The epicenter of the original outbreak in China has high male smoking rates of around 50%, and early reported death rates have an emphasis on older males, therefore the likelihood of smokers being overrepresented in fatalities is high. In Iran, China, Italy, and South Korea, female smoking rates are much lower than males. Fewer females have contracted the virus. If this analysis is correct, then Indonesia would be expected to begin experiencing high rates of Covid-19 because its male smoking rate is over 60% (Tobacco Atlas). Smokers are vulnerable to respiratory viruses.Smoking can upregulate angiotensin-converting enzyme-2 (ACE2) receptor, the known receptor for both the severe acute respiratory syndrome (SARS)-coronavirus (SARS-CoV) and the human respiratory coronavirus NL638. This could also be true for new electronic smoking devices such as electronic cigarettes and "heat-not-burn" IQOS devices. ACE2 could be a novel adhesion molecule for SARS-CoV-2 causing Covid-19 and a potential therapeutic target for the prevention of fatal microbial infections, and therefore it should be fast tracked and prioritized for research and investigation. Data on smoking status should be collected on all identified cases of Covid-19.Little attention has been given to the role of smoking in either the transmission of the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, actual virus) or mortality rate of Covid-19 (name of the disease caused). Smokers contract more respiratory ailments, including colds (commonly rhinoviruses, but also coronaviruses) than non-smokers. Smokers also show double the influenza rate and increased rates of bacterial pneumonia and tuberculosis [1][2][3][4][5]. The damage caused to the lungs by smoking makes patients more susceptible to pulmonary infections, both bacterial and viral [6]. Smokers are 34% more likely than non-smokers to contract the flu [6]. Han and colleagues conclude that literature evidence showed that smoking was consistently associated with a higher risk of hospital admissions after influenza infection [7]. Smoking is the primary etiological factor behind chronic obstructive pulmonary disease (COPD) in the developed world, but environmental pollution and degrading air quality are also responsible in developing countries. It is now the fourth leading cause of death in the world [8]. Vaccination against influenza is strongly recommended for patients with COPD, as the frequency and progression of exacerbations are strongly linked to respiratory viruses

Epithelial-mesenchymal transition (EMT) plays key roles during lung development and many lung diseases such as chronic obstructive pulmonary disease (COPD), lung cancer, and pulmonary fibrosis. Here, integrating morphological observations with underlying molecular mechanisms, we highlight the functional role of EMT in lung development and injury repair, and discuss how it can contribute to pathogenesis of chronic lung disease. We discuss the evidence of manifestation of EMT and its potential driving role in COPD, idiopathic pulmonary fibrosis (IPF), bronchiolitis obliterans syndrome (BOS), and lung cancer, while noting that all cells need not display a full EMT in any of these contexts, i.e., often cells co-express epithelial and mesenchymal markers but do not fully convert to extracellular matrix (ECM) -producing fibroblasts. Finally, we discuss recent therapeutic attempts to restrict EMT in chronic lung disease. Developmental Dynamics 247:346-358, 2018. V C 2017 Wiley Periodicals, Inc.

We explore potential dysregulation of macrophage phenotypes in COPD pathogenesis through integrated study of human small airway tissue, bronchoalveolar lavage (BAL) and an experimental murine model of COPD. We evaluated human airway tissue and BAL from healthy controls, normal lung function smokers (NLFS), and COPD subjects. Both small airways and BAL cells were immunohistochemically stained with anti-CD68 for total macrophages and with anti-CD163 for M2, and anti-iNOS for M1 macrophages. Multiplex ELISA measured BAL cytokines. Comparable cigarette smoke-induced experimental COPD mouse model was assessed for relevant mRNA profiles. We found an increase in pro-inflammatory M1s in the small airways of NLFS and COPD compared to controls with a reciprocal decrease in M2 macrophages, which remained unchanged among pathological groups. However, luminal macrophages showed a dominant M2 phenotype in both NLFS and COPD subjects. BAL cytokine skewed towards an M2 profile with increase in CCL22, IL-4, IL-13, and IL-10 in both NLFS and COPDs. The mouse-model of COPD showed similar increase in mRNA for M2 markers. Our finding suggests abnormal macrophage switching in both mucosal and luminal areas of COPD patients, that strongly associated with cytokine balance. There may be potential for beneficial therapeutic cytokine manipulation of macrophage phenotypes in COPD.

