The consequences of smoking on the body are well documented. Nicotine affects various body organs including the heart, lungs, nervous system, stomach and bones. It can damage the DNA, leading to cancer. But its reach does not stop there. New research is showing everyday that nicotine can inhibit the immune system and lower our bodies’ abilities to fight infections and prevent inflammatory diseases. By inhibiting the immune system, nicotine also allows for cancer cells to evade immune cells and progress into malignant tumors.1
To expand on how nicotine affects the immune system, a new study examined the role of nicotine on the generation and function of macrophages that are derived from bone marrow stem cells. The researchers first discovered that the nicotinic acetylcholine receptors (nAChRs) are expressed on bone marrow stem cells and macrophage progenitors. When the researchers derived macrophages from bone marrow stem cells and added nicotine to the in vitro cultures, they discovered that those macrophages generated in the presence of nicotine were fewer in number, produced fewer inflammatory cytokines, and had less capacity to divide and survive. Nicotine-exposed macrophages also did not respond well to inflammatory stimuli such as LPS, a bacterial product, further confirming that bone marrow derived macrophages in presence of nicotine are dysfunctional.2
We at HemaCare are interested in the results of this study as it shows how the nicotinic acetylcholine receptors can be used to alter the immune system response. With the correct manipulation, scientists can use this information to adjust the level of macrophage response. We provide human samples of macrophages and their precursors in bone marrow stem cells that can be used to study the role of macrophages in different disease models. You can call us at (877) 397-3087 if you have any questions or would like to place an order.
2 St-Pierre S., et al. 2016. Nicotinic Acetylcholine Receptors Modulate Bone Marrow-Derived Pro-Inflammatory Monocyte Production and Survival. PLOS ONE, 11(2): e0150230. doi:10.1371/ journal.pone.0150230.