tetano
Editor, Senior Moderator
Environ Int. 2019 Apr 15;127:720-729. doi: 10.1016/j.envint.2019.03.054. [Epub ahead of print]
[h=1]Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice.[/h] Chandler JD[SUP]1[/SUP], Hu X[SUP]1[/SUP], Ko EJ[SUP]2[/SUP], Park S[SUP]2[/SUP], Fernandes J[SUP]1[/SUP], Lee YT[SUP]2[/SUP], Orr ML[SUP]1[/SUP], Hao L[SUP]1[/SUP], Smith MR[SUP]1[/SUP], Neujahr DC[SUP]1[/SUP], Uppal K[SUP]1[/SUP], Kang SM[SUP]2[/SUP], Jones DP[SUP]3[/SUP], Go YM[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Cadmium (Cd) is a toxic, pro-inflammatory metal ubiquitous in the diet that accumulates in body organs due to inefficient elimination. Responses to influenza virus infection are variable, particularly severity of pneumonia. We used a murine model of chronic low-dose oral exposure to Cd to test if increased lung tissue Cd worsened inflammation in response to sub-lethal H1N1 infection. The results show that Cd-treated mice had increased lung tissue inflammatory cells, including neutrophils, monocytes, T lymphocytes and dendritic cells, following H1N1 infection. Lung genetic responses to infection (increasing TNF-α, interferon and complement, and decreasing myogenesis) were also exacerbated. To reveal the organization of a network structure, pinpointing molecules critical to Cd-altered lung function, global correlations were made for immune cell counts, leading edge gene transcripts and metabolites. This revealed that Cd increased correlation of myeloid immune cells with pro-inflammatory genes, particularly interferon-γ and metabolites. Together, the results show that Cd burden in mice increased inflammation in response to sub-lethal H1N1 challenge, which was coordinated by genetic and metabolic responses, and could provide new targets for intervention against lethal inflammatory pathology of clinical H1N1 infection.
Copyright ? 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.
[h=4]KEYWORDS:[/h] Environmental safety; Exposome; Heavy metals; Influenza A virus; Public health
PMID: 30999129 DOI: 10.1016/j.envint.2019.03.054
[h=1]Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice.[/h] Chandler JD[SUP]1[/SUP], Hu X[SUP]1[/SUP], Ko EJ[SUP]2[/SUP], Park S[SUP]2[/SUP], Fernandes J[SUP]1[/SUP], Lee YT[SUP]2[/SUP], Orr ML[SUP]1[/SUP], Hao L[SUP]1[/SUP], Smith MR[SUP]1[/SUP], Neujahr DC[SUP]1[/SUP], Uppal K[SUP]1[/SUP], Kang SM[SUP]2[/SUP], Jones DP[SUP]3[/SUP], Go YM[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Cadmium (Cd) is a toxic, pro-inflammatory metal ubiquitous in the diet that accumulates in body organs due to inefficient elimination. Responses to influenza virus infection are variable, particularly severity of pneumonia. We used a murine model of chronic low-dose oral exposure to Cd to test if increased lung tissue Cd worsened inflammation in response to sub-lethal H1N1 infection. The results show that Cd-treated mice had increased lung tissue inflammatory cells, including neutrophils, monocytes, T lymphocytes and dendritic cells, following H1N1 infection. Lung genetic responses to infection (increasing TNF-α, interferon and complement, and decreasing myogenesis) were also exacerbated. To reveal the organization of a network structure, pinpointing molecules critical to Cd-altered lung function, global correlations were made for immune cell counts, leading edge gene transcripts and metabolites. This revealed that Cd increased correlation of myeloid immune cells with pro-inflammatory genes, particularly interferon-γ and metabolites. Together, the results show that Cd burden in mice increased inflammation in response to sub-lethal H1N1 challenge, which was coordinated by genetic and metabolic responses, and could provide new targets for intervention against lethal inflammatory pathology of clinical H1N1 infection.
Copyright ? 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.
[h=4]KEYWORDS:[/h] Environmental safety; Exposome; Heavy metals; Influenza A virus; Public health
PMID: 30999129 DOI: 10.1016/j.envint.2019.03.054