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@ARTICLE{CampiSantos:284097,
      author       = {Campi Santos, Patricia and Santos, Daniel Assis and Secchim
                      Ribeiro, Lucas and Fagundes, Caio Tavares and de Paula,
                      Talles Prosperi and Avila, Thiago Vinícius and Baltazar,
                      Ludmila de Matos and Madeira, Mila Moreira and Cruz, Rosana
                      de Carvalho and Dias, Ana Carolina Fialho and Machado,
                      Fabiana Simão and Teixeira, Mauro Martins and Cisalpino,
                      Patrícia Silva and Souza, Danielle G.},
      title        = {{T}he {P}ivotal {R}ole of 5-{L}ipoxygenase-{D}erived {LTB}4
                      in {C}ontrolling {P}ulmonary {P}aracoccidioidomycosis},
      journal      = {PLoS neglected tropical diseases},
      volume       = {7},
      number       = {8},
      issn         = {1935-2727},
      address      = {Lawrence, Kan.},
      publisher    = {PLoS},
      reportid     = {DZNE-2026-00105},
      pages        = {e2390},
      year         = {2013},
      abstract     = {Leukotrienes (LTs) produced from arachidonic acid by the
                      action of 5-lipoxygenase (5-LO) are classical mediators of
                      inflammatory responses. However, studies published in the
                      literature regarding these mediators are contradictory and
                      it remains uncertain whether these lipid mediators play a
                      role in host defense against the fungal pathogen
                      Paracoccidioides brasiliensis. To determine the involvement
                      of LTs in the host response to pulmonary infection,
                      wild-type and LT-deficient mice by targeted disruption of
                      the 5-lipoxygenase gene (knockout mice) were studied
                      following intratracheal challenge with P. brasiliensis
                      yeasts. The results showed that infection is uniformly fatal
                      in 5-LO-deficient mice and the mechanisms that account for
                      this phenotype are an exacerbated lung injury and higher
                      fungal pulmonary burden. Genetic ablation or pharmacological
                      inhibition of LTs resulted in lower phagocytosis and
                      fungicidal activity of macrophages in vitro, suggesting that
                      deficiency in fungal clearance seems to be secondary to the
                      absence of activation in 5-LO(-/-) macrophages. Exogenous
                      LTB4 restored phagocytosis and fungicidal activity of
                      5-LO(-/-) macrophages. Moreover, P. brasiliensis killing
                      promoted by LTB4 was dependent on nitric oxide (NO)
                      production by macrophages. Taken together, these results
                      reveal a fundamental role for 5-LO-derived LTB4 in the
                      protective response to P. brasiliensis infection and
                      identify relevant mechanisms for the control of fungal
                      infection during the early stages of the host immune
                      response.},
      keywords     = {Animals / Arachidonate 5-Lipoxygenase: metabolism / Colony
                      Count, Microbial / Disease Models, Animal / Leukotriene B4:
                      metabolism / Lung: microbiology / Lung: pathology / Male /
                      Mice / Mice, Knockout / Paracoccidioides: immunology /
                      Paracoccidioidomycosis: immunology / Survival Analysis /
                      Leukotriene B4 (NLM Chemicals) / Arachidonate 5-Lipoxygenase
                      (NLM Chemicals)},
      ddc          = {610},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1371/journal.pntd.0002390},
      url          = {https://pub.dzne.de/record/284097},
}