Smoking Promotes Bacteria and Infection

Smoking affects neutrophils, the short-lived white blood cells that defend against infection, by reducing their ability to seek and destroy bacteria.

Smoking is a health hazard known to all. But if you’re still not able to kick the habit, here’s another reason why you should - smoking encourages infection, says a new study.

According to a new study, nicotine affects neutrophils, the short-lived white blood cells that defend against infection, by reducing their ability to seek and destroy bacteria.

Neutrophils are generated by our bone marrow, which they leave as terminally differentiated cells.

Although nicotine is known to affect neutrophils, there has been no study until now of the mechanisms at work when nicotine is present during neutrophil differentiation.

David Scott from the Oral Health and Systemic Disease Research Group at the University of Louisville School of Dentistry, Kentucky, USA, along with a team of international colleagues decided to investigate how nicotine influenced the differentiation process.

The authors suggest the processes they observed as contributing to impaired neutrophil function partially explain chronic tobacco users’ increased susceptibility to bacterial infection and inflammatory diseases.

In the study, the research team modeled the neutrophil differentiation process beginning with promyelocytic HL-60 cells, which differentiated into neutrophils following dimethylsulfoxide (DMSO) treatment both with and without nicotine.

The researchers found that nicotine increased the percentage of cells in late differentiation phases (metamyelocytes, banded neutrophils and segmented neutrophils) compared to DMSO alone, but did not affect other neutrophil differentiation markers that they examined.

However, the nicotine treated neutrophils were less able to seek and destroy bacteria than nicotine-free neutrophils. The nicotine suppressed the oxidative burst in HL-60 cells, a function that helps kill invading bacteria. Nicotine also increased MMP-9 release, a factor involved in tissue degradation.

"It must be acknowledged that our study model, DMSO-differentiated HL-60 cells, are not entirely similar to normal neutrophils. However, this leukemic human cell line does permit the reproducible study of differentiation while retaining many of the key effector functions of primary neutrophils," said Scott.

The study is published in the open access journal BMC Cell Biology.

Source-ANI
SPH/L