Anti-Endotoxin Monoclonal Antibodies Inhibit Secretion of Tumor Necrosis Factor-a by Two Distinct Mechanisms

Burd, Randall S.; Battafarano, Richard J.; Cody, Carolyn S.; Farber, Mitchell S.; Ratz, Craig A.; Dünn, David L.

doi:10.1097/00000658-199309000-00004

Cited by 14 publications

(7 citation statements)

References 34 publications

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“…They could affect the immune response of the mother mice and consequently that of the neonate by neutralization of LPS. An effect of anti‐LPS antibodies on the cytokine production profile of macrophages has been previously reported [31]. In conclusion our study provides first experimental evidence for the concept that prenatal exposure to microbial components — LPS in this study – act as potent immuno‐modulators for the development of respiratory allergies later in life.…”

Section: Discussionsupporting

confidence: 76%

Prenatal lipopolysaccharide‐exposure prevents allergic sensitization and airway inflammation, but not airway responsiveness in a murine model of experimental asthma

Blümer

Herz

Wegmann

et al. 2005

Clin Experimental Allergy

169

109

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Section: Discussionsupporting

confidence: 76%

Prenatal lipopolysaccharide‐exposure prevents allergic sensitization and airway inflammation, but not airway responsiveness in a murine model of experimental asthma

Blümer

Herz

Wegmann

et al. 2005

Clin Experimental Allergy

169

109

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“…Historically, anti-LPS mAbs have been very successful in animal models in blocking sepsis and improving survival when administered prior to a septic insult (15,(31)(32)(33). These results were so promising and sepsis has such a high mortality that two anti-LPS mAbs were developed for human use.…”

Section: Discussionmentioning

confidence: 99%

Anti-Endotoxin Monoclonal Antibodies are Protective against Hepatic Ischemia/Reperfusion Injury in Steatotic Mice

Fiorini¹,

Shafizadeh²,

Polito³

et al. 2004

American Journal of Transplantation

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Steatotic mice are particularly susceptible to hepatic ischemia/reperfusion injury compared with their lean littermates. We have previously demonstrated that livers of mice having a spontaneous mutation in the leptin gene (ob/ob), resulting in global obesity and liver steatosis, are ATP depleted, are endotoxin sensitive, and do not survive (I/R) injury. We hypothesize that administration of an anti-LPS monoclonal antibody (mAb) prior to initiation of I/R would be protective from that insult. Steatotic mice (ob/ob) were subjected to 15 min of ischemia via complete porta-hepatis occlusion and varying lengths of reperfusion with or without pre-treatment with an anti-LPS mAb. There was 14-31% survival of isotype matched control mAb treated ob/ob mice after 15 min of ischemia and 24 h of reperfusion. In contrast, 75-83% of ob/ob mice pre-treated with an anti-LPS mAb prior to initiation of I/R survived both ischemia and 24 h of reperfusion. Furthermore, there was a decrease in ALT and circulating endotoxin levels when treated with an anti-LPS mAb compared with control antibodies. Attenuation of the endotoxin load with anti-LPS mAb, prior to initiation of I/R, was cytoprotective and improved survival. Consequently, these studies might offer a solution to the problems associated with using steatotic livers in clinical transplantation.

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“…Because of the higher opsonic activity of IgM antibodies, one can expect that IgM anti-LPS will enhance the complement-mediated internalization of LPS by macrophages better than will IgG anti-LPS [22,35]. Fc-mediated and opsonin-mediated antibody interactions may play an important role in the protective activity of anti-LPS antibodies [10]. The lack of the IgM fraction might also explain the limited protection of i.v.…”

Section: Discussionmentioning

confidence: 99%

Protective capacity of a IgM/IgA-enriched polyclonal immunoglobulin-G preparation in endotoxemia

1998

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Animal experiments were carried out to investigate whether a protective effect can be achieved in endotoxemia by intravenous (i.v.) application of a polyclonal immunoglobulin preparation (IVIG-IgG/A/M) enriched with 12% IgM and 12% IgA. Following administration of IVIG-IgG/A/M (500 mg/kg), endotoxemia was induced by intraperitoneal inoculation of a sublethal dose (5x10(8) CFU/kg) of Escherichia coli (E. coli) and subsequent i.v. administration of an antimicrobial agent (Imipenem). Plasma endotoxin activity, IL-6 activity, mean arterial pressure, and skeletal muscle oxygen pressure (tpO2) were measured at regular intervals over a total observation period of 7 h. Prophylactic administration of IVIG-IgG/A/M was found to significantly attenuate (P<0.01) the antibiotic-induced increase in endotoxin activity as compared to the albumin control group. Limited endotoxemia in the IgG/A/M group was associated with reduced levels of circulating IL-6 (P<0.01). Both lipopolysaccharide-induced hypotension and depression of tissue oxygenation were attenuated (P<0.01) by pre-treatment with IVIG-IgG/A/M. The experimental results suggest that in endotoxemia the polyclonal immunoglobulin preparation has a prophylactic protective effect on the acute phase responses and reduces the cardiodepressant effects of E. coli septicaemia.

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Anti-Endotoxin Monoclonal Antibodies Inhibit Secretion of Tumor Necrosis Factor-a by Two Distinct Mechanisms

Cited by 14 publications

References 34 publications

Prenatal lipopolysaccharide‐exposure prevents allergic sensitization and airway inflammation, but not airway responsiveness in a murine model of experimental asthma

Prenatal lipopolysaccharide‐exposure prevents allergic sensitization and airway inflammation, but not airway responsiveness in a murine model of experimental asthma

Anti-Endotoxin Monoclonal Antibodies are Protective against Hepatic Ischemia/Reperfusion Injury in Steatotic Mice

Protective capacity of a IgM/IgA-enriched polyclonal immunoglobulin-G preparation in endotoxemia

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