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22 results for “PTX3”
Dataset related to article "The Long Pentraxin PTX3 Controls Klebsiella Pneumoniae Severe Infection "
<p>This record contains raw data related to article “The Long Pentraxin PTX3 Controls <em>Klebsiella Pneumoniae</em> Severe Infection"</p> <p><em>Klebsiella pneumoniae</em> is a common pathogen in human sepsis. The emergence of multidrug-resistant <em>K. pneumoniae</em> strains represents a major clinical challenge in nosocomial and community acquired infections. The long pentraxin PTX3, a key component of humoral innate immunity, is involved in resistance to selected pathogens by promoting opsonophagocytosis. We investigated the relevance of PTX3 in innate immunity against <em>K. pneumoniae</em> infections using <em>Ptx3</em> <sup>-/-</sup> mice and mouse models of severe <em>K. pneumoniae</em> infections. Local and systemic PTX3 expression was induced following <em>K. pneumoniae</em> pulmonary infection, in association with the up-regulation of TNF-α and IL-1β. PTX3 deficiency in mice was associated with higher bacterial burden and mortality, release of pro-inflammatory cytokines as well as IL-10 in the lung and systemically. The analysis of the mechanisms responsible of PTX3-dependent control of <em>K. pneumoniae</em> infection revealed that PTX3 did not interact with <em>K. pneumoniae</em>, or promote opsonophagocytosis. The comparison of susceptibility of wild-type, <em>Ptx3<sup>-/-</sup>, C3<sup>-/-</sup></em> and <em>Ptx3<sup>-/-</sup></em> /<em>C3<sup>-/-</sup></em> mice to the infection showed that PTX3 acted in a complement-independent manner. Lung histopathological analysis showed more severe lesions in <em>Ptx3</em> <sup>-/-</sup> mice with fibrinosuppurative, necrotizing and haemorrhagic bronchopneumonia, associated with increased fibrin deposition in the lung and circulating fibrinogen consumption. These findings indicate that PTX3 contributes to the control of <em>K. pneumoniae</em> infection by modulating inflammatory responses and tissue damage. Thus, this study emphasizes the relevance of the role of PTX3 as regulator of inflammation and orchestrator of tissue repair in innate responses to infections</p>
Dataset related to article "Regulation of inflammation and protection against invasive pneumococcal infection by the long pentraxin PTX3"
<p>This record contains raw data related to article "Regulation of inflammation and protection against invasive pneumococcal infection by the long pentraxin PTX3". </p><p><strong>Abstract</strong></p><p><i>Streptococcus pneumoniae</i> is a major pathogen in children, elderly subjects, and immunodeficient patients. Pentraxin 3 (PTX3) is a fluid-phase pattern recognition molecule (PRM) involved in resistance to selected microbial agents and in regulation of inflammation. The present study was designed to assess the role of PTX3 in invasive pneumococcal infection. In a murine model of invasive pneumococcal infection, PTX3 was strongly induced in non-hematopoietic (particularly, endothelial) cells. The IL-1β/MyD88 axis played a major role in regulation of the <i>Ptx3</i> gene expression. <i>Ptx3</i>-/- mice presented more severe invasive pneumococcal infection. Although high concentrations of PTX3 had opsonic activity in vitro, no evidence of PTX3-enhanced phagocytosis was obtained in vivo. In contrast, <i>Ptx3</i>-deficient mice showed enhanced recruitment of neutrophils and inflammation. Using <i>P-selectin-</i>deficient mice, we found that protection against pneumococcus was dependent upon PTX3-mediated regulation of neutrophil inflammation. In humans, <i>PTX3</i> gene polymorphisms were associated with invasive pneumococcal infections. Thus, this fluid-phase PRM plays an important role in tuning inflammation and resistance against invasive pneumococcal infection.</p>
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International Brain Laboratory public data
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OpenNeuro
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