<?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>S0028-37462023000300162</article-id>
<article-id pub-id-type="doi">10.35366/116815</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[¿Los neutrófilos como células de defensa? Inmunobiología y fisiopatología en las enfermedades infecciosas respiratorias humanas]]></article-title>
<article-title xml:lang="en"><![CDATA[Neutrophils as defense cells? Immunobiology and pathophysiology in human respiratory infectious diseases]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rojas-Valles]]></surname>
<given-names><![CDATA[Edwin U]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Magaña-González]]></surname>
<given-names><![CDATA[Carlos Alberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Herrera-Barrios]]></surname>
<given-names><![CDATA[María Teresa]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México Facultad de Medicina ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad Autónoma del Estado de Hidalgo  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2023</year>
</pub-date>
<volume>82</volume>
<numero>3</numero>
<fpage>162</fpage>
<lpage>173</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0028-37462023000300162&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0028-37462023000300162&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0028-37462023000300162&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: El sistema inmunológico nos protege de las infecciones y la entrada de cualquier patógeno activa la inmunidad innata. Los neutrófilos son parte de este tipo de respuesta y son los más abundantes en la sangre con una vida media corta que se incrementa cuando están activados. Se generan en la médula ósea durante la granulopoyesis y su liberación a la sangre depende de la unión de CXCR4-CXCL12. Son las primeras células en llegar al sitio de infección o inflamación, y sus mecanismos bactericidas son la fagocitosis, la desgranulación, la producción de especies reactivas de oxígeno, trampas extracelulares de neutrófilos, citocinas y quimiocinas. Durante las infecciones, llevan a cabo la fagocitosis caracterizada por la fusión directa fagosoma-gránulo, y los patógenos mueren por la acción de proteínas granulares tóxicas y moléculas oxidantes (especies reactivas de oxígeno y ácido hipocloroso). Los patógenos o citocinas favorecen la desgranulación que, junto con la producción de especies reactivas de oxígeno y ácido hipocloroso, actúan sobre las proteínas, ADN y las membranas bacterianas favoreciendo su eliminación. Los neutrófilos producen trampas extracelulares de neutrófilos para atrapar los patógenos y evitar su propagación y, además, son fuente de citocinas y quimiocinas, por lo que participan en la regulación de la respuesta inmune. En las enfermedades infecciosas humanas su participación puede ayudar, o contribuir a un mal pronóstico, provocando daño tisular. Esta revisión tiene como objetivo conocer las generalidades de los neutrófilos y su participación en enfermedades respiratorias humanas como COVID-19, influenza, tuberculosis e histoplasmosis.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: The immune system protects us from infections and the entry of any pathogen activates innate immunity. Neutrophils are part of this type of response and are the most abundant in the blood with a short half-life that increases when they are activated. They are generated in the bone marrow during granulopoiesis and their release into the blood depends on the binding of CXCR4-CXCL12. They are the first cells to reach the site of infection or inflammation, and their bactericidal mechanisms are phagocytosis, degranulation, production of ROS, NET, cytokines, and chemokines. During infections, they carry out phagocytosis characterized by direct phagosome-granule fusion, and the pathogens are killed by the action of toxic granule proteins and oxidant molecules (ROS and hypochlorous acid). Pathogens or cytokines promote degranulation which, together with the production of ROS and hypochlorous acid, act on proteins, DNA, and bacterial membranes favoring their elimination. Neutrophils produce NET to trap pathogens and prevent their spread, and they are also a source of cytokines and chemokines, which is why they participate in the regulation of the immune response. In human infectious diseases, their participation can help, or contribute to a poor prognosis, causing tissue damage. This review aims to know the generalities of neutrophils and their participation in human respiratory diseases such as COVID-19 and influenza, tuberculosis, and histoplasmosis.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[neutrófilos]]></kwd>
<kwd lng="es"><![CDATA[COVID-19]]></kwd>
<kwd lng="es"><![CDATA[influenza]]></kwd>
<kwd lng="es"><![CDATA[tuberculosis]]></kwd>
<kwd lng="es"><![CDATA[histoplasmosis]]></kwd>
<kwd lng="en"><![CDATA[neutrophils]]></kwd>
<kwd lng="en"><![CDATA[COVID-19]]></kwd>
<kwd lng="en"><![CDATA[influenza]]></kwd>
<kwd lng="en"><![CDATA[tuberculosis]]></kwd>
<kwd lng="en"><![CDATA[histoplasmosis]]></kwd>
</kwd-group>
</article-meta>
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