<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0028-3746</journal-id>
<journal-title><![CDATA[Neumología y cirugía de tórax]]></journal-title>
<abbrev-journal-title><![CDATA[Neumol. cir. torax]]></abbrev-journal-title>
<issn>0028-3746</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Mexicana de Neumología y Cirugía de Tórax; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas; Sociedad Cubana de Neumología; Sociedad Paraguaya de Neumología; Sociedad Boliviana de Neumología.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0028-37462018000400267</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[El IFN-&#947; induce LL-37 pero no controla el crecimiento de M. tuberculosis en macrófagos alveolares]]></article-title>
<article-title xml:lang="en"><![CDATA[IFN-&#947; induces LL-37 but does not control the intracellular growth of M. tuberculosis in alveolar macrophages]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Herrera]]></surname>
<given-names><![CDATA[María Teresa]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[González]]></surname>
<given-names><![CDATA[Yolanda]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Juárez]]></surname>
<given-names><![CDATA[Esmeralda]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2018</year>
</pub-date>
<volume>77</volume>
<numero>4</numero>
<fpage>267</fpage>
<lpage>275</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0028-37462018000400267&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0028-37462018000400267&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0028-37462018000400267&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: El interferón-&#947; (IFN-&#947;) es una de las citocinas más importantes de la inmunidad en la tuberculosis pulmonar ya que su función principal es la activación de los mecanismos bactericidas de los macrófagos. Los pacientes con deficiencias en la producción de IFN-&#947; no tienen la capacidad para controlan la infección por Mycobacterium tuberculosis (M. tuberculosis), entonces la aplicación exógena de esta citocina es una alternativa de tratamiento.  Objetivo:  Evaluar el efecto del IFN-&#947; recombinante humano (rhIFN-&#947;) sobre los macrófagos alveolares humanos infectados con M. tuberculosis.  Métodos:  Los macrófagos alveolares de los sujetos sanos fueron infectados con la cepa virulenta M. tuberculosis H37Rv y tratados o no con rhIFN-&#947; y evaluamos la expresión del péptido antimicrobiano LL-37 y la proteína IRGM (asociado a autofagia) por PCR (polymerase chain reaction) cuantitativo en tiempo real (qPCR), la producción del factor de necrosis tumoral &#945; (TNF-&#945;) por la técnica de ELISA y el control de la infección mediante la determinación de las unidades formadoras de colonia (UFC) de M. tuberculosis.  Resultados:  El rhIFN-&#947; indujo la expresión significativa de IRGM en macrófagos no infectados y de LL-37 en los macrófagos infectados. Sin embargo, la adición del rhIFN-&#947; no tuvo un efecto significativo en la producción de TNF-&#945; ni en el control del crecimiento intracelular bacteriano.  Conclusión:  Aunque el rhIFN-&#947; induce la expresión de LL-37 en los macrófagos infectados, no contribuye en el control de crecimiento intracelular de M. tuberculosis, lo que sugiere que existen otros mecanismos independientes del IFN-&#947; involucrados en la eliminación de la micobacteria.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: Interferon-&#947; (IFN-&#947;) is one of the most important cytokines in pulmonary tuberculosis immune responses. Its main function is to activate antimicrobial mechanisms in macrophages. Patients with IFN-&#947; deficiencies are unable to control M. tuberculosis, thus the addition of rhIFN-&#947; is an alternative treatment.  Objective:  To evaluate the effects of recombinant human IFN-&#947; (rhIFN-&#947;) on human alveolar macrophages infected with M. tuberculosis.  Methods:  We infected alveolar macrophages from healthy volunteers with M. tuberculosis H37Rv and treated them with rhIFN-&#947; to evaluate the gene expression of antimicrobial peptide LL-37 and the IRGM protein (related to autophagy) by real time PCR (qPCR), tumoral necrosis factor-&#945; (TNF-&#945;) production by ELISA and intracellular growth control by colony forming units (CFU) of M. tuberculosis.  Results:  Uninfected macrophages over expressed IRGM after rhIFN-&#947; treatment, whereas infected macrophages over expressed LL-37. However, the addition of rhIFN-&#947; did not have a significant effect on production TNF-&#945; production and intracellular growth control of M. tuberculosis.  Conclusion:  Although LL-37 expression was induced, it was not associated with the killing of M. tuberculosis, suggesting that there are IFN-&#947;-independent mechanisms involved in the pathogen elimination.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Macrófagos alveolares humanos]]></kwd>
<kwd lng="es"><![CDATA[M. tuberculosis]]></kwd>
<kwd lng="es"><![CDATA[rhIFN-&#947;]]></kwd>
<kwd lng="es"><![CDATA[TNF-&#945;]]></kwd>
<kwd lng="es"><![CDATA[LL-37]]></kwd>
<kwd lng="es"><![CDATA[IRGM]]></kwd>
<kwd lng="en"><![CDATA[Human alveolar macrophages]]></kwd>
<kwd lng="en"><![CDATA[M. tuberculosis]]></kwd>
<kwd lng="en"><![CDATA[rhIFN-&#947;]]></kwd>
<kwd lng="en"><![CDATA[TNF-&#945;]]></kwd>
<kwd lng="en"><![CDATA[LL-37]]></kwd>
<kwd lng="en"><![CDATA[IRGM]]></kwd>
</kwd-group>
</article-meta>
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