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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Inhaled tobacco smoke delivers multiple harmful particles that cause inflammatory&#44; genotoxic&#44; and proliferative changes in the entire lung anatomy from the airway to the parenchyma&#46; Lung cancer and chronic obstructive pulmonary disease are the lung diseases most commonly associated with smoking&#44; but today it is estimated that 8&#37;&#8211;10&#37; of smokers have some associated interstitial lung abnormalities&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> This association is dose-dependent&#44; i&#46;e&#46;&#44; the greater the exposure to tobacco smoke&#44; the greater the risk&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">1&#44;2</span></a> As our knowledge of how tobacco injures the lung increases&#44; so does our understanding of the heterogeneous breadth of the spectrum of smoking-related interstitial lung diseases &#40;ILD&#41;&#46; These pathologies primarily include respiratory bronchiolitis-interstitial lung disease&#44; desquamative interstitial pneumonia&#44; pulmonary Langerhans cell histiocytosis&#44; acute eosinophilic pneumonia&#44; combined pulmonary fibrosis and emphysema&#44; smoking-related interstitial fibrosis&#44; and idiopathic pulmonary fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">At the biological level&#44; it is plausible that smoking-induced cell abnormalities associated with small airway changes and alveolar wall destruction also affect the interstitium&#46; Pathogenic studies are still lacking&#44; but ILD may be associated with mechanisms that parallel those of chronic obstructive pulmonary disease and lung cancer&#44; primarily&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">a&#41;</span><p id="par0015" class="elsevierStylePara elsevierViewall">Immune response changes</p><p id="par0020" class="elsevierStylePara elsevierViewall">Cigarette smoke can affect the immune system at different levels&#46; It can chemically modify signaling pathways and extracellular matrix by acetylation&#44; nitrosylation&#44; carbonylation and oxidation&#44; which can impact the survival&#44; activation and differentiation of immune cells&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a> These immunological modifications can have two types of opposing consequences&#58; they can either trigger a proinflammatory cascade&#44; or they can have an immunosuppressive effect&#44;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">5</span></a> due to reduced macrophage phagocytic ability&#44;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">6</span></a> and decreased NK cell function&#44; immunoglobulin activity&#44; dendritic cell maturation&#44; and lymphocyte function&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a> As a result of these mechanisms&#44; pulmonary fibrosis is often characterized by elevated neutrophils&#44; monocytes and macrophages that promote a moderate proinflammatory state with the production of cytokines IL-8&#44; IL-6 and CCL2 and an increase in senescent T lymphocytes that produce Th2 cytokines&#44; considered profibrotic&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">7</span></a> Prasse et al&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a> demonstrated that osteopontine&#44; a glycoprotein with cytokine-like properties&#44; is increased in the extracellular matrix of bone as a result of chronic exposure to nicotine in patients with smoking-related ILDs&#44; particularly in desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">b&#41;</span><p id="par0025" class="elsevierStylePara elsevierViewall">Oxidative stress</p><p id="par0030" class="elsevierStylePara elsevierViewall">It is well established that tobacco causes oxidative stress due to the inability of endogenous pulmonary antioxidant mechanisms to combat the increased levels of free radicals caused by cigarette smoke&#46; This process leads to increased transcription of inflammatory genes&#44; among other mechanisms&#44; which&#44; through the release of cytokines and chemokines&#44; perpetuate the inflammatory response and induce rapid lung aging by increasing the activity of proteases and other mediators &#40;both in the large and small airways and the parenchyma&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">9</span></a></p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">c&#41;</span><p id="par0035" class="elsevierStylePara elsevierViewall">Premature aging</p><p id="par0040" class="elsevierStylePara elsevierViewall">It has been associated with both COPD and idiopathic pulmonary fibrosis&#46; In addition to oxidative stress&#44; telomere shortening&#44; cellular senescence&#44; epigenetic changes &#40;histone acetylation and hypermethylation&#41;&#44; loss of proteostasis&#44; mitochondrial dysfunction&#44; and DNA damage are considered distinctive of the aging process&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">10&#44;11</span></a> Many of these mechanisms are associated with smoking&#58; for