<?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>0120-4157</journal-id>
<journal-title><![CDATA[Biomédica]]></journal-title>
<abbrev-journal-title><![CDATA[Biomédica]]></abbrev-journal-title>
<issn>0120-4157</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Salud]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0120-41572018000300437</article-id>
<article-id pub-id-type="doi">10.7705/biomedica.v38i3.3688</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Nueva teoría sobre la depresión: un equilibrio del ánimo entre el sistema nervioso y el inmunológico, con regulación de la serotonina-quinurenina y el eje hipotálamo-hipófiso-suprarrenal]]></article-title>
<article-title xml:lang="en"><![CDATA[A new theory of depression based on the serotonin/kynurenine relationship and the hypothalamicpituitary- adrenal axis]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ramírez]]></surname>
<given-names><![CDATA[Leslie Alejandra]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez-Padilla]]></surname>
<given-names><![CDATA[Elsy Arlene]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[García-Oscos]]></surname>
<given-names><![CDATA[Francisco]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Salgado]]></surname>
<given-names><![CDATA[Humberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Atzori]]></surname>
<given-names><![CDATA[Marco]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pineda]]></surname>
<given-names><![CDATA[Juan Carlos]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Autónoma de Yucatán Centro de Investigaciones Regionales &#8220;Dr. Hideyo Noguchi&#8221; Departamento de Neurociencias]]></institution>
<addr-line><![CDATA[Mérida ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Autónoma de Yucatán Licenciatura en Rehabilitación Facultad de Medicina]]></institution>
<addr-line><![CDATA[Mérida ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,University of Texas Deparment of Neuroscience ]]></institution>
<addr-line><![CDATA[Dallas TX]]></addr-line>
<country>USA</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Universidad Autónoma de San Luis Potosí Facultad de Ciencias Laboratorio de Neurobiología del Estrés]]></institution>
<addr-line><![CDATA[San Luis Potosí ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,University of Texas at Dallas School of Behavioral and Brain Sciences ]]></institution>
<addr-line><![CDATA[Richardson TX]]></addr-line>
<country>USA</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2018</year>
</pub-date>
<volume>38</volume>
<numero>3</numero>
<fpage>437</fpage>
<lpage>450</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0120-41572018000300437&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0120-41572018000300437&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0120-41572018000300437&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La hipótesis sobre las causas de la depresión basada en la acción de la serotonina y del sistema inmunológico, propone que ciertos tipos de estrés distorsionan la relación entre la actividad del sistema inmunitario innato y la del sistema nervioso central. El estrés causado por una infección o el estrés psicológico excesivo activan receptores de tipo toll, como el TLR-4, el factor de transcripción NF-kB, el inflamasoma NLRP3, así como la secreción de interleucina 1 beta (IL-1&#946;) e interleucina 6 (IL-6); esto causa, en primer lugar, los síntomas generales de enfermedad que aparecen con cualquier infección, pero también los síntomas característicos de la depresión como disforia y anhedonia. Las evidencias indican que, si el estímulo persiste o se repite en las siguientes 24 horas, se activa la enzima indolamina 2,3-dioxigenasa (IDO) de la vía metabólica de la quinurenina, lo cual incrementa la síntesis del ácido quinolínico y reduce la síntesis de serotonina. El ácido quinolínico activa los receptores de N-metil-D-aspartato (NMDA) en el sistema nervioso central y estimula la secreción de, entre otras, las interleucinas IL-6 e 1L-1&#946;, las cuales promueven la hiperactividad del eje hipotálamohipófiso- suprarrenal y refuerzan la desviación del metabolismo del triptófano hacia la producción de ácido quinolínico, así como de las interleucinas de la inmunidad innata, con lo cual se reduce más la síntesis de serotonina y se consolida el proceso depresivo. Este proceso puede ser iniciado por las interleucinas estimuladas por una infección, así como por algunas vacunas o por un estrés psicológico excesivo que active el eje hipotálamo-hipófiso-suprarrenal simultáneamente con la respuesta inmunológica innata, con lo que se provocaría un proceso de inflamación estéril en el sistema nervioso central.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract The serotonergic and immunological hypothesis of depression proposes that certain types of excessive stress distort the relationship between the activities of the innate immune and central nervous systems, so that the stress caused by an infection, or excessive psychological stress, activate toll-like receptors such as the TLR-4, the transcription factor NF-kB, the inflammasome NLRP3, as well as the secretion of interleukin-1 beta (IL-1&#946;), interleukin-6 (IL-6) and other factors of the innate immune response, causing first, the general symptoms of the disease which appear with any infection, but also those characteristic of depressive illness such as dysphoria and anhedonia. The evidence indicates that, if the stimulus persists or recurs within 24 hours, the indole-2, 3-dioxygenase enzyme (IDO) of the kynurenine metabolic pathway, which increases the synthesis of quinolinic acid, is activated with an associated reduction of serotonin synthesis. Quinolinic acid activates NMDA receptors in the central nervous system and stimulates the secretion of interleukins IL-6 and 1L-1&#946;, among others, promoting hyper-activity of the HPA axis and reinforcing a bias of the tryptophan metabolism to produce quinolinic acid, and interleukins by the innate immune system, further reducing the synthesis of serotonin and consolidating the depressive process. We discuss the evidence showing that this process can be initiated by either interleukin stimulated by an infection or some vaccines or excessive psychological stress that activates the HPA axis together with said innate immune response, causing a process of aseptic inflammation in the central nervous system.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[depresión]]></kwd>
<kwd lng="es"><![CDATA[sistema nervioso]]></kwd>
<kwd lng="es"><![CDATA[sistema inmunológico]]></kwd>
<kwd lng="es"><![CDATA[serotonina]]></kwd>
<kwd lng="es"><![CDATA[inmunidad innata, interleucina-1beta]]></kwd>
<kwd lng="es"><![CDATA[interleucina-6]]></kwd>
<kwd lng="es"><![CDATA[interleucina-10]]></kwd>
<kwd lng="es"><![CDATA[interferón gamma]]></kwd>
<kwd lng="es"><![CDATA[neuroglia]]></kwd>
<kwd lng="es"><![CDATA[sistema hipotálamohipófiso-suprarrenal.]]></kwd>
<kwd lng="en"><![CDATA[Depression]]></kwd>
<kwd lng="en"><![CDATA[nervous system]]></kwd>
<kwd lng="en"><![CDATA[immune system]]></kwd>
<kwd lng="en"><![CDATA[serotonin]]></kwd>
<kwd lng="en"><![CDATA[immunity, innate]]></kwd>
<kwd lng="en"><![CDATA[interleukin-1beta]]></kwd>
<kwd lng="en"><![CDATA[interleukin-6]]></kwd>
<kwd lng="en"><![CDATA[interleukin-10, interferon gamma]]></kwd>
<kwd lng="en"><![CDATA[neuroglia]]></kwd>
<kwd lng="en"><![CDATA[pituitary-adrenal system]]></kwd>
</kwd-group>
</article-meta>
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