Brief Report: Increased Cotinine Concentrations are Associated With Reduced Expression of Cathelicidin (LL-37) and NOD-2 in Alveolar Macrophages of PLWH Who Smoke.
Diaz. Philip T PT; Ferketich. Amy A; Wewers. Mary E ME; Browning. Kristine K; Gavrilin. Mikhail A MA; Sarkar. Anasuya A; Hollyfield. Jennifer J; Trinka. Teresa T; Wewers. Mark M
Key Findings
- Higher salivary cotinine levels correlate with reduced LL‑37 expression in alveolar macrophages
- Cotinine also inversely correlates with NOD‑2 expression
- The negative link between cotinine and LL‑37 is especially strong
Practical Outcomes
- Avoid smoking or nicotine exposure to preserve LL‑37‑mediated lung immunity. If you smoke, consider strategies that may boost LL‑37 (e.g., vitamin D, certain probiotics) and monitor lung health closely. No specific dosing guidance for LL‑37 is provided.
Summary
In people with HIV who smoke, higher levels of the nicotine marker cotinine are linked to lower levels of the natural antimicrobial peptide LL‑37 and the immune receptor NOD‑2 in lung immune cells, suggesting smoking weakens lung defenses.
Abstract
There is a strong link between cigarette smoking and pulmonary complications among people living with HIV. However, the effects of smoking on the local lung immune environment in this population remain unclear. Bronchoalveolar lavage and saliva were collected from HIV-infected smokers involved in a prospective study investigating alveolar macrophage expression of host defense molecules. Salivary cotinine concentrations were inversely related to expression of the immune cell receptor nucleotide-binding oligomerization domain-2 and the cathelicidin antimicrobial peptide LL-37. The negative correlation between salivary cotinine and LL-37 was particularly strong. Our study provides insight into how nicotine may adversely affect lung innate immunity in HIV.
Study Information
pubmed
2020
2020-12-15T00:00:00.000Z
10.1097/qai.0000000000002491