In vitro studies revealed that IL-6 transsignaling increases chemokine activation of CXCL5, CXCL6, and
CCL8 [16].
ACKR2 binds most inflammatory CC-chemokines (CCL2, CCL5, CCL3, CCL4, CCL7,
CCL8, CCL11, CCL13, CCL17, CCL22, CCL23, and CCL24) leading to their degradation, thereby reducing local levels of inflammatory chemokines.
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CCL8 (MCP-2), CCL7 (MCP-3), XCL1 (linfotactina) y XCL2.
Quercetin also reduced the gene expression of specific factors implicated in local vascular inflammation including IL-1R,
Ccl8, IKK, and STAT3.
Quantitative RT-PCR analyses of livers using a Mouse Inflammatory Cytokines and Receptors PCR Array (Qiagen) revealed seven genes that were significantly downregulated in [LDLR.sup.-/-]; [macLRP1.sup.-/-] mice: Ccl3, Ccl4,
Ccl8, Ccr1, Ccr2, Cxcl9, and Tnf (Figure 2(a)).
In a similar manner, SF-derived exosomes induced the release of several chemokines (
CCL8, CCL15, CCL20, and CXCL1), while downregulating the production of others (CCL7 in particular; Figures 4(a) and 4(c)).
Gene specific human Taqman[R] primers MMP1 (Hs00899659_m1), MMP13 (Hs00233992_ml), CCL2 (Hs00234140_m1)
CCL8 (Hs04187715_m1), CXCL6 (Hs00605742_m1), C3 (Hs00163811_ml), CH25H (Hs02379634_s1), and LBP (Hs01084621_ml) (Applied Biosystems) were used for gene expression analysis.
Indeed, the genes encoding for CCL2,
CCL8, CCL7, RANTES, CCL3, and CCL11 chemokines, as well as those encoding for CCR1, CCR2, CCR3, and CCR5, were found upregulated in the adipose tissue of morbidly obese compared with lean subjects [62].
The positive self-feedback loop of
CCL8 secretion recruits further neutrophils to the infarct for the phagocytosis of necrotic, autophagic, or apoptosed cardiac tissue [51].