The Environmental Pollutant Cadmium Promotes Influenza Virus Replication in MDCK Cells by Altering Their Redox State

Checconi, Paola; Sgarbanti, Rossella; Celestino, Ignacio; Limongi, Dolores; Amatore, Donatella; Iuvara, Alessandra; Alimonti, Andrea; Garaci, Enrico; Palamara, Anna Teresa; Nencioni, Lucia

doi:10.3390/ijms14024148

Cited by 32 publications

(24 citation statements)

References 53 publications

(62 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Initial damage following exposure to Cd may be caused by a disturbance in thiol homeostasis and/or the production of ROS, what is in accordance with previous report indicating that Cd induces a decrease in GSH level in epithelial cells60. One of the possible resulting effects is an increased susceptibility to influenza viral infection, as Cd-induced OS directly increases the ability of influenza virus to replicate in the host-cell.…”

Section: Discussionsupporting

confidence: 90%

Disulfiram moderately restores impaired hepatic redox status of rats subchronically exposed to cadmium

Begić

Djurić

Ninković

et al. 2017

Journal of Enzyme Inhibition and Medicinal Chemistry

View full text Add to dashboard Cite

Examination of cadmium (Cd) toxicity and disulfiram (DSF) effect on liver was focused on oxidative stress (OS), bioelements status, morphological and functional changes. Male Wistar rats were intraperitoneally treated with 1 mg CdCl2/kg BW/day; orally with 178.5 mg DSF/kg BW/day for 1, 3, 10 and 21 days; and co-exposed from 22nd to 42nd day. The co-exposure nearly restored previously suppressed total superoxide dismutase (SOD), catalase (CAT) and increased glutathione peroxidase (GPx) activities; increased previously reduced glutathione reductase (GR) and total glutathione-S-transferase (GST) activities; reduced previously increased superoxide anion radical (O2 ·−) and malondialdehyde (MDA) levels; increased zinc (Zn) and iron (Fe), and decreased copper (Cu) (yet above control value), while magnesium (Mg) was not affected; and decreased serum alanine aminotransferases (ALT) levels. Histopathological examination showed signs of inflammation process as previously demonstrated by exposure to Cd. Overall, we ascertained partial liver redox status improvement, compared with the formerly Cd-induced impact.

show abstract

Section: Discussionsupporting

confidence: 90%

Disulfiram moderately restores impaired hepatic redox status of rats subchronically exposed to cadmium

Begić

Djurić

Ninković

et al. 2017

Journal of Enzyme Inhibition and Medicinal Chemistry

View full text Add to dashboard Cite

show abstract

“…Host-cell redox changes leading to activation of redox-regulated cellular pathways involved in the control of virus life-cycle have been reported during IV infection [ 42 – 45 ]. Interestingly, the Endoplasmic Reticulum oxidative stress causes the over-expression of the receptor Gp96 observed in CD patients [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Influenza A Virus Infection of Intestinal Epithelial Cells Enhances the Adhesion Ability of Crohn’s Disease Associated Escherichia coli Strains

Aleandri¹,

Conte²,

Simonetti³

et al. 2015

PLoS ONE

Self Cite

View full text Add to dashboard Cite

Modifications of intestinal glycoreceptors expression, in particular CEACAM6, typically found in ileal Crohn's disease (CD), favor, among the commensal species of microbiota, the enrichment in Escherichia coli. Removal of protein glycosidic residues by neuraminidase, a sialidase typical of influenza virus, increases adhesion ability of Escherichia coli to Caco-2 intestinal cells. In this study we investigated whether influenza virus infection of human intestinal epithelial cells could influence the adhesiveness of different Escherichia coli strains isolated from CD patients by altering surface glycoreceptors. Influenza virus infection of intestinal cells increased exposure of galactose and mannose residues on the cell surface. In particular, glycoreceptors Thomsen-Friedenreich and CEACAM6 were over-expressed in influenza virus infected cells. In the same experimental conditions, a significant increase in bacterial adhesiveness was observed, independently of their own adhesive ability. The increase was reverted by treatment with anti-TF and anti-CEACAM6 antibodies. Interestingly, influenza virus was able to efficiently replicate in human primary intestinal cells leading to TF exposure. Finally, intestinal infected cells produced high levels of pro-inflammatory cytokines compared to control. Overall these data suggest that influenza virus infection, could constitute an additional risk factor in CD patients.

show abstract

“…Influenza virus causes redox changes in infected cells and GSH depletion favors virus replication [10][11][12][13]16,17 ; hence, at day 8 pi we investigated whether infection and/or GSH-C4 treatment modified GSH content in spleen, lymph nodes, lungs, pancreas, and brain of old mice. Surprisingly, GSH content was increased in all the organs of infected mice, except in the brain (Figure 3).…”

Section: Gsh Concentration In Organs Of Infected Micementioning

confidence: 99%

Glutathione increase by the n‐butanoyl glutathione derivative (GSH‐C4) inhibits viral replication and induces a predominant Th1 immune profile in old mice infected with influenza virus

et al. 2019

Self Cite

View full text Add to dashboard Cite

During aging, glutathione (GSH) content declines and the immune system undergoes a deficiency in the induction of Th1 response. Reduced secretion of Th1 cytokines, which is associated with GSH depletion, could weaken the host defenses against viral infections. We first evaluated the concentration of GSH and cysteine in organs of old mice; then, the effect of the administration of the N‐butanoyl GSH derivative (GSH‐C4) on the response of aged mice infected with influenza A PR8/H1N1 virus was studied through the determination of GSH concentration in organs, lung viral titer, IgA and IgG1/IgG2a production, and Th1/Th2 cytokine profile. Old mice had lower GSH than young mice in organs. Also the gene expression of endoplasmic reticulum (ER) stress markers involved in GSH metabolism and folding of proteins, that is, Nrf2 and PDI, was reduced. Following infection, GSH content remained low and neither infection nor GSH‐C4 treatment affected Nrf2 expression. In contrast, PDI expression was upregulated during infection and appeared counterbalanced by GSH‐C4. Moreover, the treatment with GSH‐C4 increased GSH content in organs, reduced viral replication and induced a predominant Th1 response. In conclusion, GSH‐C4 treatment could be used in the elderly to contrast influenza virus infection by inducing immune response, in particular the Th1 profile.

show abstract

The Environmental Pollutant Cadmium Promotes Influenza Virus Replication in MDCK Cells by Altering Their Redox State

Cited by 32 publications

References 53 publications

Disulfiram moderately restores impaired hepatic redox status of rats subchronically exposed to cadmium

Disulfiram moderately restores impaired hepatic redox status of rats subchronically exposed to cadmium

Influenza A Virus Infection of Intestinal Epithelial Cells Enhances the Adhesion Ability of Crohn’s Disease Associated Escherichia coli Strains

Glutathione increase by the n‐butanoyl glutathione derivative (GSH‐C4) inhibits viral replication and induces a predominant Th1 immune profile in old mice infected with influenza virus

Contact Info

Product

Resources

About