Human phagocytes lack the ability to kill Mycobacterium gordonae, a non-pathogenic mycobacteria

Se ha desarrollado un modelo de infección en fagocitos humanos para poner a prueba su capacidad de matar dos cepas de M. Gordonae, HL184G y una variedad atenuada, HL184Gat. Como controles se incluyeron una cepa de M.Tuberculosis (HL186T) y otro de L. Pneumophila (ATCC13151). Se observa que los fagocitos humanos carecen de la capacidad intrínseca de eliminar ya sea M. Gordonae o M. Tuberculosis, pero matan a la cepa atenuada. Pudimos observar una relación entre la patogenicidad y el patrón de producción de citoquinas. Así, tanto el patógeno M. tuberculosis y L. Pneumophila, pero no la no patógeno M. Gordonae, induce la producción de niveles significativamente diferentes de IL-1A, IL-6 y TNF-C en monocitos y IL-8 en los neutrófilos. Aunque tanto monocitos y neutrófilos mataron HL184Gat, pero no HL184G, los patrones de la producción de citoquinas inducida por cualquiera de las cepas eran idénticas. La adición de INF-D y / o TNF-C no mejoró la actividad antimicobacteriana de los fagocito

Apoptosis and oxidative burst in neutrophils infected with Mycobacterium spp.

Los neutrófilos son las especies reactivas de oxígeno (ROS) y la inducción de apoptosis. Su importancia en las infecciones por micobacterias es el objetivo a analizar Se analizó de forma simultánea en los neutrófilos infectados con cualquiera M. tuberculosis o la no patógena M. gordonae. Ninguna de las dos especies se elimina por neutrófilos, pero el patrón exhibido para ambas actividades es completamente diferente. La tuberculosis induce la producción de ROS y la apoptosis y la M. Gordonae no lo hace. La evidencia adicional fue proporcionada por una cepa atenuada de M. gordonae que, aunque se ha convertido en susceptibles a la actividad antimicrobiana de los neutrófilos, todavía no hace promover la producción de ROS o apoptosis. Por lo tanto no se pudo establecer ninguna relación entre cualquiera de estas actividades y la capacidad de los neutrófilos para matar las micobacterias. Hemos observado que la concentración de neutrófilos, una variable que es importante en la actividad antimicrobiana frente a otros patógenos, no tiene ninguna influencia en el micobacteriana crecimiento intracelula

CCL20 is overexpressed in Mycobacterium tuberculosis infected monocytes and inhibits the production of reactive oxygen species (ROS)

CCL20 es una quimiocina que atrae las células dendríticas inmaduras. Se demuestra que los monocitos, células características de la respuesta inmune innata, infectadas con Mycobacterium la tuberculosis expresan el gen CCL20 a nivel mucho más alto que las mismas células infectadas con microbacterias no tuberculosas. INFE, una citoquina fundamental en la respuesta inmune a la tuberculosis, inhibe fuertemente tanto la transcripción y la traducción de CCL20. También hemos confirmado que las células dendríticas son un huésped adecuado para la proliferación de microbacterias, aunque no parece CCL20 de influir en su intracelular tasa de multiplicación. La quimioquina, sin embargo, regula a la baja la característica producción de especies reactivas de oxígeno (ROS) inducida por M. tuberculosis en monocitos, que pueden afectar a la actividad de las células. La apoptosis mediada por las micobacterias, posiblemente ROS-dependiente, también fue inhibido por CCL2

Leptin levels and Q223R leptin receptor gene polymorphism in obese Mexican young adults

Introduction: The Q223R polymorphism of the leptin receptor (LEPR) gene is one of the most common polymorphisms and it is believed to be associated with a damaged capacity of LEPR signaling and with high circulating leptin levels. Methods: An observational, cross-sectional, analytical study was carried out in the Autonomous University of Ciudad Juarez, Mexico, where a sample of young adult participants (ranging from 18 to 30 years of age) was obtained. They were classified based on the results of body mass index: non-obese, and overweight/ obese. The polymorphic variant was determined by Polymerase Chain Reaction (PCR) from the DNA sample and serum leptin levels were measured by EnzymeLinked Immuno Sorbent Assay Results: A total of 159 participants were included (nonobese, n=103; overweight/obese, n=56). Leptin levels were 15.14±12.3 ng/mL in the non-obese group and 26.13±19.0 ng/mL in the overweight/ obese group (p≤0.001). The allelic frequencies of the Q and R alleles of the LEPR gene in the studied subjects were as follows: non-obese, Q=0.56, R=0.44; overweight/obese, Q=0.62, R=0.38. The relative risk for the Q/Q genotype was 1.18 (CI 0.53-2.34), for Q/R was 1.14 (CI 0.59-2.18) and for R/R was 0.59 (CI 0.23-1.50). Conclusions: This study shows that leptin levels are associated with overweight/obesity in Mexican young adults, but this is not related to the presence of the Q223R polymorphism in the LEPR gene, so the underlying mechanisms for a possible disturbance in leptin signaling in obese Mexican young adults await further studies

Neotropical ornithology: Reckoning with historical assumptions, removing systemic barriers, and reimagining the future

A major barrier to advancing ornithology is the systemic exclusion of professionals from the Global South. A recent special feature, Advances in Neotropical Ornithology, and a shortfalls analysis therein, unintentionally followed a long-standing pattern of highlighting individuals, knowledge, and views from the Global North, while largely omitting the perspectives of people based within the Neotropics. Here, we review current strengths and opportunities in the practice of Neotropical ornithology. Further, we discuss problems with assessing the state of Neotropical ornithology through a northern lens, including discovery narratives, incomplete (and biased) understanding of history and advances, and the promotion of agendas that, while currently popular in the north, may not fit the needs and realities of Neotropical research. We argue that future advances in Neotropical ornithology will critically depend on identifying and addressing the systemic barriers that hold back ornithologists who live and work in the Neotropics: unreliable and limited funding, exclusion from international research leadership, restricted dissemination of knowledge (e.g., through language hegemony and citation bias), and logistical barriers. Moving forward, we must examine and acknowledge the colonial roots of our discipline, and explicitly promote anti-colonial agendas for research, training, and conservation. We invite our colleagues within and beyond the Neotropics to join us in creating new models of governance that establish research priorities with vigorous participation of ornithologists and communities within the Neotropical region. To include a diversity of perspectives, we must systemically address discrimination and bias rooted in the socioeconomic class system, anti-Blackness, anti-Brownness, anti-Indigeneity, misogyny, homophobia, tokenism, and ableism. Instead of seeking individual excellence and rewarding top-down leadership, institutions in the North and South can promote collective leadership. In adopting these approaches, we, ornithologists, will join a community of researchers across academia building new paradigms that can reconcile our relationships and transform science. Spanish and Portuguese translations are available in the Supplementary Material.• Research conducted by ornithologists living and working in Latin America and the Caribbean has been historically and systemically excluded from global scientific paradigms, ultimately holding back ornithology as a discipline.• To avoid replicating systems of exclusion in ornithology, authors, editors, reviewers, journals, scientific societies, and research institutions need to interrupt long-held assumptions, improve research practices, and change policies around funding and publication.• To advance Neotropical ornithology and conserve birds across the Americas, institutions should invest directly in basic field biology research, reward collective leadership, and strengthen funding and professional development opportunities for people affected by current research policies.Peer reviewe