Induced Sensitization of Normal Laboratory Animals to<i>Brucella abortus</i>Endotoxin

Freedman, Henry H.; Fox, Alfred E.; Willis, R. Suzanne; Schwartz, Benjamin S.

doi:10.1128/jb.95.2.286-290.1968

Cited by 6 publications

(8 citation statements)

References 16 publications

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“…There are, however, some opposing reports, which have provided evidence for the role of LPS-associated protein (17,18), the core-oligosaccharide (29), and the 0-specific chain (4) in eliciting hypersensitivity to LPS.…”

Section: Discussionmentioning

confidence: 99%

“…(ii) Duration. The group of mice resistant to 1,000 ,ug of Re LPS on day 15 (see above) was divided into two groups (five mice per group) and challenged with Re LPS (10 Mug) on days 18 or 30, respectively. Both groups were found to be completely refractory to hypothermia [AT(2) = +0.1 ± 0.30C), showing that late tolerance persisted for at least 2 weeks after its induction.…”

Section: (Jg)mentioning

confidence: 99%

“…The degree of host susceptibility, however, can be altered by prior exposure to LPS. Thus, LPS pretreatment renders the host under certain experimental conditions either refractory (1, 2, 6, 8-10, 12, 13, 19, 25, 26, 30-32, 34, 35, 37, 39, 41, 42, 45, 47, 50) or more sensitive (6,7,8,17,18,29,33) to subsequent LPS challenge. These opposing effects have been commonly referred to as endotoxin tolerance and hypersensitivity (8), respectively.…”

mentioning

confidence: 99%

“…In contrast to tolerance, other investigators have shown that prior injection of sublethal quantities of LPS resulted in enhanced susceptibility (hypersensitivity) to subsequent LPS challenge (4,4,8,17,18,29). Immunological hypersensitivity has been implicated as a major mechanism for LPS hyperreactivity (4,8,29).…”

mentioning

confidence: 99%

“…Immunological hypersensitivity has been implicated as a major mechanism for LPS hyperreactivity (4,8,29). Again, the three main regions of LPS (4, 29,33), as weli as LPS-associated protein (17,18), have been implicated as the determinants relating to sensitization.…”

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confidence: 99%

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Lipid A-induced tolerance and hyperreactivity to hypothermia in mice

Greer¹,

Rietschel²

1978

Infect Immun

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Mice responded to lipopolysaccharide (LPS) with a dose-dependent, monophasic hypothermia reaching a maximum at 2 h postinjection. Degraded polysaccharide was not active; free lipid A, however, induced a similar pattern of hypothermia, indicating that the hypothermic principle of LPS was embedded within the lipid A component. The hypothermic response of mice to LPS was modified by prior exposure of the host to LPS. This altered reactivity was manifested by refractory periods (early and late tolerance), in which animals no longer responded with hypothermia, or a hyperreactive phase (hypersensitivity), in which hypothermic responses were greatly augmented upon LPS challenge. Thus, tolerance observed 24 h after a single injection of LPS (early tolerance) was followed, on further LPS challenge, by an enhanced hypothermic responses reaching a maximum on day 4. Further daily exposure of the animals to LPS eliminated hyperreactivity and led to the establishment of a late tolerance maximally expressed on day 8. Hyperreactivity could also be evoked on day 4 after a single injection of LPS. Mice pretreated with Salmonella S- and R-form LPS or free lipid A (Salmonella) demonstrated tolerance and hyperreactivity to both homologous and heterologous challenge. In addition, complete cross-tolerance was observed with S-form LPS derived from Shigella. It was concluded that the differential effects of LPS on host responses (tolerance and hyperreactivity) were due to lipid A.

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Section: Discussionmentioning

confidence: 99%

Section: (Jg)mentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Lipid A-induced tolerance and hyperreactivity to hypothermia in mice

Greer¹,

Rietschel²

1978

Infect Immun

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The lipid A immunity system. I. Induction of heterophile antibodies by enterobacterial lipopolysaccharides and their lipid A component

1972

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The lipid A immunity system Induction of heterophile antibodies by enterobacterial lipopolysaccharides and their lipid A componentMice were immunized either with lipopolysaccharides (LPS) or with the respective lipid A components. After four days an increase in the number of direct plaque-forming cells with complement-dependent antibody against sheep red cells was seen. Cross-reactions were observed with red cells of cattle, goats, horses and rabbits. All LPS investigated, of Shigella, Escherichia coli, and S and R form Salmonella, as well as the lipid A component evoked this immune response. We therefore conclude that all enterobacterial LPS induce an antibody which cross-reacts with SRC and that the lipid A component is responsible for this reaction. Evidence is presented that these effects, such as toxicity, fever, pyrogen tolerance, leucopenia/leucocytosis, nonspecific immunity, and tumor inhibition are mediated by lipid A-induced antibodies. Materials and methods BacteriaThe Salmonella cholerae suis strains were kindly supplied by H. Momenteau and L. LeMinor, International Salmonella Centre, Institut Pasteur, Paris, the Escherichia coli strains by F. Grskov, Statens Seruminstitut, Copenhagen, Shigella sonnei (phase 11) by M. Mulczyk, Institut Immunologii i Terapii, D&wiadczalnej, Breslau, Poland. R and S form Salmonella were provided by 0. Luderitz, Max-Planck-Institut fur Immunbiologie, Freiburg and by R. Rohde, Nationale Salmonella-Zentrale, Hygiene-Institut, Hamburg, respectively. The bacteria were kept at 4 O C on peptone agar. 2.2. Preparation of antigens Abbreviations: SRC: Sheep red blood cell(s) PFC: Direct antibody plaque-forming cell(s) LPS: Lipopolysaccharide(s) PBS: Phosphate buffered saline MBB: Modified barbital buffer i.p.: intraperitoneal 2.2.1. Lipopolysaccharides Bacterja were grown in 100 liter steel containers for 30 h at 37 C, slightly aerated, with either modified Fraser's medium [20], or in synthetic medium: 0.1 M Tris, pH 7.4; 0.0005 M KH2P04; 0.002 M sodium citrate, pH 6; 0.02 M NH4C1; 0.001 M MgS04; 1 x M FeCI3; 1 x M W.-R. Rank, R. DiPauli and U. Flie-Rank Eur.

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Endotoxins and the Immune Response

Neter

1969

Current Topics in Microbiology and Immunology

135

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Induced Sensitization of Normal Laboratory Animals toBrucella abortusEndotoxin

Cited by 6 publications

References 16 publications

Lipid A-induced tolerance and hyperreactivity to hypothermia in mice

Lipid A-induced tolerance and hyperreactivity to hypothermia in mice

The lipid A immunity system. I. Induction of heterophile antibodies by enterobacterial lipopolysaccharides and their lipid A component

Endotoxins and the Immune Response

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