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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., A housing period as little as 2 weeks in an enriched environment with an increase in spatial and sensorial stimuli improved the ability of mice to clear infections.

Little is known about the role(s) of endogenous galectin-1 (Gal-1) in arthritis. In this study we queried whether antiarthritic functions for this effector of endogenous anti-inflammation could be unveiled by studying collagen-induced arthritis in Gal-1−/− mice. Gal-1−/− and C57BL/6J [wild-type (WT)] mice received an immunization of chicken type II collagen (CII) in CFA followed by a booster on day 21, which consisted of CII in IFA. Animals were monitored for signs of arthritis from day 14 onward. Clinical and histological signs of arthritis were recorded, and humoral and cellular immune responses against CII were analyzed. A distinct disease penetrance was apparent, with ∼ 70% of Gal-1−/− mice developing arthritis compared with ∼ 50% in WT animals. Gal-1−/− mice also exhibited an accelerated disease onset and more severe arthritis characterized by significantly elevated clinical scores. Postmortem analyses (day 42) revealed higher levels of IgG1 and IgG2b anti-CII Ig isotypes in the serum of Gal-1 null animals compared with WT. Finally, T cell responses following ex vivo stimulation with CII revealed a greater degree of proliferation in T cells of Gal-1−/− mice compared with WT, which was associated with increased production of IL-17 and IL-22. These data suggest the novel idea that endogenous Gal-1 is an inhibitory factor in the development of arthritis affecting disease severity. We have also highlighted the importance of endogenous Gal-1 in regulating T cell reactivity during experimental arthritis.

The trafficking of leukocytes from the blood stream to the surrounding tissue is a fundamental feature of an inflammatory response. Although many of the adhesion molecules and chemokines that direct leukocyte trafficking have been identified, there is still much to be discovered, particularly with regard to the persistence of leukocyte infiltrates in chronic inflammation. Elucidating the molecular mechanisms involved in this process is critical to understanding and treating inflammatory pathologies. Recent studies have identified members of the galectin family as immunoregulatory proteins. Included among the actions of galectins are modulatory effects, both positive and negative, on leukocyte recruitment. The focus of this review is to summarize current knowledge on the role of galectins in leukocyte trafficking during inflammation. A better understanding of the function of this family of endogenous lectins will open new avenues for innovative drug discovery.

Numerous protocols exist for investigating leukocyte recruitment both in vitro and in vivo. Here we describe three of these methods; an in vitro flow chamber assay, intravital microscopy, and zymosan-induced peritonitis, and give details as to how they can be used to study the actions of galectins on this crucial process.

Numerous protocols exist for investigating leukocyte recruitment both in vitro and in vivo. Here we describe three of these methods; an in vitro flow chamber assay, intravital microscopy, and zymosan-induced peritonitis, and give details as to how they can be used to study the actions of galectins on this crucial process.

Studies have recently demonstrated the immune system to significantly more plastic than previously believed. Multiple external factors have been shown to influence the immune response including alterations to the host’s external environment and psychological status. This study aimed to investigate this influence utilising classic models of inflammatory disease. Following a two week period of environmental enrichment subjects were challenged with either a model of acute inflammation or bacterial sepsis; zymosan inducedperitonitis (ZIP) and caecal ligation and puncture (CLP). The results of the ZIP model revealed a markedly altered immune response, typified by heightened cell migration to and maturation at the point of immune insult. In CLP we observed analogous results,accompanied by a significant inhibition of systemic bacterial spread in enriched animals. Micro-array analysis supported these findings, revealing the increased expression of immune-modulatory genes associated with a heightened immune response. We further discovered these changes to persist ex vivo , identifying macrophages isolated from enriched animals to possess a significantly enhanced phagocytic capacity alongside an unchanged profile of cytokine release. These results demonstrate environmental enrichment has an enhancing effect on the murine immune response: Upregulating immune-protective gene expression and heightening both leukocyte number and function to improve clearance of systemic bacterial infection. We also believe these results will aid in establishing a series of immunological models that could assess the effects of environment and psychological state on the active immune response.

The trafficking of leukocytes from the blood stream to the surrounding tissue is a fundamental feature of an inflammatory response. Although many of the adhesion molecules and chemokines that direct leukocyte trafficking have been identified, there is still much to be discovered, particularly with regard to the persistence of leukocyte infiltrates in chronic inflammation. Elucidating the molecular mechanisms involved in this process is critical to understanding and treating inflammatory pathologies. Recent studies have identified members of the galectin family as immunoregulatory proteins. Included among the actions of galectins are modulatory effects, both positive and negative, on leukocyte recruitment. The focus of this review is to summarize current knowledge on the role of galectins in leukocyte trafficking during inflammation. A better understanding of the function of this family of endogenous lectins will open new avenues for innovative drug discovery.