CC chemokines, a subfamily of 27 chemotactic cytokines, are a component of intercellular communication, which is crucial for the functioning of the tumor microenvironment. Although many individual chemokines have been well researched, there has been no comprehensive review presenting the role of all known human CC chemokines in the hallmarks of cancer, and this paper aims at filling this gap. The first part of this review discusses the importance of CCL1, CCL3, CCL4, CCL5, CCL18, CCL19, CCL20, CCL21, CCL25, CCL27, and CCL28 in cancer. Here, we discuss the significance of CCL2 (MCP-1), CCL7, CCL8, CCL11, CCL13, CCL14, CCL15, CCL16, CCL17, CCL22, CCL23, CCL24, and CCL26. The presentation of each chemokine includes its physiological function and then the role in tumor, including proliferation, drug resistance, migration, invasion, and organ-specific metastasis of tumor cells, as well as the effects on angiogenesis and lymphangiogenesis. We also discuss the effects of each CC chemokine on the recruitment of cancer-associated cells to the tumor niche (eosinophils, myeloid-derived suppressor cells (MDSC), tumor-associated macrophages (TAM), tumor-associated neutrophils (TAN), regulatory T cells (Treg)). On the other hand, we also present the anti-cancer properties of CC chemokines, consisting in the recruitment of tumor-infiltrating lymphocytes (TIL).

CC chemokines (or β-chemokines) are 28 chemotactic cytokines with an N-terminal CC domain that play an important role in immune system cells, such as CD4+ and CD8+ lymphocytes, dendritic cells, eosinophils, macrophages, monocytes, and NK cells, as well in neoplasia. In this review, we discuss human CC motif chemokine ligands: CCL1, CCL3, CCL4, CCL5, CCL18, CCL19, CCL20, CCL21, CCL25, CCL27, and CCL28 (CC motif chemokine receptor CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 ligands). We present their functioning in human physiology and in neoplasia, including their role in the proliferation, apoptosis resistance, drug resistance, migration, and invasion of cancer cells. We discuss the significance of chemokine receptors in organ-specific metastasis, as well as the influence of each chemokine on the recruitment of various cells to the tumor niche, such as cancer-associated fibroblasts (CAF), Kupffer cells, myeloid-derived suppressor cells (MDSC), osteoclasts, tumor-associated macrophages (TAM), tumor-infiltrating lymphocytes (TIL), and regulatory T cells (Treg). Finally, we show how the effect of the chemokines on vascular endothelial cells and lymphatic endothelial cells leads to angiogenesis and lymphangiogenesis.

Glycogen metabolism has important implications for the functioning of the brain, especially the cooperation between astrocytes and neurons. According to various research data, in a glycogen deficiency (for example during hypoglycemia) glycogen supplies are used to generate lactate, which is then transported to neighboring neurons. Likewise, during periods of intense activity of the nervous system, when the energy demand exceeds supply, astrocyte glycogen is immediately converted to lactate, some of which is transported to the neurons. Thus, glycogen from astrocytes functions as a kind of protection against hypoglycemia, ensuring preservation of neuronal function. The neuroprotective effect of lactate during hypoglycemia or cerebral ischemia has been reported in literature. This review goes on to emphasize that while neurons and astrocytes differ in metabolic profile, they interact to form a common metabolic cooperation.

Vanadium belongs to the group of transition metals and is present in the air and soil contaminants in large urban agglomerations due to combustion of fossil fuels. It forms numerous inorganic compounds (vanadyl sulfate, sodium metavanadate, sodium orthovanadate, vanadium pentoxide) as well as complexes with organic compounds (BMOV, BEOV, METVAN). Depending on the research model, vanadium compounds exhibit antitumor or carcinogenic properties. Vanadium compounds generate ROS as a result of Fenton's reaction or of the reaction with atmospheric oxygen. They inactivate the Cdc25B(2) phosphatase and lead to degradation of Cdc25C, which induces G(2)/M phase arrest. In cells, vanadium compounds activate numerous signaling pathways and transcription factors, including PI3K-PKB/Akt-mTOR, NF-κB, MEK1/2-ERK, that cause cell survival or increased expression and release of VEGF. Vanadium compounds inhibit p53-dependent apoptosis and promote entry into the S phase of cells containing functional p53 protein. In addition, vanadium compounds, in particular organic derivatives, have insulin-mimetic and antidiabetic properties. Vanadium compounds lower blood glucose levels in animals and in clinical trials. They also inhibit the activity of protein tyrosine phosphatase 1B. By activating the PI3K-PKB/Akt pathway, vanadium compaunds increase the cellular uptake of glucose by the GLUT4 transporter. The PKB/Akt pathway is also used to inactivate glycogen synthase kinase-3. The impact of vanadium compounds on inflammatory reactions has not been fully studied. Vanadium pentoxide causes expression of COX-2 and the release of proinflammatory cytokines in a human lung fibroblast model. Other vanadium compounds activate NF-κB in macrophages by activating IKKβ.

