The Role of Exosome-Derived microRNA on Lung Cancer Metastasis Progression.

The high mortality from lung cancer is mainly attributed to the presence of metastases at the time of diagnosis. Despite being the leading cause of lung cancer death, the underlying molecular mechanisms driving metastasis progression are still not fully understood. Recent studies suggest that tumor cell exosomes play a significant role in tumor progression through intercellular communication between tumor cells, the microenvironment, and distant organs. Furthermore, evidence shows that exosomes release biologically active components to distant sites and organs, which direct metastasis by preparing metastatic pre-niche and stimulating tumorigenesis. As a result, identifying the active components of exosome cargo has become a critical area of research in recent years. Among these components are microRNAs, which are associated with tumor progression and metastasis in lung cancer. Although research into exosome-derived microRNA (exosomal miRNAs) is still in its early stages, it holds promise as a potential target for lung cancer therapy. Understanding how exosomal microRNAs promote metastasis will provide evidence for developing new targeted treatments. This review summarizes current research on exosomal miRNAs' role in metastasis progression mechanisms, focusing on lung cancer.

Mechanisms of Lung Damage and Development of COPD Due to Household Biomass-Smoke Exposure: Inflammation, Oxidative Stress, MicroRNAs, and Gene Polymorphisms.

Chronic exposure to indoor biomass smoke from the combustion of solid organic fuels is a major cause of disease burden worldwide. Almost 3 billion people use solid fuels such as wood, charcoal, and crop residues for indoor cooking and heating, accounting for approximately 50% of all households and 90% of rural households globally. Biomass smoke contains many hazardous pollutants, resulting in household air pollution (HAP) exposure that often exceeds international standards. Long-term biomass-smoke exposure is associated with Chronic Obstructive Pulmonary Disease (COPD) in adults, a leading cause of morbidity and mortality worldwide, chronic bronchitis, and other lung conditions. Biomass smoke-associated COPD differs from the best-known cigarette smoke-induced COPD in several aspects, such as a slower decline in lung function, greater airway involvement, and less emphysema, which suggests a different phenotype and pathophysiology. Despite the high burden of biomass-associated COPD, the molecular, genetic, and epigenetic mechanisms underlying its pathogenesis are poorly understood. This review describes the pathogenic mechanisms potentially involved in lung damage, the development of COPD associated with wood-derived smoke exposure, and the influence of genetic and epigenetic factors on the development of this disease.

Role of IL-10-Producing Natural Killer Cells in the Regulatory Mechanisms of Inflammation during Systemic Infection.

Natural killer (NK) cells have the dual ability to produce pro-inflammatory (IFNγ) and anti-inflammatory (IL-10) cytokines during systemic infection, which points to their crucial role both as inflammatory effectors for infection clearance and as regulators to counterbalance inflammation to limit immune-mediated damage to the host. In particular, immunosuppressive IL-10 secretion by NK cells has been described to occur in systemic, but not local, infections as a recent immunoregulatory mechanism of inflammation that may be detrimental or beneficial, depending on the timing of release, type of disease, or the infection model. Understanding the factors that drive the production of IL-10 by NK cells and their impact during dualistic inflammatory states, such as sepsis and other non-controlled inflammatory diseases, is relevant for achieving effective therapeutic advancements. In this review, the evidence regarding the immunoregulatory role of IL-10-producing NK cells in systemic infection is summarized and discussed in detail, and the potential molecular mechanisms that drive IL-10 production by NK cells are considered.

Identificación molecular de Candida lusitaniae en infección de tracto respiratorio inferior / Molecular identification of Candida lusitaniae in lower repiratory tract infection

Candida lusitaniae es una levadura que ha sido descrita como un patógeno nosocomial emergente de baja frecuencia en infecciones profundas. La identificación oportuna de C. lusitaniae es importante porque puede desarrollar resistencia in vivo a la anfotericina B durante la terapia. Comunicamos el aislamiento de C. lusitaniae como agente etiológico de infección de tracto respiratorio inferior en un paciente masculino. Los cultivos de orina y esputo fueron negativos para bacterias y positivos para esta levadura. Los aislamientos fueron identificados por métodos fenotípicos de rutina y confirmados por secuenciación y polimorfismos de longitud de fragmentos de restricción y PCR de la región espaciadora interna del ADN ribosómico

Candida lusitaniae is a yeast that has emerged as a low frequency nosocomial pathogen in deep infections. Although it usually shows in vitro susceptibility to all antifungal agents, in vivo resistance to amphotericin B has been observed in several clinical cases. Therefore, its early identification in the course of therapy is important. We report the isolation of C. lusitaniae as an etiologic agent of a lower respiratory tract infection in a male patient. Urine and sputum cultures were negative for bacteria and positive for this yeast. Isolates were identified by routine phenotypic methods and confirmed by sequencing and restriction fragment length polymorphism analysis of PCR internal spacer of ribosomal DNA