Abstract
Nutrients transiently or chronically modulate functional and biochemical characteristics of cells and tissues both in vivo and in vitro. The influence of tomato aqueous extract (TAE) on the in vitro inflammatory response of activated human peripheral blood leukocytes (PBLs) and macrophages was investigated. Its effect on endothelial dysfunction (ED) was analyzed in human umbilical vein endothelial cells (HUVECs). Murine macrophages (RAW264.7 cells), PBLs and HUVECs were incubated with TAE. They were activated with LPS or TNF-α in order to induce inflammatory processes and ED, respectively. Inflammatory mediators and adhesion molecules were measured by immune assay-based multiplex analysis. Gene expression was quantified by RT-PCR. TAE altered the production of interleukins (IL-1β, IL-6, IL-10, IL-12) and chemokines (CCL2/MCP-1, CCL3/MIP-1α, CCL5/RANTES, CXCL8/IL-8, CXCL10/IP-10) in PBLs. TAE reduced ED-associated expression of adhesion molecules (ICAM-1, VCAM-1) in endothelial cell. In macrophages, the production of nitric oxide, PGE2, cytokines and ILs (TNF-α, IL-1β, IL-6, IL-12), which reflects chronic inflammatory processes, was reduced. Adenosine was identified as the main bioactive of TAE. Thus, TAE had cell-specific and context-dependent effects. We infer from these in vitro data, that during acute inflammation TAE enhances cellular alertness and therefore the sensing of disturbed immune homeostasis in the vascular-endothelial compartment. Conversely, it blunts inflammatory mediators in macrophages during chronic inflammation. A novel concept of immune regulation by this extract is proposed.
Highlights
Numerous epidemiological studies established the beneficial relationship between a diet rich in fruit and vegetables and health conditions like cardiovascular diseases (CVD), diabetes, obesity, neuro-degeneration and arthritis
We investigated the influence of tomato aqueous extract (TAE) on the inflammatory profile of murine macrophages (i.e., RAW267.4 cells) stimulated with E. coli lipopolysaccharide (LPS), which triggered numerous metabolic changes [10]
TAE reduced the LPS-induced production of nitric oxide (NO) and it significantly diminished the secretion of COX-2 dependent prostaglandin E2 (PGE2) (Figure 1)
Summary
Numerous epidemiological studies established the beneficial relationship between a diet rich in fruit and vegetables and health conditions like cardiovascular diseases (CVD), diabetes, obesity, neuro-degeneration and arthritis. Low-grade inflammation is a common feature of these chronic diseases. This is reflected by an unbalanced production of inflammatory mediators including cytokines and chemokines, a disturbed homeostasis of cellular oxidants and mediators of inflammation such as prostaglandins, nitric oxide or the status of the extracellular matrix (ECM). A hallmark of acute inflammation is the increased production of cytokines and chemokines. These enable and enhance inflammatory processes that are essential to recruit immune cells to the sites of inflammation and eliminate pathogens. Chronic inflammation maintains a status of un-coordinated production of mediators and metabolites that cause tissue and organ damage. We found that TAE markedly altered the production of metabolites related to the acute inflammatory response. We show that TAE orchestrates the response of cells to inflammatory stimuli or altered homeostasis in a cell- and compartment-specific way
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