Este artículo debe citarse como: Rico-Rosillo MG, Vega-Robledo GB. Sueño y sistema inmune. Rev Alerg Mex. 2018;65(2):160-170 ORCID María Guadalupe Rico-Rosillo, ORCID: 0000-0002-3117-1617; Gloria Bertha Vega-Robledo, ORCID: 0000-0002-5816-1910 AbstractSleep is a process that occupies one third part of the life of the human being, and it is essential in order for the individual to be able to maintain body homeostasis. It emerges as an important regulator of the immune system since, during sleep, the necessary functions to maintain its balance are carried out. On the other hand, decreased sleep has deleterious eff ects that alter the metabolism and produce an increase in the secretion of C-reactive protein, interleukin (IL)-6 and tumor necrosis factor (TNF). These cytokines activate NF-κB; therefore, sleep disturbance can be a risk factor for the development of chronic infl ammatory and metabolic diseases. Pro-infl ammatory cytokines IL-1, IL-6 and TNF increase non-rapid eye movement sleep, whereas anti-infl ammatory cytokines such as IL-4 and IL-10 decrease it. Sleep can modify the immune system function by inducing changes in the hypothalamus-pituitary-adrenal axis and the sympathetic nervous system. In turn, the circadian rhythm of hormones such as cortisol and adrenaline, which have a nocturnal decrease, favors diff erent activities of the immune system. The purpose of the present review is to address diff erent aspects of sleep and their relationship with the immune system.

Many modified genes are products regulated by the Nuclear Factor-kappaB and Mitogen Activated Protein Kinase pathways, suggesting MLIF involvement with these two major pathways for the modulation of the inflammation and immune responses.

El asma ocupacional es la forma más común de enfermedad pulmonar causada por factores que se atribuyen a un ambiente laboral específico en países industrializados. Causa limitación variable del flujo aéreo e hiperrespuesta de las vías aéreas debido al contacto con agentes específicos presentes en un ambiente de trabajo y no a estímulos encontrados fuera de este lugar. Se reconoce cada vez con más frecuencia y muchos agentes son capaces de causar asma ocupacional por diferentes mecanismos fisiopatológicos. Se conocen más de 400 agentes causantes de asma ocupacional y cada año se detectan nuevos desencadenantes. Numerosos factores contribuyen a la patogénesis de asma ocupacional inducida químicamente, incluidos mecanismos inmunológicos, no inmunológicos, de daño epitelial, remodelación de las vías aéreas, estrés oxidativo, inflamación neurogénica y factores genéticos. Entre los factores de riesgo de asma ocupacional están: la atopia, el tabaquismo y factores genéticos. El diagnóstico se basa en la historia clínica del paciente, pruebas cutáneas, inmunológicas y estudios funcionales. El tratamiento principal es la remoción del trabajador del sitio de exposición tan pronto como sea posible. El avance en el conocimiento de la patogénesis del asma ocupacional influirá de manera importante en la prevención y el tratamiento de esta enfermedad.

El tejido adiposo, actualmente considerado un órgano con funciones neuroinmunoendocrinas, participa en la homeostasis del organismo. Posee gran plasticidad y variabilidad funcional acorde con la ingesta de nutrientes o con el incremento o la disminución de su volumen tisular, el cual modifica la función y el número de las células que lo integran o llegan a él. Los elementos liberados anormalmente por estas células, entre otros citocinas y adipocinas, ocasionan inflamación local y sistémica, predominantemente cuando provienen del tejido adiposo visceral y pueden afectar diversos órganos como el hígado y el sistema cardiovascular. Se ha señalado que la obesidad implica un mayor riesgo de padecer enfermedades inflamatorias, metabólicas, autoinmunes, alérgicas, alteraciones en la cicatrización y cáncer.

The bone tissue, previously considered as a mechanical support or structure and movement, has shown an important participation in the homeostasis of the body, including energy metabolism and adipose tissue. Currently, it is considered an endocrine organ that synthesizes regulatory molecules of metabolism called osteokines. At the same time, the adipose issue, considered as an internal secretion gland, helps to maintain the body energy and produces proteins and molecules such as adipokines, some of which affect the bone directly. The analysis of bone resorption/formation cycle shows that bone mass is a reflection of the balance between both. When this balance is lost and there is a reduction of bone mass with increased fragility, osteoporosis appears and increases the risk of fracture. One in three women and one in five men over 50 years old have a fracture due to osteoporosis. The interaction between adipose tissue and bone is mediated by cytokines, osteokines and adipokines. Obesity may affect the bone by several mechanisms, among which the inflammatory is included and those induced by cytokines secreted by adipocytes such as leptin and adiponectin which can modify bone metabolism. Evidence supports the negative effect of obesity on bone health, although studies about it are still contradictory. Keywords: Obesity; bone; adipokines; osteoporosis; osteoblast; osteoclast.

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Senescence is an irreversible process by which cells enter to a permanent cell cycle arrest with generalized molecular changes. Senescent cells remain metabolically active and most of them show a secretory phenotype; through its secretion may induce senescence or cancer in other cells. The secretory cells in the so-called transient senescence may participate in embryogenesis, tissue regeneration and immune response. The deleterious changes associated with age affect the immune system members and the immune senescence cause poor response to vaccines and susceptibility to cancer and infections. These latter are a frequent cause of asthma mostly in the elderly, the incidence is increasing in old people, and it may be related with those anatomical, physiological and immune changes caused by age, asthma chronicity and external agents. Comorbidity in the elderly worsens the ailment and hinders diagnosis, therefore, knowledge and handling of these clinical entities must be in control by the physicians responsible of the first level attention to old patients. Senescencia del sistema inmune y alteraciones relacionadas con el asma