Cigarette smoking and mechanisms of susceptibility to infections of the respiratory tract and other organ systems

Feldman, Charles; Anderson, Ronald

doi:10.1016/j.jinf.2013.05.004

Cited by 202 publications

(200 citation statements)

References 180 publications

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“…This duality blurs the definition of a commensal member of the respiratory tract. Instead, it's likely that this body site harbours an indigenous microbiota whose members behave differently, depending on factors such as their location in the body (Blaser and Falkow, 2009), bacterial community disturbance (Lynch, 2013), environmental pressures (Feldman and Anderson, 2013) and/or immune responses in the host (Starkey et al, 2013). Unlike many acute infectious diseases where a single microbe can be targeted and eradicated, lung infections are often polymicrobial (Bakaletz, 2004;Han et al, 2012;Huang et al, 2012Huang et al, , 2014Dickson et al, 2013) and the organisms recovered from respiratory and invasive infections are often a mixture of common URT microbes (Laupland et al, 2000, Sibley et al, 2008.…”

Section: Introductionmentioning

confidence: 99%

Culture and molecular-based profiles show shifts in bacterial communities of the upper respiratory tract that occur with age

et al. 2015

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The upper respiratory tract (URT) is a crucial site for host defense, as it is home to bacterial communities that both modulate host immune defense and serve as a reservoir of potential pathogens. Young children are at high risk of respiratory illness, yet the composition of their URT microbiota is not well understood. Microbial profiling of the respiratory tract has traditionally focused on culturing common respiratory pathogens, whereas recent culture-independent microbiome profiling can only report the relative abundance of bacterial populations. In the current study, we used both molecular profiling of the bacterial 16S rRNA gene and laboratory culture to examine the bacterial diversity from the oropharynx and nasopharynx of 51 healthy children with a median age of 1.1 years (range 1-4.5 years) along with 19 accompanying parents. The resulting profiles suggest that in young children the nasopharyngeal microbiota, much like the gastrointestinal tract microbiome, changes from an immature state, where it is colonized by a few dominant taxa, to a more diverse state as it matures to resemble the adult microbiota. Importantly, this difference in bacterial diversity between adults and children accompanies a change in bacterial load of three orders of magnitude. This indicates that the bacterial communities in the nasopharynx of young children have a fundamentally different structure from those in adults and suggests that maturation of this community occurs sometime during the first few years of life, a period that includes ages at which children are at the highest risk for respiratory disease.

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Section: Introductionmentioning

confidence: 99%

Culture and molecular-based profiles show shifts in bacterial communities of the upper respiratory tract that occur with age

et al. 2015

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“…The wide-ranging suppressive effects of smoking, encompassing both innate and adaptive airway host defences, have been described elsewhere [45] and are summarised in figures 1 and 2 and table 1. These immunosuppressive and pro-inflammatory effects of smoking result from constant exposure of the airways to the vast array of low molecular toxicants generated during the combustion of tobacco.…”

Section: Smoking and Immunitymentioning

confidence: 99%

Impact of HIV infection and smoking on lung immunity and related disorders

2015

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HIV-infected persons not only have higher rates of smoking than the general population, but are also unusually vulnerable to the associated adverse health effects, both infective and noninfective in origin. Indeed, in the setting of well-organised care and availability of highly active antiretroviral therapy, HIV-infected smokers lose more life-years to smoking than to HIV infection per se, presenting a major challenge to healthcare providers. Not surprisingly, the respiratory system is particularly susceptible to the damaging interactive chronic inflammatory and immunosuppressive effects of HIV and smoking, intensifying the risk of the development of opportunistic infections, as well as lung cancer and obstructive lung disorders. The impact of smoking on the immunopathogenesis and frequencies of these respiratory conditions in the setting of HIV infection, as well as on the efficacy of antiretroviral therapy, represent the primary focus of this review. @ERSpublications Smoking exacerbates the immunosuppressive/pro-inflammatory effects of HIV, increasing the risk of pulmonary disease

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“…Cigarette smoking is closely associated with the development and progression of various respiratory diseases including lung cancer, chronic obstructive pulmonary disease (COPD), interstitial lung diseases and bronchial asthma (1,2). In particular, lung cancer and COPD are the main causes of death related to cigarette smoking in the world.…”

Section: Introductionmentioning

confidence: 99%

RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

Hao

et al. 2015

Oncology Reports

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Abstract. Cigarette smoking is closely associated with various respiratory diseases. Oxidants and carcinogens in cigarettes are reported to induce various airway epithelial injuries. However, the underlying mechanisms remain unclear. The aims of the present study were to determine the involvement of RNA-binding motif protein 5 (RBM5) and Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury, as well as the interaction between both. A549 cells were treated with cigarette smoke extract (CSE). The MTT assay was used to assess the effects of CSE on cell viability. The levels of RBM5 and Wnt/β-catenin/GSK3β were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis. A luciferase assay was used to assess the activity of β-catenin/T-cell factor (TCF) signaling. The results revealed that CSE inhibited A549 cell viability in both a dose-and time-dependent manner. Cytosolic and nuclear β-catenin levels were significantly increased following CSE treatment, compared with those in the control cells (P<0.05). The luciferase activity in CSE-exposed cells transfected with the TCF luciferase reporter wild-type plasmid (pGL3-OT) was significantly greater than that in cells without CSE exposure (33,167±3,085 vs. 19,978±1,916, respectively, P<0.05). Both the mRNA and protein levels of RBM5 in the CSE-treated cells were significantly reduced compared to the levels in the controls (all P<0.05). The overexpression of RBM5 inhibited Wnt/β-catenin signaling in the A549 cells, while silencing of RBM5 enhanced Wnt/β-catenin signaling. The β-catenin/TCF signaling inhibitor ICG-001 had no apparent effect on the RBM5 levels. Downregulation of RBM5 and activation of Wnt/β-catenin signaling are involved in CSE-induced alveolar epithelial injury. RBM5 acts as an upstream molecule that negatively regulates the activity of Wnt/β-catenin signaling.

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Cigarette smoking and mechanisms of susceptibility to infections of the respiratory tract and other organ systems

Cited by 202 publications

References 180 publications

Culture and molecular-based profiles show shifts in bacterial communities of the upper respiratory tract that occur with age

Culture and molecular-based profiles show shifts in bacterial communities of the upper respiratory tract that occur with age

Impact of HIV infection and smoking on lung immunity and related disorders

RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

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