abolish expression of suppressor T cell activity

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