Abstract
Living in a mentally and physically stimulating environment has been suggested to have a beneficial effect on the immune response. This study investigates these effects, utilizing a 2-week program of environmental enrichment (EE) and 2 models of acute inflammation: zymosan-induced peritonitis (ZIP) and the cecal ligation and puncture (CLP) model of sepsis. Our results revealed that following exposure to EE, mice possessed a significantly higher circulating neutrophil to lymphocyte ratio compared with control animals. When subject to ZIP, EE animals exhibit enhanced neutrophil and macrophage influx into their peritoneal cavity. Corresponding results were found in CLP, where we observed an improved capacity for enriched animals to clear systemic microbial infection. Ex vivo investigation of leukocyte activity also revealed that macrophages from EE mice presented an enhanced phagocytic capacity. Supporting these findings, microarray analysis of EE animals revealed the increased expression of immunomodulatory genes associated with a heightened and immunoprotective status. Taken together, these results provide potentially novel mechanisms by which EE influences the development and dynamics of the immune response.
Highlights
Inflammation plays a pivotal role in the normal function of many living organisms, serving both as an initiator of the immune response and a key modulator of tissue homeostasis [1]
Further assessment revealed a significant difference in the relative percentages of circulating cell types, with the blood of EE mice consistently showing a higher percentage of neutrophils and a correspondingly lower percentage of lymphocytes compared with the standard environment (SE) group (Figure 2D)
This study sought to assess whether defined enhancements to an animal’s housing conditions could have a modulating effect on its immune status. We have used this experimental system to model the effects of external environmental factors on the inflammatory response and to investigate the possible underpinning cellular and molecular mechanisms behind these effects
Summary
Inflammation plays a pivotal role in the normal function of many living organisms, serving both as an initiator of the immune response and a key modulator of tissue homeostasis [1]. Inflammation is distinct from other homeostatic mechanisms in that damage to self is an unavoidable and often necessary part of its process. While a long-studied field of research [2], recent innovations in cellular and molecular biology have greatly expanded our knowledge of the factors regulating (and dysregulating) the inflammatory response. Such knowledge has allowed us to divide this process into several subtypes, such as silent inflammation (due to aging or lifestyle), sterile inflammation (e.g., gouty arthritis) [3], para-inflammation (e.g., macular degeneration) [4], and cellular stress responses [5], each with its own distinct effects and etiologies. We appreciate that inflammation is a multifaceted and adaptive process, sensitive to alterations both internal and external to the host
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