3 results match your criteria: "San Raffaele Research Center[Affiliation]"

Moving from the earlier periods in which the lungs were believed to represent sterile environments, our knowledge on the lung microbiota has dramatically increased, from the first descriptions of the microbial communities inhabiting the healthy lungs and the definition of the ecological rules that regulate its composition, to the identification of the changes that occur in pathological conditions. Despite the limitations of lung as a microbiome reservoir due to the low microbial biomass and abundance, defining its microbial composition and function in the upper and lower airways may help understanding the impact on local homeostasis and its disruption in lung diseases. In particular, the understanding of the metabolic and immune significance of microbes, their presence or lack thereof, in health and disease states could be valuable in development of novel druggable targets in disease treatments.

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Article Synopsis
  • * Recent research indicates that the gut microbiome plays a crucial role in cardiovascular health by activating immune and inflammatory responses, impacting various CVDs.
  • * This review focuses on how metabolites from gut microbiota, particularly those derived from tryptophan, interact with immune systems, potentially leading to new, microbiome-based strategies for CVD treatment.
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Stress system activity, innate and T helper cytokines, and susceptibility to immune-related diseases.

Ann N Y Acad Sci

June 2006

Laboratory of Neuro-Endocrine-Immunology, San Raffaele Research Center, via della Pisana 235, 00163 Rome, Italy.

Associations between stress and health outcomes have now been carefully documented, but the mechanisms by which stress specifically influences disease susceptibility and outcome remain poorly understood. Recent evidence indicates that glucocorticoids (GCs) and catecholamines (CAs), the major stress hormones, inhibit systemically IL-12, TNF-alpha, and INF-gamma, but upregulate IL-10, IL-4, and TGF-beta production. Thus, during an immune and inflammatory response, the activation of the stress system, through induction of a Th2 shift may protect the organism from systemic "overshooting" with T helper lymphocyte 1 (Th1)/proinflammatory cytokines.

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