Corrigendum to ‘Human monocytes and macrophages undergo M1-type inflammatory polarization in response to high levels of glucose’ [Immunol. Lett. 176 (2016) 81–89]

Paradoxical Pro-inflammatory Responses by Human Macrophages to an Amoebae Host-Adapted Legionella Effector

“…However, unlike amoebae, the response to cytosolic hyper-glucose in infected macrophages triggers aerobic glycolysis, which triggers a rapid M1-like pro-inflammatory differentiation. This may mimic the M1 pro-inflammatory polarization of macrophages upon exposure to high levels of glucose (Erbel et al, 2016;Haidet et al, 2012;Kraakman et al, 2014;Pan et al, 2012;Reinhold et al, 1996;Torres-Castro et al, 2016). Although import of extracellular glucose represents a bottleneck, LamA-mediated hyper-glucose bypasses the glucose import bottleneck.…”

“…We tested the hypothesis that in response to the cytosolic hyperglucose, hMDMs mount a pro-inflammatory response (Erbel et al, 2016;Haidet et al, 2012;Kraakman et al, 2014;Pan et al, 2012;Reinhold et al, 1996;Torres-Castro et al, 2016). At 6 h post-infection of hMDMs, the levels of pro-and anti-inflammatory cytokines released into the culture supernatant were measured.…”

“…A growing body of data in vitro, in animal models, and in diabetic patients show that excessive amounts of glucose triggers upregulation of aerobic glycolysis, which directly polarizes monocytes-macrophages toward a M1 pro-inflammatory phenotype (Bradshaw et al, 2009;Bustos and Sobrino, 1992;Haidet et al, 2012;Pan et al, 2012;Reinhold et al, 1996;Torres-Castro et al, 2016). Importantly, upon exposure of human monocytes/macrophages to high levels of glucose in vitro, they undergo M1 polarization along with an increased import of glucose, and monocytes/macrophages from patients with Type 1 diabetes exhibit a M1 pro-inflammatory profile (Erbel et al, 2016;Haidet et al, 2012;Kraakman et al, 2014;Pan et al, 2012;Reinhold et al, 1996;Torres-Castro et al, 2016).…”

Metabolic Reprogramming of Immunity in Obesity and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2).

“…Surmi et al had found a large number of monocytes and differentiated macrophages in adipose tissues owing to a high number of macrophage attractant adipocyte-secreted cytokines, particularly leukotriene B3 (LTB3), macrophage inflammatory proteins (MIP), macrophage migration inhibitory factor (MIF), and monocyte chemotactic protein-3 (MCP30 [22]. Once residing inside adipose tissues, these macrophages undergo M1-phenotype transformation, resulting in inflammatory mediators' production, specifically nitric oxide, TNF-𝛼𝛼, and IL-1𝛽𝛽 [23]. Oddly, some others have found that leptin induces macrophages to undergo M2-phenotype transformation but secrete M1-typical cytokines such as TNF-𝛼𝛼, IL-6, IL-1𝛽𝛽, IL-1R𝛼𝛼, IL-10, MCP-1, and MIP1-𝛼𝛼 [24,25] to favour an inflammatory response.…”