Comparative methods for multiplex analysis of cytokine protein expression in plasma of lipopolysaccharide-treated mice

Bobrowski, Walter F.; McDuffie, J. Eric; Sobocinski, Gregg; Chupka, Jonathan; Olle, Eric W.; Bowman, Amy; Albassam, Mudher

doi:10.1016/j.cyto.2005.09.007

Cited by 27 publications

(23 citation statements)

References 8 publications

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“…In agreement with this hypothesis, we observed that mice inoculated with E. coli did not present an increase in circulating sTNFR1 levels and showed increased levels of TNF-␣ in serum at 2 and 4 h after challenge (data not shown). These results agree with previous observations for mice challenged with LPS, where TNF-␣ was found in the circulation at 2 h postinoculation, while sTNFR1 was detected only at 24 h (35). To further demonstrate the neutralization of TNF-␣ by sTNFR1 in vivo, we compared the levels of TNF-␣ in serum from TNFR1-deficient (tnfr1 Ϫ/Ϫ ) and wild-type (C57BL/6) mice under basal conditions and after S. aureus inoculation.…”

Section: Fig 5 Tnf-␣ Expression During S Aureus Infection Mice Weresupporting

confidence: 83%

“…Activation of ADAM17 and shedding of TNFR1 by immune cells have been reported in response to septic stimuli in vitro (13,47) and in animal models of LPS-induced endotoxemia (19,35). Shedding of TNFR1, which occurs between 6 and 24 h after LPS inoculation, was critical for the neutralization of TNF-␣ signaling and the arrest of inflammation (19).…”

Section: Fig 7 Inflammatory Response Induced During Systemic S Aureumentioning

confidence: 99%

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Shedding of Tumor Necrosis Factor Receptor 1 Induced by Protein A Decreases Tumor Necrosis Factor Alpha Availability and Inflammation during Systemic Staphylococcus aureus Infection

et al. 2013

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Staphylococcus aureus infections are an important public health concern due to their increasing incidence and high rates of mortality. The success of S. aureus as a pathogen is highly related to its enormous capacity to evade the host immune response. The critical role of tumor necrosis factor alpha (TNF-␣) in the initial host defense against systemic staphylococcal infection has been demonstrated in experimental models and may partially explain the lack of significant benefits observed in clinical trials attempting to neutralize this cytokine in septic patients. S. aureus protein A plays a key role in regulating inflammation through its ability to bind and signal through the TNF-␣ receptor 1 (TNFR1). In this study, we demonstrate that S. aureus, via protein A-mediated signaling, induces early shedding of TNFR1, which precedes the secretion of TNF-␣ in vitro and in vivo. The results obtained using a protein A-deficient mutant and tnfr1 ؊/؊ mice strongly suggest that the increased levels of soluble TNFR1 present during experimental S. aureus infection may neutralize circulating TNF-␣ and impair the host inflammatory response. Early shedding of TNFR1 induced by protein A may constitute a novel mechanism by which S. aureus subverts the host immune response.

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Section: Fig 5 Tnf-␣ Expression During S Aureus Infection Mice Weresupporting

confidence: 83%

Section: Fig 7 Inflammatory Response Induced During Systemic S Aureumentioning

confidence: 99%

Shedding of Tumor Necrosis Factor Receptor 1 Induced by Protein A Decreases Tumor Necrosis Factor Alpha Availability and Inflammation during Systemic Staphylococcus aureus Infection

et al. 2013

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“…The mechanism of inf lammationinduced PK2 gene transcription in granulocytes is yet unknown. Inf lammatory stimuli in mice and rats are known to produce an early and rapid increase in plasma levels of granulocyte colony-stimulating factor (G-CSF) (24), and, among the numerous cytokines released by inf lammatory stimulation, G-CSF is the only cytokine able to activate PK2 transcription in CD11bϩGr1ϩ bone marrow-derived cells (25). G-CSF is a principal regulator of granulopoiesis and neutrophil mobilization from the bone marrow; thus, the early increase of G-CSF levels in plasma of CFA-inf lamed animals could explain the enhanced PK2 transcription in spleen and paw granulocytes.…”

Section: Discussionmentioning

confidence: 99%

The chemokine Bv8/prokineticin 2 is up-regulated in inflammatory granulocytes and modulates inflammatory pain

Giannini

Lattanzi

Nicotra

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

111

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Neutrophil migration into injured tissues is invariably accompanied by pain. Bv8/prokineticin 2 (PK2), a chemokine characterized by a unique structural motif comprising five disulfide bonds, is highly expressed in inflamed tissues associated to infiltrating cells. Here, we demonstrate the fundamental role of granulocyte-derived PK2 (GrPK2) in initiating inflammatory pain and driving peripheral sensitization. In animal models of complete Freund's adjuvantinduced paw inflammation the development and duration of pain temporally correlated with the expression levels of PK2 in the inflamed sites. Such an increase in PK2 mRNA depends mainly on a marked up-regulation of PK2 gene transcription in granulocytes. A substantially lower up-regulation was also detected in macrophages. From a pool of peritoneal granulocytes, elicited in rats by oyster glycogen, we purified the GrPK2 protein, which displayed high affinity for the prokineticin receptors (PKRs) and, when injected into the rat paw, induced hypersensitivity to noxious stimuli as the amphibian prokineticin Bv8 did. Mice lacking PKR1 or PKR2 developed significantly less inflammation-induced hyperalgesia in comparison with WT mice, confirming the involvement of both PKRs in inflammatory pain. The inflammation-induced upregulation of PK2 was significantly less in pkr1 null mice than in WT and pkr2 null mice, demonstrating a role of PKR1 in setting PK2 levels during inflammation. Pretreatment with a nonpeptide PKR antagonist, which preferentially binds PKR1, dose-dependently reduced and eventually abolished both prokineticin-induced hypernociception and inflammatory hyperalgesia. Inhibiting PK2 formation or antagonizing PKRs may represent another therapeutic approach for controlling inflammatory pain.hypernociception ͉ inflammation ͉ prokineticin receptors

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“…The lower limit of cytokine detection was 3.2 pg/ml, whereas the higher limit was 10,000 pg/ml. Cytokine concentrations were automatically calculated as previously described [15].…”

Section: Monocyte Cytokine Productionmentioning

confidence: 99%

Impairment of stimulation ability of very-preterm neonatal monocytes in response to lipopolysaccharide

et al. 2010

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Comparative methods for multiplex analysis of cytokine protein expression in plasma of lipopolysaccharide-treated mice

Cited by 27 publications

References 8 publications

Shedding of Tumor Necrosis Factor Receptor 1 Induced by Protein A Decreases Tumor Necrosis Factor Alpha Availability and Inflammation during Systemic Staphylococcus aureus Infection

Shedding of Tumor Necrosis Factor Receptor 1 Induced by Protein A Decreases Tumor Necrosis Factor Alpha Availability and Inflammation during Systemic Staphylococcus aureus Infection

The chemokine Bv8/prokineticin 2 is up-regulated in inflammatory granulocytes and modulates inflammatory pain

Impairment of stimulation ability of very-preterm neonatal monocytes in response to lipopolysaccharide

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