A comparison of specificity and biological activity of polyclonal and monoclonal antibodies raised against Salmonella minnesota R595 lipopolysaccharide

Mehta, Ninad; Wilson, B. M.; Rapson, N. T.; Easmon, C. S. F.

doi:10.1099/00222615-31-2-85

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1991

1993

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Cited by 2 publications

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“…We find that the Sm5G also inhibited murine splenocyte proliferation induced by R595 lipid A (20). Furthermore, Metha et al (26) have reported that rabbit anti-R595 LPS antiserum inhibited both mitogenicity (murine splenocytes) and lethal toxicity (chick embryo) of the Re LPS, while MAbs inhibited the mitogenesis but were not able to neutralize the lethality.…”

Section: Discussionmentioning

confidence: 99%

Neutralization of Shwartzman‐Inducing Activity by Antibodies Recognizing the Re Core or Lipid A Structures of Lipopolysaccharide from Salmonella minnesota R595 and Pseudomonas vesicularis JCM1477

Mashimo

Mita

Kasai

1991

Microbiology and Immunology

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Section: Discussionmentioning

confidence: 99%

Neutralization of Shwartzman‐Inducing Activity by Antibodies Recognizing the Re Core or Lipid A Structures of Lipopolysaccharide from Salmonella minnesota R595 and Pseudomonas vesicularis JCM1477

Mashimo

Mita

Kasai

1991

Microbiology and Immunology

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Inhibition of Lipid A- and Lipopolysaccharide-Induced Cytokine Secretion, B Cell Mitogenesis, and Lethal Shock by Lipid A-Specific Murine Monoclonal Antibodies

Ramachandra

Berczi

Sehon

et al. 1993

Journal of Infectious Diseases

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Three murine hybridomas secreting IgM monoclonal antibodies (MAbs) to lipid A (LA) of Salmonella minnesota R595 were generated. These MAbs serologically cross-reacted with LA and lipopolysaccharide (LPS) of unrelated gram-negative bacterial species. All three MAbs significantly suppressed the ability of LA and LPS from various gram-negative bacteria to induce tumor necrosis factor (TNF)-alpha (36%-67%) and interleukin-1 (30%-98%) in murine peritoneal macrophages and to stimulate B lymphocytes (37%-78%). Lipid A-induced TNF alpha production was also suppressed in mice (86%-88%). All three antibodies protected adrenalectomized mice against lethal shock induced by LA of S. minnesota R595. Optimal protection was achieved with one of the antibodies (MLA-1), if it was administered 2 h before injection of lipid A, and full protection persisted < or = 24 h. Moreover, MLA-1 was able to protect adrenalized or D(+)-galactosamine-sensitized mice against lethal shock induced by LPS derived from various gram-negative bacteria. This cross-protection could be predicted on the basis of serologic cross-reactivity and cross-neutralization by MLA-1 of the bioactivity of the heterologous LA or LPS in vitro.

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A comparison of specificity and biological activity of polyclonal and monoclonal antibodies raised against Salmonella minnesota R595 lipopolysaccharide

Cited by 2 publications

References 28 publications

Neutralization of Shwartzman‐Inducing Activity by Antibodies Recognizing the Re Core or Lipid A Structures of Lipopolysaccharide from Salmonella minnesota R595 and Pseudomonas vesicularis JCM1477

Neutralization of Shwartzman‐Inducing Activity by Antibodies Recognizing the Re Core or Lipid A Structures of Lipopolysaccharide from Salmonella minnesota R595 and Pseudomonas vesicularis JCM1477

Inhibition of Lipid A- and Lipopolysaccharide-Induced Cytokine Secretion, B Cell Mitogenesis, and Lethal Shock by Lipid A-Specific Murine Monoclonal Antibodies

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