Exposure to Cigarette Smoke Enhances Pneumococcal Transmission Among Littermates in an Infant Mouse Model

Abstract

Streptococcus pneumoniae, one of the most common commensal pathogens among children, is spread by close contact in daycare centers or within a family. Host innate immune responses and bacterial virulence factors promote pneumococcal transmission. However, investigations into the effects of environmental factors on transmission have been limited. Passive smoking, a great concern for children’s health, has been reported to exacerbate pneumococcal diseases. Here, we describe the effect of cigarette smoke exposure on an infant mouse model of pneumococcal transmission. Our findings reveal that the effect of cigarette smoke exposure significantly promotes pneumococcal transmission by enhancing bacterial shedding from the colonized host and by increasing susceptibility to pneumococcal colonization in the new host, both of which are critical steps of transmission. Local inflammation, followed by mucosal changes (such as mucus hypersecretion and disruption of the mucosal barrier), are important underlying mechanisms for promotion of transmission by smoke exposure. These effects were attributable to the constituents of cigarette smoke rather than smoke itself. These findings provide the first experimental evidence of the impact of environmental factors on pneumococcal transmission and the mechanism of pathogenesis.

Chronic obstructive pulmonary disease and cigarette smoke exposure lead to dysregulated MAIT cell activation by bronchial epithelial cells

“…Notably, MAIT cell responses to infected BEC from all donor groups were significantly reduced by CSE treatment (Figure 5a-b, Table 2-3). The decreased response with CSE treatment was unexpected, given previous reports indicating that cigarette smoke treatment increases Sp infection of respiratory tract epithelial cells [35][36][37] . As such, we examined the efficiency of Sp infection in these cells as described above.…”

Direct toxicity of cigarette smoke extract on cardiac function mediated by mitochondrial dysfunction in Sprague-Dawley rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes

“…CSE was produced by bubbling a stream of smoke from 50 Hi-Lite cigarettes (Japan Tobacco Inc., Tokyo, Japan) into a 50-mL saline solution (1 cigarette/mL), which was defined as 100% CSE [ 12 ]. Such CSE was purchased from CMIC Pharmascience Corporation (Yamanashi, Japan) [ 13 ] and stored at –80 °C until use, as previously described [ 14 ].…”

Hubungan Merokok Dengan Terbentuknya Lesi Kavitas Paru Pada Pasien Tuberkulosis RSUP H Adam Malik

“…20 Penelitian kepada hewan percobaan telah beberapa kali dilakukan untuk melihat efek asap rokok pada saluran pernafasan secara langsung, didapati bahwa paparan asap rokok menciptakan lingkungan yang baik bagi mikroba untuk berkolonisasi sehingga kerusakan pada paru semakin parah dan tingkat penularan menjadi sangat tinggi. [20][21][22] Kerusakan parenkim paru oleh paparan asap rokok dapat meningkatkan kerentanan seseorang terkena suatu penyakit, hal ini sejalan dengan banyaknya penelitian yang mendapati hubungan merokok dengan kejadian tuberkulosis paru. 9,11,13 Sistem pertahanan pada paru pasien yang merokok dan tidak merokok sangat berbeda dimana kondisi paru pasien yang merokok akan sangat mudah untuk terinfeksi.…”