Exposure to cigarette smoke and Chlamydia pneumoniae infection in mice: Effect on infectious burden, systemic dissemination and cytokine responses: A pilot study. (2nd January 2016)

• Record Type: Journal Article
• Authors: Kumar, Swati; Smith-Norowitz, Tamar A.; Kohlhoff, Stephan; Apfalter, Petra; Roblin, Patricia; Kutlin, Andrei; Harkema, Jack; Ng, Sheung P.; Doherty-Lyons, Shannon; Zelikoff, Judith T.; Hammerschlag, Margaret R.
• Is Part Of: Journal of immunotoxicology. Volume 13:Number 1(2016)
• Page Start: 77
• Page End: 83
• Publication Date: 2016-01-02
• Subjects: Chlamydia pneumoniae -- cigarette smoke -- mice -- cytokines; Immunotoxicology -- Periodicals; Poisons -- Immunology -- Periodicals; Environmental health -- Periodicals; 616.97
• DOI: 10.3109/1547691X.2015.1006346
• Languages: English
• ISSNs: 1547-691X

Abstract

Abstract: Cigarette smoke exposure has been considered a risk factor for infection with Chlamydia pneumoniae. C. pneumoniae infection is associated with respiratory tract infection and chronic respiratory disease, which is a serious public health concern. To determine whether prior exposure to cigarette smoke worsens C. pneumoniae infection (specifically, increases infectious burden and systemic dissemination) as well as alters cytokine responses in mice, adult female C57BL/6 mice were exposed to either filtered air (FA) or mainstream cigarette smoke (MCS) (15 mg/m 3, total suspended particulates) for 5 days/week for 2 weeks and then infected with C. pneumoniae (10 5 IFU) via intratracheal instillation. Mice were euthanized on Days 7, 14 or 26 post-infection (p.i.). Chlamydial burdens in the lungs and spleen were quantified by quantitative PCR (qPCR) and histologic analyses were performed; cytokine levels (TNF α, IL-4, IFN γ ) in bronchoalveolar lavage fluid and serum were assayed by enzyme-linked immunosorbent assay (ELISA). The results indicated that: (1) mice exposed to either FA or MCS had similar chlamydial burdens in the lungs and spleen on Days 14 and 26 p.i.; (2) proximal and distal airway inflammation was observed on Day 14 p.i. in both FA and MCS mice, but persisted in MCS mice until Day 26 p.i.; FA exposed mice demonstrated resolution of distal airway inflammation; and (3) MCS mice displayed higher serum levels of IFN γ and IL-4 on Day 26 p.i. These findings indicate that exposure of mice to MCS (at a concentration equivalent to smoking < 1 pack cigarettes/day) led to greater C. pneumoniae -induced inflammation, as indicated by prolonged inflammatory changes.