AI Article Synopsis

  • Tissue-resident natural killer (trNK) cells in the lungs may play a significant role in respiratory immunity, especially in chronic lung diseases like COPD, but their exact functions are not well understood.
  • Researchers conducted a study on mice exposed to cigarette smoke to mimic COPD and analyzed trNK cell behaviors in both mouse and human lung tissues when infected with influenza A virus.
  • Findings revealed that specific NK cell populations, especially CD49a NK cells, exhibited altered functions during COPD, showing increased activity when confronted with viral infections, which could lead to heightened inflammation in COPD patients.

Article Abstract

Tissue-resident natural killer (trNK) cells have been identified in numerous organs, but little is known about their functional contribution to respiratory immunity, in particular during chronic lung diseases such as chronic obstructive pulmonary disease (COPD). To investigate the phenotype and antiviral responses of trNK cells in murine cigarette smoke-induced experimental COPD and in human lung parenchyma from COPD donors. Mice were exposed to cigarette smoke for 12 weeks to induce COPD-like lung disease. Lung trNK cell phenotypes and function were analyzed by flow cytometry in both murine and human disease with and without challenge with influenza A virus. In the mouse lung, CD49aCD49bEOMES and CD49aCD49bEOMES NK cell populations had a distinct phenotype compared with CD49a circulating NK cells. CD49a NK cells were more extensively altered earlier in disease onset than circulating NK cells, and increased proportions of CD49a NK cells correlated with worsening disease in both murine and human COPD. Furthermore, the presence of lung disease delayed both circulating and trNK cell functional responses to influenza infection. CD49a NK cells markedly increased their NKG2D, CD103, and CD69 expression in experimental COPD after influenza infection, and human CD49a NK cells were hyperactive to influenza infection in COPD donors. Collectively, these results demonstrate that trNK cell function is altered in cigarette smoke-induced disease and suggests that smoke exposure may aberrantly prime trNK cell responsiveness to viral infection. This may contribute to excess inflammation during viral exacerbations of COPD.

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Source
http://dx.doi.org/10.1164/rccm.202205-0848OCDOI Listing

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