Abstract
Obese adipose tissue (AT) is characterized by increased recruitment and infiltration of multiple immune cell populations, in particular T cells (CD4+ or CD8+ subsets) and macrophages, that interact with adipocytes through paracrine signaling (i.e., cross-talk).
Highlights
This invited Commentary is on the methods paper entitled “Studying adipocyte and immune cell cross talk using a co-culture system” in Immunometabolism: Methods and Protocols [1]
Co-culturing individual immune cell populations with adipocytes represents a model system to study the paracrine interactions between cell types that can impact adipose tissue (AT) function. This is relevant in obese AT, wherein paracrine interactions between cell types promotes the secretion of inflammatory mediators that contribute to increased local and systemic low-grade inflammation and metabolic dysfunction, including insulin resistance (IR) [2,3,4,5]
We will discuss the development of the adipocyte-immune cell co-culture models and highlight our research findings demonstrating the ability of n-3 polyunsaturated fatty acids (PUFA) to mitigate paracrine signaling between co-cultured adipocytes and T cells (CD8+ and CD4+) or macrophages with an emphasis on the secretory profile, it is worth noting that we have shown a beneficial impact of n-3 PUFA on the NLRP3 inflammasome and/or macrophage M1/M2 polarization status in these models [29,31,32,37]
Summary
This invited Commentary is on the methods paper entitled “Studying adipocyte and immune cell cross talk using a co-culture system” in Immunometabolism: Methods and Protocols [1]. In our co-culture model (using a physiologically relevant cellular ratio and LPS concentration) adipocytes were co-cultured in direct cell contact with primary splenicderived purified CD4+ T cells from lean mice fed isocaloric diets enriched with either n-3 or n-6 PUFA Using this approach, n-3 PUFA increased mRNA expression and/ or secreted protein of Th2 polarization markers (GATA3, IL-4) and reduced expression of Th1 polarization markers (Tbet, IFNγ), in addition to reducing the secretion of other inflammatory and macrophage chemotactic mediators (IL-1β, IL-6, MCP-1, MCP-3 and MIP-1α) [32]. Attenuating macrophage-muscle inflammatory cross-talk represents another potential target for n-3 PUFA to improve obesity-associated insulin sensitivity In this connection, RAW264.7 macrophages were stimulated with fatty acids [DHA (n-3 PUFA) versus palmitic acid (saturated fatty acid control)] and a physiologically relevant LPS dose (described above) to generate macrophage conditioned media (MCM), which contained secreted cytokines and chemokines that could impact muscle cell function in a cell contact-independent manner. Skeletal muscle cell (myotube)/macrophage co-culture models represent a relevant future direction to elucidate the underlying mechanisms contributing to obesity-associated IR
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