Cessation from Smoking Improves Innate Host Defense and Clearance of Experimentally Inoculated Nasal Staphylococcus aureus

• Published in: Infection and immunity Vol. 86; no. 4
• Main Authors: Cole, Amy L., Schmidt-Owens, Mary, Beavis, Ashley C., Chong, Christine F., Tarwater, Patrick M., Schaus, James, Deichen, Michael G., Cole, Alexander M.
• Format: Journal Article
• Language: English
• Published: United States American Society for Microbiology 01.04.2018
• Subjects: Host Response and Inflammation; nasal carriage; smoking cessation; humans; Staphylococcus aureus; host defense; experimental colonization
• ISSN: 0019-9567; 1098-5522; 1098-5522
• DOI: 10.1128/IAI.00912-17

Staphylococcus aureus nasal carriage is transient in most humans and usually benign, but dissemination of S. aureus to extranasal sites causes the majority of clinical infections, and S. aureus is a major cause of serious infections in the United States. A better understanding of innate nasal decolonization mechanisms is urgently needed, as are relevant models for studying S. aureus clearance. Here, we screened a population of healthy smokers for nasal S. aureus carriage and compared the participants' abilities to clear experimentally applied nasal S. aureus before and after completion of a smoking cessation program. We determined that cigarette smoking increases the mean nasal S. aureus load (2.6 × 10 4 CFU/swab) compared to the load observed in healthy nonsmokers (1.7 × 10 3 CFU/swab) and might increase the rate of S. aureus nasal carriage in otherwise-healthy adults: 22 of 99 smokers carried S. aureus at the screening visit, while only 4 of 30 nonsmokers screened positive during the same time period. Only 6 of 19 experimental inoculation studies in active smokers resulted in S. aureus clearance within the month of follow-up, while in the cessation group, 6 of 9 subjects cleared nasal S. aureus and carriage duration averaged 21 ± 4 days. Smoking cessation associated with enhanced expression of S. aureus -associated interleukin-1β (IL-1β) and granulocyte colony-stimulating factor (G-CSF) in nasal fluids. Participants who failed to clear S. aureus exhibited a higher nasal S. aureus load and elevated nasal interleukin-1 receptor antagonist (IL-1RA) expression at the preexperiment study visits. We conclude that smokers exhibit higher S. aureus loads than nonsmokers and that innate immune pathways, including G-CSF expression and signaling through the IL-1 axis, are important mediators of nasal S. aureus clearance.