Modulation of Immune Response by Bacterial Lipopolysaccharide (LPS): Roles of Macrophages and T Cells in <i>In Vitro</i> Adjuvant Effect of LPS on Antibody Response to T Cell‐Dependent and T Cell‐Independent Antigens

Uchiyama, Takehiko

doi:10.1111/j.1348-0421.1982.tb00173.x

Cited by 17 publications

(14 citation statements)

References 24 publications

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“…Perhaps this discrepancy would be based on the difference between titers of O-antigen-specific antibodies in our anti-porin serum and those of Saxen et al, because Saxen et al have used hyperimmune serum of rabbits. In addition, O-antigen-specific antibodies would protect such a low challenge dose as used by Saxen et al Therefore, a contamination of low amounts of LPS in porin might be necessary as an adjuvant to porin and enhance the immune response (27,31). However, it seemed unlikely that LPS was a protective antigen which could induce the CMI, because we found that neither DTH reaction nor IL-2 production were induced by the immunization with LPS alone in mice.…”

Section: Discussionmentioning

confidence: 77%

Protective Immunity Induced by Porin in Experimental Mouse Salmonellosis

Matsui

Arai

1989

Microbiology and Immunology

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Section: Discussionmentioning

confidence: 77%

Protective Immunity Induced by Porin in Experimental Mouse Salmonellosis

Matsui

Arai

1989

Microbiology and Immunology

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“…Whereas in the CASP model no published work to date has determined the state of the immune response beyond 24 h, different parameters associated with immunosuppression have been reported in other models. Old work reports that the injection of moderate doses of LPS daily reduces the capacity to generate antibodies for between 1 and 7 days (42,43), and using the CLP model, a low clearance capacity and an increased sensitivity to a second infection were observed (40,50).…”

Section: Discussionmentioning

confidence: 99%

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

et al. 2011

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Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-induced immune deactivation. Although the contribution of experimental models to the knowledge of pathophysiological and therapeutic aspects of human sepsis is undeniable, most of the current studies using animal models have focused on the acute, proinflammatory phase. We developed a murine model that reproduces the early acute phases but also the long-term consequences of human sepsis. We induced polymicrobial acute peritonitis (AP) by establishing a surgical connection between the cecum and the peritoneum, allowing the exit of intestinal bacteria. Using this model, we observed an acute phase with high mortality, leukopenia, increased interleukin-6 levels, bacteremia, and neutrophil activation. A peak of leukocytosis on day 9 or 10 revealed the persistence of the infection within the lung and liver, with inflammatory hepatic damage being shown by histological examination. Long-term (20 days) derangements in both innate and adaptive immune responses were found, as demonstrated by impaired systemic tumor necrosis factor alpha production in response to an inflammatory stimulus; a decreased primary humoral immune response and T cell proliferation, associated with an increased number of myeloid suppressor cells (Gr-1 ؉ CD11b ؉ ) in the spleen; and a low clearance capacity. This model provides a good approach to attempt novel therapeutic interventions directed to augmenting host immunity during late sepsis.Local inflammatory mechanisms triggered by an infection are usually enough to eradicate the pathogen. However, if the infection is not contained, the pathogen, its toxins, and diverse mediators of the host are released to the circulation, producing a systemic inflammatory response syndrome that can cause severe sepsis or septic shock (8). Sepsis is usually treated in intensive care units (ICUs), and about 30% of the patients with severe sepsis die; this percentage rises to 50 to 70% if septic shock, the main cause of mortality in the ICU, develops (46).As death by septic shock has been associated with an early excessive inflammatory response, most of the treatment strategies have been designed to block the inflammatory mediators involved in this phenomenon. This theory is based on animal models where the administration of large amounts of bacteria or lipopolysaccharide (LPS), a major component of the outer membrane of Gram-negative bacteria, generates a cytokine storm and where the blockade of these molecules increases the survival of animals (11). Nevertheless, clinical trials designed to neutralize inflammatory mediators have failed (45). The sepsis syndrome is not restricted to the activation of the inflammatory response, as compensatory anti-inflammatory mechanisms are also triggered, usually leading to immunosuppressio...

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“…Like other microbial compounds /products such as b-glucan and dsRNA, LPS possesses certain conserved structural sequences that have profound effects on the immune system of many animals. It can either enhance or suppress the immunity by affecting T cells, B cells, macrophages, and other immune components in different animal species [94,95].…”

Section: Effects Of Endotoxin On Fish Immunitymentioning

confidence: 99%