Effect of Deficiency of Tumor Necrosis Factor Alpha or Both of Its Receptors on<i>Streptococcus pneumoniae</i>Central Nervous System Infection and Peritonitis

Wellmer, Andreas; Gerber, Joachim; Ragheb, Jasmin; Zysk, Gregor; Kunst, Tammo; Smirnov, Alexandr; Brück, Wolfgang; Nau, Roland

doi:10.1128/iai.69.11.6881-6886.2001

Cited by 87 publications

(62 citation statements)

References 43 publications

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“…Furthermore, anti-TNF␣-treated mice died of pneumococcal pneumonia significantly sooner than control mice. Moreover, in a murine model of pneumococcal peritonitis, 100 colony-forming units of S pneumoniae produced fatal peritonitis in TNF␣-deficient mice, but not in wild-type mice (32). TNF deficiency also led to a substantial increase in the level of pneumococci in blood and the spleen.…”

Section: Tnf␣ Inhibition and Sepsismentioning

confidence: 99%

Infections and anti–tumor necrosis factor α therapy

Ellerin¹,

Rubin²,

Weinblatt³

2003

Arthritis & Rheumatism

267

125

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Section: Tnf␣ Inhibition and Sepsismentioning

confidence: 99%

Infections and anti–tumor necrosis factor α therapy

Ellerin¹,

Rubin²,

Weinblatt³

2003

Arthritis & Rheumatism

267

125

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“…In this regard it will be interesting to define whether MBL interacts with TLRs that play a key role in NF-B-dependent secretion of TNF-␣. It is clear from clinical studies with TNF-␣ antagonists and in TNF null mice that TNF-␣ plays a key role in host defense, thus the sluggish TNF-␣ response in MBL null mice is likely to contribute toward the susceptibility of these mice to infection (24,63,64).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Møller-Kristensen

Ip²,

Shi³

et al. 2006

The Journal of Immunology

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Burn injury disrupts the mechanical and biological barrier that the skin presents against infection by symbionts like the Pseudomonas aeruginosa, a Gram-negative bacteria. A combination of local factors, antimicrobial peptides, and resident effector cells form the initial response to mechanical injury of the skin. This activity is followed by an inflammatory response that includes influx of phagocytes and serum factors, such as complement and mannose-binding lectin (MBL), which is a broad-spectrum pattern recognition molecule that plays a key role in innate immunity. A growing consensus from studies in humans and mice suggests that lack of MBL together with other comorbid factors predisposes the host to infection. In this study we examined whether MBL deficiency increases the risk of P. aeruginosa infection in a burned host. We found that both wild-type and MBL null mice were resistant to a 5% total body surface area burn alone or s.c. infection with P. aeruginosa alone. However, when mice were burned then inoculated s.c. with P. aeruginosa at the burn site, all MBL null mice died by 42 h from septicemia, whereas only one-third of wild-type mice succumbed (p = 0.0005). This result indicates that MBL plays a key role in containing and preventing a systemic spread of P. aeruginosa infection following burn injury and suggests that MBL deficiency in humans maybe a premorbid variable in the predisposition to infection in burn victims.

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“…Several reports have shown that proinflammatory cytokines, such as IL-1, tumor necrosis factor alpha (TNF-␣), IL-6, and IL-18, play protective roles against pneumococcal infection (22,26,48,54,55). Moreover, gamma interferon has been demonstrated to protect mice against infection with S. pneumoniae by promoting the accumulation of neutrophils in the infected lung (34).…”

mentioning

confidence: 99%

Critical Involvement of Pneumolysin in Production of Interleukin-1α and Caspase-1-Dependent Cytokines in Infection withStreptococcus pneumoniaeIn Vitro: a Novel Function of Pneumolysin in Caspase-1 Activation

et al. 2008

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Pneumolysin is a pore-forming cytolysin known as a major virulence determinant of Streptococcus pneumoniae. This protein toxin has also been shown to activate the Toll-like receptor 4 (TLR4) signaling pathway. In this study, a mutant S. pneumoniae strain deficient in pneumolysin (⌬ply) and a recombinant pneumolysin protein (rPLY) were constructed. Upon infection of macrophages in vitro, the ability to induce the production of interleukin-1␣ (IL-1␣), IL-1␤, and IL-18 was severely impaired in the ⌬ply mutant, whereas there was no marked difference in the induction of tumor necrosis factor alpha (TNF-␣) and IL-12p40 between the wild type and the ⌬ply mutant of S. pneumoniae. When macrophages were stimulated with rPLY, the production of IL-1␣, IL-1␤, and IL-18 was strongly induced in a TLR4-dependent manner, whereas lipopolysaccharide, a canonical TLR4 agonist, hardly induced these cytokines. In contrast, lipopolysaccharide was more potent than rPLY in inducing the production of TNF-␣, IL-6, and IL-12p40, the cytokines requiring no caspase activation. Activation of caspase-1 was observed in macrophages stimulated with rPLY but not in those stimulated with lipopolysaccharide, and the level of activation was higher in macrophages infected with wild-type S. pneumoniae than in those infected with the ⌬ply mutant. These results clearly indicate that pneumolysin plays a key role in the host response to S. pneumoniae, particularly in the induction of caspase-1-dependent cytokines.

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Effect of Deficiency of Tumor Necrosis Factor Alpha or Both of Its Receptors onStreptococcus pneumoniaeCentral Nervous System Infection and Peritonitis

Cited by 87 publications

References 43 publications

Infections and anti–tumor necrosis factor α therapy

Infections and anti–tumor necrosis factor α therapy

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Critical Involvement of Pneumolysin in Production of Interleukin-1α and Caspase-1-Dependent Cytokines in Infection withStreptococcus pneumoniaeIn Vitro: a Novel Function of Pneumolysin in Caspase-1 Activation

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