Inhibitory effects of carbocisteine on type A seasonal influenza virus infection in human airway epithelial cells.

@article{Yamaya2010InhibitoryEO,
  title={Inhibitory effects of carbocisteine on type A seasonal influenza virus infection in human airway epithelial cells.},
  author={Mutsuo Yamaya and Hidekazu Nishimura and Kyoko Shinya and Yukimasa Hatachi and Takahiko Sasaki and Hiroyasu Yasuda and Motoki Yoshida and Masanori Asada and Naoya Fujino and Takaya Suzuki and Xue Deng and Hiroshi Kubo and Ryoichi Nagatomi},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2010},
  volume={299 2},
  pages={
          L160-8
        }
}
Type A human seasonal influenza (FluA) virus infection causes exacerbations of bronchial asthma and chronic obstructive pulmonary disease (COPD). l-carbocisteine, a mucolytic agent, reduces the frequency of common colds and exacerbations in COPD. However, the inhibitory effects of l-carbocisteine on FluA virus infection are uncertain. We studied the effects of l-carbocisteine on FluA virus infection in airway epithelial cells. Human tracheal epithelial cells were pretreated with l-carbocisteine… 
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20 Citations

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Citation Type

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The results suggest that LVFX inhibits major-group rhinovirus infections in part by reducing ICAM-1 expression levels and the number of acidic endosomes, and may also modulate airway inflammation inrhinoviral infections.
Increased severity of 2009 pandemic influenza A virus subtype H1N1 infection in alveolar type II cells from patients with pulmonary fibrosis.
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It is hypothesized that the infection of ATII cells with A(H1N1) pdm09 is more severe for cells from pulmonary fibrotic lungs than for cells in diseased lungs, and viral titers in the culture supernatants are compared.
Effect of Influenza Virus Infection in a Murine Model of Asthma.
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In a murine model of asthma, influenza-induced airway inflammation appeared to be caused by simultaneous activation of neutrophilic and eosinophilic inflammation.
Virus Infection-Induced Bronchial Asthma Exacerbation
  • M. Yamaya
  • Medicine, Biology
    Pulmonary medicine
  • 2012
TLDR
Several drugs used for the treatment of bronchial asthma reduce viral and pro-inflammatory cytokine release from airway epithelial cells infected with viruses, and the modulation of viral infection-induced airway inflammation is reviewed.
Carbocisteine reduces virus-induced pulmonary inflammation in mice exposed to cigarette smoke.
TLDR
The findings suggest that S-CMC reduces pulmonary inflammation and mucus overproduction in mice exposed to CS after infection with FluV via the activation of Nrf2.
Serine Proteases and their Inhibitors in Human Airway Epithelial Cells: Effectson Influenza Virus Replication and Airway Serine Proteases and their Inhibitors in Human Airway Epithelial Cells: Effects on Influenza Virus Replication and Airway Inflammation
TLDR
Serine proteases expressed by human tracheal epithelial cells induce the proteolytic activation of influenza viruses and that serine protease inhibitors may reduce viral replication and the resultant production of inflammatory cytokines are suggested.
T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
TLDR
It is found that both T cells and ILC2s contribute to influenza‐induced exacerbation of allergic airway inflammation, but with different kinetics.
N-Acetylcysteine: An Old Drug With Variable Anti-Influenza Properties
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N-acetylcysteine was shown to limit lung inflammation, damage associated with the virus, and limit viral growth, at least in vitro, however, the antiviral activity was highly variable depending on the influenza A strain.
Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways
TLDR
Carbocisteine effectively suppresses TNF-α-induced inflammation in A549 cells via suppressing NF-κB and ERK1/2 MAPK signaling pathways.
Redox Biology of Respiratory Viral Infections
TLDR
Changes in redox homeostasis in infected cells are one of the key events that is linked to infection with respiratory viruses and linked to inflammation and subsequent tissue damage.
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