Coffee, being one of the world’s most popular beverages, is a rich source of dietary antioxidants. The aim of this study was to determine the mineral content and antioxidant activity as well as acidity of coffee beverages depending on the brewing technique. We tested coffee brews made and served at a popular urban coffee shop (Szczecin, Poland). Five coffee brewing techniques were used: Aeropress, drip, espresso machine, French press, and simple infusion. Our findings showed that the brewing method had a significant effect on all parameters tested in the study. The antioxidant activity of the beverages was high (31%–42% inhibition of DPPH (2,2-diphenyl-1-picrylhydrazyl); reduction potential from 3435.06 mol Fe3+/mL to 4298.19 mol Fe3+/mL). Polyphenolic content ranged from 133.90 g (French press) to 191.29 g of gallic acid/L (Aeropress brew), depending on the coffee extraction method. Mineral content was also found to differ between brewing methods. Coffees prepared by simple infusion and Aeropress provided a valuable source of magnesium, manganese, chromium, cobalt, and potassium, whereas the drip brew was found to be a good source of silicon.

The human immune system is constantly exposed to xenobiotics and pathogens from the environment. Although the mechanisms underlying their influence have already been at least partially recognized, the effects of some factors, such as lead (Pb), still need to be clarified. The results of many studies indicate that Pb has a negative effect on the immune system, and in our review, we summarize the most recent evidence that Pb can promote inflammatory response. We also discuss possible molecular and biochemical mechanisms of its proinflammatory action, including the influence of Pb on cytokine metabolism (interleukins IL-2, IL-4, IL-8, IL-1b, IL-6), interferon gamma (IFNγ), and tumor necrosis factor alpha (TNF-α); the activity and expression of enzymes involved in the inflammatory process (cyclooxygenases); and the effect on selected acute phase proteins: C-reactive protein (CRP), haptoglobin, and ceruloplasmin. We also discuss the influence of Pb on the immune system cells (T and B lymphocytes, macrophages, Langerhans cells) and the secretion of IgA, IgE, IgG, histamine, and endothelin.

Cadmium is a toxic and carcinogenic heavy metal that nowadays constitutes a serious environmental health problem. The aim of this study is to review the effects of cadmium on selected inflammatory mediators and markers, such as NF-κB and AP-1 transcription factors, IL-6, TNF-α, IL-1β cytokines, IL-8 or MIP-2 chemokine, MPO, iNOS, MMPs and COX-2 enzymes, PGE 2 (product of COX-2 enzyme), ICAM-1, VCAM-1 and PECAM-1 adhesion molecules, and CRP. The research strategy identified articles available in Medline, published between 1998 and 2012; we included both in vivo and in vitro studies carried out on humans and rodents. Most of the reviewed research findings suggest that cadmium in micromolar concentrations (especially in the 1-10 μM range) causes up-regulation of the mediators and markers of inflammation, and appears to have pro-inflammatory properties. However, it is worth mentioning that a contradictory or even opposite hypothesis exists, which suggests cadmium to be an anti-inflammatory factor. Further research including detailed histological analyses should solve this discrepancy. Nevertheless, it appears that the main reason for these contradictory findings is the experimental setup: different biological systems analyzed and different doses of cadmium applied.

That the nervous system is the main target of lead (Pb) has long been considered an established fact until recent evidence has linked the Pb effect on the immune system to the toxic effects of Pb on the nervous system. In this paper, we present recent literature reports on the effect of Pb on the inflammatory processes in the brain, particularly the expression of selected cytokines in the brain (interleukin 6, TGF-β1, interleukin 16, interleukin 18, and interleukin 10); expression and activity of enzymes participating in the inflammatory processes, such as cyclooxygenase 2, caspase 1, nitrogen oxide synthase (NOS 2) and proteases (carboxypeptidases, metalloproteinases and chymotrypsin); and the expression of purine receptors P2X4 and P2X7. A significant role in the development of inflammatory processes in the brain is also played by microglia (residual macrophages in the brain and the spinal cord), which act as the first line of defense in the central nervous system, and astrocytes—Whose most important function is to maintain homeostasis for the proper functioning of neurons. In this paper, we also present evidence that exposure to Pb may result in micro and astrogliosis by triggering TLR4-MyD88-NF-κB signaling cascade and the production of pro-inflammatory cytokines.