example&#44; smokers who develop pulmonary fibrosis show telomere shortening &#40;present in the circulating leukocytes of smokers&#44; and more pronounced the greater the cumulative exposure to tobacco smoke<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">12</span></a>&#41;&#46; The aggression from cigarette smoke causes aging mesenchymal stem cells in the bone marrow to accumulate DNA damage and lose their response to soluble factors&#46; This could impair their ability to repair damaged organs&#44; which could increase susceptibility to the development of fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">10</span></a> Moreover&#44; senescent epithelial cells produce numerous profibrotic mediators that&#44; together with senescent fibroblasts&#44; may favor pulmonary fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">In conclusion&#44; there is evidence that smoking plays a role in the pathogenesis of ILD that is not yet well established&#46; Prevention and treatment of smoking are essential to treat such diseases&#44; although in many cases cessation is not enough to prevent progression&#46; It is therefore extremely important to characterize the cell pathways by which tobacco smoke induces different interstitial lung diseases&#44; because understanding the relevant pathogenic pathways will help us develop new drugs aimed at specific targets and thus change the course of these diseases&#46;</p></li></ul></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0050" class="elsevierStylePara elsevierViewall">This study was funded by the SLT008&#47;18&#47;00176 grant and the <span class="elsevierStyleGrantSponsor" id="gs1">Department of Health of the Generalitat de Catalunya</span>&#44; in the 2019&#8211;2021 call for applications for competitive grants for funding programs and instrumental actions included in the Strategic Plan for Health Research and Innovation 2016&#8211;2020&#46; It was also funded by <span class="elsevierStyleGrantSponsor" id="gs2">SEPAR</span><span class="elsevierStyleGrantNumber" refid="gs2">2018-562</span>&#44; <span class="elsevierStyleGrantNumber" refid="gs2">2019-792</span>&#44; <span class="elsevierStyleGrantSponsor" id="gs3">SOCAP</span><span class="elsevierStyleGrantNumber" refid="gs3">2017</span>&#44; <span class="elsevierStyleGrantSponsor" id="gs4">FUCAP</span><span class="elsevierStyleGrantNumber" refid="gs4">2018</span>&#46;</p></span></span>"
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Editorial
Smoking and Interstitial Lung Damage/Effects: A Plausible Association?
Tabaco y alteraciones intersticiales: ¿una asociación plausible?
Nuria Albacara, Rosa Fanerb,c, Jacobo Sellarésa,b,c,
Corresponding author


Corresponding author.
a Servei de Pneumologia, Respiratory Institute, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain
b Centro de Investigación Biomedica en Red-Enfermedades Respiratorias (CIBERES), Spain
c Institut d’investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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    "titulo" => "Smoking and Interstitial Lung Damage&#47;Effects&#58; A Plausible Association&#63;"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Inhaled tobacco smoke delivers multiple harmful particles that cause inflammatory&#44; genotoxic&#44; and proliferative changes in the entire lung anatomy from the airway to the parenchyma&#46; Lung cancer and chronic obstructive pulmonary disease are the lung diseases most commonly associated with smoking&#44; but today it is estimated that 8&#37;&#8211;10&#37; of smokers have some associated interstitial lung abnormalities&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> This association is dose-dependent&#44; i&#46;e&#46;&#44; the greater the exposure to tobacco smoke&#44; the greater the risk&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">1&#44;2</span></a> As our knowledge of how tobacco injures the lung increases&#44; so does our understanding of the heterogeneous breadth of the spectrum of smoking-related interstitial lung diseases &#40;ILD&#41;&#46; These pathologies primarily include respiratory bronchiolitis-interstitial lung disease&#44; desquamative interstitial pneumonia&#44; pulmonary Langerhans cell histiocytosis&#44; acute eosinophilic pneumonia&#44; combined pulmonary fibrosis and emphysema&#44; smoking-related interstitial fibrosis&#44; and idiopathic pulmonary fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">At the biological level&#44; it is plausible that smoking-induced cell abnormalities associated with small airway changes and alveolar wall destruction also affect the interstitium&#46; Pathogenic studies are still lacking&#44; but ILD may be associated with mechanisms that parallel those of chronic obstructive pulmonary disease and lung cancer&#44; primarily&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">a&#41;</span><p id="par0015" class="elsevierStylePara elsevierViewall">Immune response changes</p><p id="par0020" class="elsevierStylePara elsevierViewall">Cigarette smoke can affect the immune