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While cigarette smoking still remains one of the most pressing global health issues of our time, newer forms of smoking device have been introduced across the globe in the last decade [1]. Electronic nicotine/non-nicotine delivery systems commonly known as electronic cigarettes (eCig) heat a solution (e-liquid) to create vapour [2]; the latest addition to this list is the introduction of heat-not-burn (HNBs) tobacco products branded as IQOS [3]. HNBs are hybrids between eCigs and traditional cigarettes i.e. they are equipped with a device that heats the product, without burning to generate aerosol and the product being heated is not a liquid but real tobacco [4, 5]. eCig vaping is comparatively new but its use is increasing at an alarming rate; it is believed it will surpass the use of traditional cigarettes in next 5 years, with global sales reaching US$10 billion [6]. Since its launch in Italy and Japan in 2014, IQOS has become the leader in the HNB market [4, 7]. To date, IQOS is available in 41 countries, including 22 from the WHO-European region, and its market share has now reached the level of cigars in Italy [4]. Emerging data shows that eCig use, particularly in the young, is associated with future cigarette use [8]. Similarly, over half of the people interested in IQOS are never-smokers [4]. Therefore, both eCigs and IQOS may represent a gateway for nicotine addiction among never-smokers rather than a substitute used for harm-reduction purposes in current smokers [4]. It is now clear that eCig vapour contains high levels of toxic compounds [9], which adversely affect respiratory, gastrointestinal and cardiovascular systems both in vitro and in vivo [10–12]. It is also important to recognise that IQOS products are comparatively new but emerging research suggests that IQOS emits substantially high levels of carbonyls [13]. There is as yet no published comparison between the effect of eCigs, IQOS and tobacco smoke on human lungs. Here, we examine whether exposure to IQOS has the same damaging effect on human airway epithelial and smooth muscle cells as traditional tobacco cigarette and eCigs in vitro.

Chronic obstructive pulmonary disease (COPD) is primarily an airway condition, which mainly affects cigarette smokers and presents with shortness of breath that is progressive and poorly reversible. In COPD research, there has been a long held belief that airway disease progression is due to inflammation. Although this may be true in the airway lumen with innate immunity activated by the effect of smoke or secondary to infection, the accurate picture of inflammatory cells in the airway wall, where the pathophysiological COPD remodeling occurs, is uncertain and debatable. Areas covered: The current review provides a comprehensive literature survey of the changes in the main inflammatory cells in human COPD patients and focuses on contrarian views that affect the prevailing dogma on inflammation. The review also delves into the role of oxidative stress and inflammasomes in modulating the immune response in COPD. Further, the effects of inflammation in affecting the epithelium, fibroblasts, and airway remodeling are discussed. Expert commentary: Inflammation as a driving force for airway wall damage and remodelling in early COPD is at the very least 'oversimplified' and is likely to be misleading. This has serious implications for rational thinking about the illness, including pathogenesis and designing therapy.

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Introduction: COVID-19 is a recent emerging pandemic whose prognosis is still unclear. Diagnostic tools are the main players that not only indicate a possible infection but can further restrict the transmission and can determine the extent to which disease progression would occur. Areas covered: In this paper, we have performed a narrative and critical review on different technology-based diagnostic strategies such as molecular approaches including real-time reverse transcriptase PCR, serological testing through enzyme-linked immunosorbent assay, laboratory and point of care devices, radiology-based detection through computed tomography and chest X-ray, and viral cell cultures on Vero E6 cell lines are discussed in detail to address COVID-19. This review further provides an overview of emergency use authorized immunodiagnostic and molecular diagnostic kits and POC devices by FDA for timely and efficient conduction of diagnostic tests. The majority of the literature cited in this paper is collected from guidelines on protocols and other considerations on diagnostic strategies of COVID-19 issued by WHO, CDC, and FDA under emergency authorization. Expert opinion: Such information holds importance to the health professionals in conducting error-free diagnostic tests and researches in producing better clinical strategies by addressing the limitations associated with the available methods.