Oral exposure to cadmium chloride triggers an acute inflammatory response in the intestines of mice, initiated by the over-expression of tissue macrophage inflammatory protein-2 mRNA

Zhao, Zhaohui; Hyun, Ja Shil; Satsu, Hideo; Kakuta, Shigeru; Shimizu, Makoto

doi:10.1016/j.toxlet.2005.12.004

Cited by 54 publications

(34 citation statements)

References 43 publications

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“…As shown in Fig. 9, absorption could be amplified after chronic Cd exposure, because Cd-induced cell death may cause a leak in the epithelial layer, resulting in a larger amount of Cd permeating from within the enterocytes to the portal blood (8,41). Moreover, Cd-induced disruption of tight junctions may lead to an intercellular leak, providing an abnormal path for Cd to pass through the intestinal barrier (6,7,41).…”

Section: Discussionmentioning

confidence: 99%

“…For the general population, food and drinking water are the main sources of Cd exposure due to the biomagnification of Cd within the food chain (4); therefore, the intestinal tract is the first organ that is susceptible to Cd contamination. Early in vitro and animal studies have shown that the intestinal barrier plays a crucial role in limiting Cd absorption (5,6), and Cd exposure causes an inflammatory response, death of epithelial cells, and damage to tight junctions in the intestines, leading to the disruption of the intestinal barrier and the amplification of Cd absorption (6)(7)(8)(9)(10). A recent research study also revealed that subchronic oral Cd exposure significantly affects the gut ecology and susceptibility to colitis in mice (11).…”

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confidence: 99%

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Oral Administration of Probiotics Inhibits Absorption of the Heavy Metal Cadmium by Protecting the Intestinal Barrier

Zhai

Tian

Zhang

et al. 2016

Appl Environ Microbiol

170

105

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The heavy metal cadmium (Cd) is an environmental pollutant that causes adverse health effects in humans and animals. Our previous work demonstrated that oral administration of probiotics can significantly inhibit Cd absorption in the intestines of mice, but further evidence is needed to gain insights into the related protection mode. The goal of this study was to evaluate whether probiotics can inhibit Cd absorption through routes other than the Cd binding, with a focus on gut barrier protection. In the in vitro assay, both the intervention and therapy treatments of

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Oral Administration of Probiotics Inhibits Absorption of the Heavy Metal Cadmium by Protecting the Intestinal Barrier

Zhai

Tian

Zhang

et al. 2016

Appl Environ Microbiol

170

105

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“…Blocking of MIP-2 bioactivity by anti-MIP-2 antibodies results in significantly decreased neutrophil influx[26,27]. When injected in vivo as recombinant chemokines, KC and MIP-2 in models of inflammation, can cause neutrophil influx[28,29]. The results of other studies have highlighted MIP-2 as the major chemoattractant[29].…”

Section: Mip-2 Mediates Inflammation By Neutrophil Recruitmentmentioning

confidence: 99%

“…When injected in vivo as recombinant chemokines, KC and MIP-2 in models of inflammation, can cause neutrophil influx[28,29]. The results of other studies have highlighted MIP-2 as the major chemoattractant[29]. In liver injury, neutralizing KC and MIP-2 result in less neutrophil extravasation and reduce neutrophil-induced injury in a mouse model of cholestatic liver damage[30].…”

Section: Mip-2 Mediates Inflammation By Neutrophil Recruitmentmentioning

confidence: 99%

Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

Qin

Liu

et al. 2017

WJG

116

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Macrophage inflammatory protein (MIP)-2 is one of the CXC chemokines and is also known as chemokine CXC ligand (CXCL2). MIP-2 affects neutrophil recruitment and activation through the p38 mitogen-activated-protein-kinase-dependent signaling pathway, by binding to its specific receptors, CXCR1 and CXCR2. MIP-2 is produced by a variety of cell types, such as macrophages, monocytes, epithelial cells, and hepatocytes, in response to infection or injury. In liver injury, activated Kupffer cells are known as the major source of MIP-2. MIP-2-recruited and activated neutrophils can accelerate liver inflammation by releasing various inflammatory mediators. Here, we give a brief introduction to the basic molecular and cellular sources of MIP-2, and focus on its physiological and pathological functions in acute liver injury induced by concanavalin A, lipopolysaccharides, irradiation, ischemia/reperfusion, alcohol, and hypoxia, and hepatectomy-induced liver regeneration and tumor colorectal metastasis. Further understanding of the regulatory mechanisms of MIP-2 secretion and activation may be helpful to develop MIP-2-targeted therapeutic strategies to prevent liver inflammation.

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“…We have found that cadmium, a heavy metal known as a contaminant in many agricultural products, induces inflammatory reactions in IECs. 77,78) These stress factors induce stimulation of immune cells in the intestinal epithelium. The mild activation of immune cells is thought to be an adaptive response to risk factors, and is called controlled inflammation.…”

Section: Inflammatory Bowel Diseasesmentioning

confidence: 99%

Interaction between Food Substances and the Intestinal Epithelium

Shimizu

2010

Bioscience, Biotechnology, and Biochemistry

Self Cite

130

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The small intestine is an organ responsible for nutrient absorption, barrier functions, signal recognition/transduction, and the production of bioactive compounds. These functions are known to be regulated by such factors as hormones and cytokines, but substances contained in the daily diet are also thought to play roles as major modulators of intestinal functions. Intestinal epithelial cells (IECs), which form a monolayer covering the inside surface of the intestinal tract, are particularly important in this modulation, because they directly interact with intestinal contents, including food substances, their digests, and gut microbial components. Using cell-based in vitro assays, we investigated the food-IEC interactions at the cellular and molecular levels, and found that a variety of food substances affected the transporter activity, tight junction permeability, metabolic enzyme expression, immune functions, and so on. Modulation of the intestinal functions by dietary substances is therefore essential to promote health.

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Oral exposure to cadmium chloride triggers an acute inflammatory response in the intestines of mice, initiated by the over-expression of tissue macrophage inflammatory protein-2 mRNA

Cited by 54 publications

References 43 publications

Oral Administration of Probiotics Inhibits Absorption of the Heavy Metal Cadmium by Protecting the Intestinal Barrier

Oral Administration of Probiotics Inhibits Absorption of the Heavy Metal Cadmium by Protecting the Intestinal Barrier

Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

Interaction between Food Substances and the Intestinal Epithelium

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