The effects of cadmium exposure in the induction of inflammation

Abstract

Inflammation is a physiological process essential for maintaining homeostatic mechanisms in human, but however, exaggerated inflammatory responses are closely related to many chronic diseases. Cadmium (Cd) is a heavy metal with high toxicity when present in food, water and air has the potential of eliciting inflammatory reactions, with a major health risk to human. This review aimed to elucidate on the major routes of Cd exposure, the main organs affected by the exposure, the degree of toxicity as well as the roles of the toxic effects on the immune system which results to inflammatory responses. Immune modulation by Cd may cause serious adverse health effects in humans. Various studies have highlighted the ability of Cd as an environmental pollutant involved in the modulation of the innate, adaptive and mucosal immune responses in relations to the release of chemokine, gene expression, and susceptibility to microbial infections.

Keywords:

• Cadmium
• toxicity
• inflammation
• cytokine
• chemokine

Disclosure statement

No potential conflict of interest was reported by the authors.

Figure 1. The major routes of cadmium exposure and its toxic effects on different parts of the body.

Figure 2. Proinflammatory effects of cadmium on monocyte lineage. Cd induces inflammation, DNA damage and apoptosis through different mechanisms. ROS: reactive oxygen species; COX2: cyclooxygenase-2; PGE2: Prostaglandin E2; PI3K/AKT: Phosphatidylinositol-3-Kinase and Protein Kinase B; MIP-2: macrophage inflammatory protein 2-alpha; IL-6: interleukin 6; IL-8: interleukin 8; TNF- α: Tumor necrosis factor alpha; IL-1β interleukin 1 beta.

Figure 3. Proinflammatory and pro-oxidative effects of cadmium exposure on neutrophils and macrophages. Cadmium increase inflammatory cytokines and chemokines, induction of neutrophil and macrophage recruitment and tissue damage. Cd upregulates caspase 3 and causes cell apoptosis. ROS: Reactive oxygen species; COX2: cyclooxygenase-2; MMPs: matrix metallopeptidases; LTB4: leukotriene B4; NFkB: nuclear factor kappa-light-chain-enhancer of activated B cells; AP-1: activator protein 1; MIP-2: macrophage inflammatory protein 2-alpha; IL-6: interleukin 6; IL-8: interleukin 8; TNF- α: tumor necrosis factor alpha; IL-1β: interleukin 1 beta.

Correction Statement

This article has been republished with minor change. This change do not impact the academic content of the article.