The effects of ethanol, tumor necrosis factor, and granulocyte colony-stimulating factor on lung antibacterial defenses.

@article{Nelson1991TheEO,
  title={The effects of ethanol, tumor necrosis factor, and granulocyte colony-stimulating factor on lung antibacterial defenses.},
  author={Steve Nelson and Gregory J. Bagby and Jan Andresen and C Nakamura and Judd E. Shellito and W. Summer},
  journal={Advances in experimental medicine and biology},
  year={1991},
  volume={288},
  pages={
          245-53
        }
}
In summary, evidence is emerging indicating that alcohol-abusing hosts are seriously undermined by profound disturbances in cytokine production and activity. These alterations likely play a critical role in the development and clinical sequelae of their immunosuppressed status. Recombinant technology currently provides the clinician with the potential to immunologically reconstitute and restore host defenses in these hosts. While the ultimate role of these agents in patients will require… 
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At least two mechanisms, suppressed chemokine production and impaired neutrophil adhesion molecule expression, likely work in concert in the alcohol-intoxicated host to impair neutrophils adhesion and migration into the lung during pneumococcal infection.
Alcohol Impairment of Granulocyte Function During Lung Infection
TLDR
Present knowledge supports the conclusion that defects in neutrophil recruitment, function and production are pivotal consequences of alcohol abuse and render the host susceptible to a multitude of respiratory infections.
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TLDR
The results of these experiments strongly implicate IL-17 as an important pathway for the immunosuppression associated with alcohol abuse and support gene therapeutic approaches to augment immune function in the alcoholic host or to treat infections associated with alcoholism.
Ethanol suppresses Mycobacteria tuberculosis-induced mRNA for nitric oxide synthase in alveolar macrophages, in vivo.
TLDR
It is shown that heat-killed M. avium complex and human virulent MTB instilled into rat lungs rapidly increased mRNA for inducible NO synthase II of AMs in fluid obtained by bronchoalveolar lavage, which may offer an explanation for the increased severity of mycobacterial infections in alcoholics.
Down-regulation of tumor necrosis factor α activity by acute ethanol treatment in human peripheral blood monocytes
TLDR
It is demonstrated that acute ethanol exposure has the potential to down-regulate Mφ production of TNF α significantly regardless of the TNFα-inducing stimulus.
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