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  • 1
    Language: English
    In: Sci Rep, 2017, Vol.7(1), pp.13243-13243
    Description: Naturally produced by microbial processes in soil, nitrous oxide (NO) is an important greenhouse gas contributing to climate change. Accordingly, there is a need to accurately quantify the capability of forest ecosystems to exchange NO with the atmosphere. While NO emissions from soils have been well studied, trees have so far been overlooked in NO inventories. Here, we show that stems of mature beech trees (Fagus sylvatica) may act as a substantial sink of NO from the atmosphere under conditions of soils consuming NO. Consistent consumption of NO by all stems investigated (ranging between −2.4 and −3.8 µg m h) is a novel finding in contrast to current studies presenting trees as NO emitters. To understand these fluxes, NO exchange of photoautotrophic organisms associated with beech bark (lichens, mosses and algae) was quantified under laboratory conditions. All these organisms were net NO sinks at full rehydration and temperature of 25 °C. The consumption rates were comparable to stem consumption rates measured under field conditions. Cryptogamic stem covers could be a relevant sink of NO in European beech forests.
    Keywords: Article;
    ISSN: 2045-2322
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  • 2
    Language: English
    In: Respiratory Research, 01 July 2010, Vol.11(1), p.93
    Description: Abstract Background Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards L. pneumophila. Methods We investigated the effects of L. pneumophila and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis. Results L. pneumophila induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-κB. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on L. pneumophila replication. Conclusions Taken together, human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.
    Keywords: Medicine
    ISSN: 1465-9921
    E-ISSN: 1465-993X
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