Merck
  • Home
  • Search Results
  • Estrogen-mediated impairment of macrophageal uptake of environmental TiO2 particles to explain inflammatory effect of TiO2 on airways during pregnancy.

Estrogen-mediated impairment of macrophageal uptake of environmental TiO2 particles to explain inflammatory effect of TiO2 on airways during pregnancy.

Journal of immunotoxicology (2014-05-16)
Yiming Zhang, Lyudmila Mikhaylova, Lester Kobzik, Alexey V Fedulov
ABSTRACT

Innate defenses against environmental particulate exposures can become deficient when physiological background of the organism is unbalanced. Even those exposures considered innocuous may then become harmful. For example, one of the important inherent risks of pregnancy is increased inflammatory responsiveness in the airways, which extends to exposures considered otherwise innocuous: it has been observed that normally "inert" particulates become inflammatory in pregnancy. They lead to enhanced airway inflammation associated with increased asthma risk in the offspring in the BALB/c model. It was hypothesized that pregnancy hormones alter macrophageal uptake and clearance of particles. This study shows that the phagocytic activity of alveolar macrophages (AM) and RAW264.7 cells against titanium dioxide (TiO2) was inhibited in pregnancy by ∼ 10% and in vitro by estradiol by ∼ 20%; progesterone potentiated this effect. Hence, enhanced inflammation in pregnancy as an outcome of exposure to the "inert" TiO2 may be due to an effect of pregnancy hormones which decrease the ability of the airways to clear the particles. AM (at 10(6) cells/recipient) isogenically transplanted from pregnant mothers into airways of recipients were able to confer the phenotype of inflammatory response to TiO2 (PMN counts of 1.62 [± 0.19] × 10(5)/ml versus 0.61 [± 0.13] × 10(5)/ml in control). Because this small amount of transferred AM could not replace the AM population in the recipients' lungs, it is postulated that the effect is mediated by inhibitory signaling factors that AM produce and release; hence, a list of probable molecules was identified via genome-wide microarray.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Methanol, HPLC Plus, ≥99.9%, poly-coated bottles
Supelco
Methanol, Pharmaceutical Secondary Standard; Certified Reference Material
Progesterone for peak identification, European Pharmacopoeia (EP) Reference Standard
Progesterone for system suitability, European Pharmacopoeia (EP) Reference Standard
USP
Progesterone, United States Pharmacopeia (USP) Reference Standard
Progesterone, European Pharmacopoeia (EP) Reference Standard
Supelco
Progesterone, Pharmaceutical Secondary Standard; Certified Reference Material
Sigma-Aldrich
Methanol, for residue analysis, JIS 5000
Sigma-Aldrich
Methanol, ACS reagent, ≥99.8%
Sigma-Aldrich
Methanol, ACS reagent, ≥99.8%
Sigma-Aldrich
Methanol, puriss. p.a., ACS reagent, reag. ISO, reag. Ph. Eur., ≥99.8% (GC)
Sigma-Aldrich
Methanol, ACS reagent, ≥99.8%
Sigma-Aldrich
Methanol, Laboratory Reagent, ≥99.6%
Sigma-Aldrich
Methanol, Absolute - Acetone free
Sigma-Aldrich
Methanol, SAJ special grade
Sigma-Aldrich
Methanol, suitable for HPLC
Sigma-Aldrich
Methanol, NMR reference standard
Sigma-Aldrich
Methanol, JIS 1000, ≥99.8%, for residue analysis
Sigma-Aldrich
Methanol, ≥99.8%, suitable for absorption spectrum analysis
Sigma-Aldrich
Methanol, ≥99.8%, for chromatography
Sigma-Aldrich
Methanol, JIS special grade, ≥99.8%
Sigma-Aldrich
Methanol, SAJ first grade, ≥99.5%
Sigma-Aldrich
Methanol, JIS 300, ≥99.8%, for residue analysis
Sigma-Aldrich
Progesterone, powder, BioReagent, suitable for cell culture
Sigma-Aldrich
Progesterone, meets USP testing specifications
Sigma-Aldrich
Methanol, anhydrous, 99.8%
Supelco
Progesterone, VETRANAL®, analytical standard
Sigma-Aldrich
Progesterone, γ-irradiated, BioXtra, suitable for cell culture
Supelco
Methanol, analytical standard
Sigma-Aldrich
Methanol, ACS spectrophotometric grade, ≥99.9%