Contribution of different placental cells to the expression and stimulation of antimicrobial proteins (AMPs)

Klaffenbach, Daniela; Friedrich, Diana; Strick, Reiner; Strissel, Pamela L.; Beckmann, MW; Rascher, Wolfgang; Gessner, Alexandra; Dötsch, Jörg; Meißner, Udo; Schnare, Markus

doi:10.1016/j.placenta.2011.08.004

Cited by 27 publications

(37 citation statements)

References 21 publications

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“…The latter may be related to incubation times or peptides degradation. It is noteworthy to mention that a similar difficulty to detect AMPs in the culture media of placental cells has been previously reported by others [34].…”

Section: Protein Expression Studiessupporting

confidence: 82%

IL-10 inhibits while calcitriol reestablishes placental antimicrobial peptides gene expression

Olmos-Ortíz

Noyola-Martínez

Barrera

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Protein Expression Studiessupporting

confidence: 82%

IL-10 inhibits while calcitriol reestablishes placental antimicrobial peptides gene expression

Olmos-Ortíz

Noyola-Martínez

Barrera

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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“…The limited expression of TLRs on trophoblast cells suggested that early trophoblasts might be less able to protect embryos against pathogenic agents compared to differentiated trophoblast cells [41]. The obtained results are consistent with outcomes of another study, which indicated that TLR4 expression and related IL-8 secretion that occurred after LPS stimulation might be assigned, rather, to leukocytes, as it was no longer observed in trophoblast fraction purified from leukocytes [42]. The expression of different antimicrobial peptides and proteins was suggested to be characteristic for various placental cells and resulted from the cooperation between leukocytes and cells of embryonic origin [42].…”

Section: The Activity Of Tlrs During Pregnancysupporting

confidence: 82%

SNPs in toll-like receptor (TLR) genes as new genetic alterations associated with congenital toxoplasmosis?

Wujcicka

Wilczyński

Nowakowska

2012

Eur J Clin Microbiol Infect Dis

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Nearly 40 % of pregnant women are infected with Toxoplasma gondii. Primary infections in pregnant women result, in approximately 30–50 % of patients, in transmission of T. gondii through the placenta to the fetus and then in congenital infections with severe, sometimes fatal course. Studies still do not provide sufficient data on the genetic bases of the immunity in fetuses, newborns, and infants with congenital toxoplasmosis. Previous research showed the contribution of toll-like receptors (TLRs) to non-specific immunity against T. gondii invasion, observed in T. gondii-infected animals, especially mice. So far, the activity of TLRs in defense against T. gondii infections was observed particularly for TLR2, TLR4, and TLR9 molecules. Differential TLR activity associates with both cell types, including a variety of placental cells and stage of pregnancy. Several single-nucleotide polymorphisms (SNPs) residing in three genes encoding these receptors were reported as significant genetic modifications of TLRs associated with different pregnancy disorders. Despite those data, genetic alterations of TLRs which have contributed to innate immune response against T. gondii infections are still not precisely described. In this article, we present reasons for the research of the plausible role of SNPs residing in TLR2, TLR4, and TLR9 genes in congenital toxoplasmosis development.

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“…We speculate, however, that granulocytes, neutrophils in particular, fetal, maternal, or both, are the predominant source of increased cathelicidin level in amniotic fluid. Our assumption is supported by the work of Klaffenbach et al, where the authors assessed antimicrobial peptides and protein production by placenta [51]. Although placental tissue is capable of producing a wide range of antimicrobial peptides, granulocytes were the key source of secreted proteins.…”

Section: Discussionmentioning

confidence: 52%

Amniotic Fluid Cathelicidin in PPROM Pregnancies: From Proteomic Discovery to Assessing Its Potential in Inflammatory Complications Diagnosis

et al. 2012

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Background Preterm prelabor rupture of membranes (PPROM) complicated by microbial invasion of the amniotic cavity (MIAC) leading to histological chorioamnionitis (HCA) significantly impacts perinatal morbidity. Unfortunately, no well-established tool for identifying PPROM patients threatened by these disorders is available. Methodology/Principal Findings We performed an unbiased exploratory analysis of amniotic fluid proteome changes due to MIAC and HCA. From among the top five proteins that showed the most profound and significant change, we sought to confirm results concerning cathelicidin (P49913, CAMP_HUMAN), since an ELISA kit was readily available for this protein. In our exploratory proteomic study, cathelicidin showed a ∼6-fold higher concentration in PPROM patients with confirmed MIAC and HCA. We verified significantly higher levels of cathelicidin in exploratory samples (women without both MIAC and HCA: median 1.4 ng/ml; women with both conditions confirmed: median 3.6 ng/ml; p = 0.0003). A prospective replication cohort was used for independent validation and for assessment of cathelicidin potential to stratify women with MIAC leading to HCA from women in whom at least one of these conditions was ruled out. We confirmed the association of higher amniotic fluid cathelicidin levels with MIAC leading to HCA (the presence of both MIAC and HCA: median 3.1 ng/ml; other women: median 1.4 ng/ml; p <0.0001). A cathelicidin concentration of 4.0 ng/ml was found to be the best cut-off point for identifying PPROM women with both MIAC and HCA. When tested on the validation cohort, a sensitivity of 48%, a specificity of 90%, a likelihood ratio of 5.0, and an area under receiver-operating characteristic curve of 71% were achieved for identification of women with MIAC leading to HCA. Conclusions Our multi-stage study suggests cathelicidin as a candidate marker that should be considered for a panel of amniotic fluid proteins permitting identification of PPROM women with MIAC leading to HCA.

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Contribution of different placental cells to the expression and stimulation of antimicrobial proteins (AMPs)

Cited by 27 publications

References 21 publications

IL-10 inhibits while calcitriol reestablishes placental antimicrobial peptides gene expression

IL-10 inhibits while calcitriol reestablishes placental antimicrobial peptides gene expression

SNPs in toll-like receptor (TLR) genes as new genetic alterations associated with congenital toxoplasmosis?

Amniotic Fluid Cathelicidin in PPROM Pregnancies: From Proteomic Discovery to Assessing Its Potential in Inflammatory Complications Diagnosis

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