Exposure to cigarette smoke andChlamydia pneumoniaeinfection in mice: Effect on infectious burden, systemic dissemination and cytokine responses: A pilot study

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, IL-4, IFN) 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 and IL-4 on Day 26 p.i. These findings indicate that exposure of mice to MCS (at a concentration equivalent to smoking51 pack cigarettes/day) led to greater C. pneumoniae-induced inflammation, as indicated by prolonged inflammatory changes.

Cigarette Smoke Constituents and Nicotine Differentially Affect Cytokine Production by Human Macrophages Stimulated by TLR Ligands In Vitro: Considerations for a Standardised Protocol

“…For example, in vivo protocols vary in the amount and time of cigarette smoke exposure per day, and the number of days of exposure (from a few days to several months). [8][9][10][11][12]14,16 The procedure used here for the generation of CSE was identical to that used in our own previous studies, 22 and was similar to that used by several other authors. [23][24][25][26][27][28][29][30][31] However, studies of this type would be significantly improved by employing the internationally standardised regimes for CSE generation 37,38 (ISO 3308:2012 39 ).…”

“…5 Various cell types are implicated in COPD and in the contribution of infections to this pathology, with macrophages playing an important role in these processes. 6,7 Numerous in vivo murine models have been employed to investigate the effects of tobacco smoking on lung infections [8][9][10][11][12][13][14][15] and the effects of smoking on macrophages. 16,17 Although they have provided valuable information, these models may not completely replicate the pathology that occurs in human smokers.…”

Effects of infections on the pathogenesis of cancer

“…Impairment of lung and bronchial immunity, increased levels of IL-4 and suppression of cellular immunity could facilitate C. pneumoniae lung localization and invasion in smoking subjects. IL-8, also produced by smokers, along with IL-1β and TNF-α, may cause genetic damage 124 .…”

Can environmental factors increase the risk of multiple sclerosis? A narrative review

“…Another possibility is that some compounds in cigarettes may have direct toxic effects on the central nervous system and cause myelin loss of neurons 33 . Studies have shown that antibodies against chlamydia pneumoniae are more common in smokers than non-smokers 34 . Therefore, cigarette smoking is considered as a factor in increasing the duration and severity of respiratory infections, which may lead to infection-induced MS 35 .…”