system at different levels&#46; It can chemically modify signaling pathways and extracellular matrix by acetylation&#44; nitrosylation&#44; carbonylation and oxidation&#44; which can impact the survival&#44; activation and differentiation of immune cells&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a> These immunological modifications can have two types of opposing consequences&#58; they can either trigger a proinflammatory cascade&#44; or they can have an immunosuppressive effect&#44;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">5</span></a> due to reduced macrophage phagocytic ability&#44;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">6</span></a> and decreased NK cell function&#44; immunoglobulin activity&#44; dendritic cell maturation&#44; and lymphocyte function&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a> As a result of these mechanisms&#44; pulmonary fibrosis is often characterized by elevated neutrophils&#44; monocytes and macrophages that promote a moderate proinflammatory state with the production of cytokines IL-8&#44; IL-6 and CCL2 and an increase in senescent T lymphocytes that produce Th2 cytokines&#44; considered profibrotic&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">7</span></a> Prasse et al&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a> demonstrated that osteopontine&#44; a glycoprotein with cytokine-like properties&#44; is increased in the extracellular matrix of bone as a result of chronic exposure to nicotine in patients with smoking-related ILDs&#44; particularly in desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">b&#41;</span><p id="par0025" class="elsevierStylePara elsevierViewall">Oxidative stress</p><p id="par0030" class="elsevierStylePara elsevierViewall">It is well established that tobacco causes oxidative stress due to the inability of endogenous pulmonary antioxidant mechanisms to combat the increased levels of free radicals caused by cigarette smoke&#46; This process leads to increased transcription of inflammatory genes&#44; among other mechanisms&#44; which&#44; through the release of cytokines and chemokines&#44; perpetuate the inflammatory response and induce rapid lung aging by increasing the activity of proteases and other mediators &#40;both in the large and small airways and the parenchyma&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">9</span></a></p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">c&#41;</span><p id="par0035" class="elsevierStylePara elsevierViewall">Premature aging</p><p id="par0040" class="elsevierStylePara elsevierViewall">It has been associated with both COPD and idiopathic pulmonary fibrosis&#46; In addition to oxidative stress&#44; telomere shortening&#44; cellular senescence&#44; epigenetic changes &#40;histone acetylation and hypermethylation&#41;&#44; loss of proteostasis&#44; mitochondrial dysfunction&#44; and DNA damage are considered distinctive of the aging process&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">10&#44;11</span></a> Many of these mechanisms are associated with smoking&#58; for example&#44; smokers who develop pulmonary fibrosis show telomere shortening &#40;present in the circulating leukocytes of smokers&#44; and more pronounced the greater the cumulative exposure to tobacco smoke<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">12</span></a>&#41;&#46; The aggression from cigarette smoke causes aging mesenchymal stem cells in the bone marrow to accumulate DNA damage and lose their response to soluble factors&#46; This could impair their ability to repair damaged organs&#44; which could increase susceptibility to the development of fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">10</span></a> Moreover&#44; senescent epithelial cells produce numerous profibrotic mediators that&#44; together with senescent fibroblasts&#44; may favor pulmonary fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">In conclusion&#44; there is evidence that smoking plays a role in the pathogenesis of ILD that is not yet well established&#46; Prevention and treatment of smoking are essential to treat such diseases&#44; although in many cases cessation is not enough to prevent progression&#46; It is therefore extremely important to characterize the cell pathways by which tobacco smoke induces different interstitial lung diseases&#44; because understanding the relevant pathogenic pathways will help us develop new drugs aimed at specific targets and thus change the course of these diseases&#46;</p></li></ul></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0050" class="elsevierStylePara elsevierViewall">This study was funded by the SLT008&#47;18&#47;00176 grant and the <span class="elsevierStyleGrantSponsor" id="gs1">Department of Health of the Generalitat de Catalunya</span>&#44; in the 2019&#8211;2021 call for applications for competitive grants for funding programs and instrumental actions included in the Strategic Plan for Health Research and Innovation 2016&#8211;2020&#46; It was also funded by <span class="elsevierStyleGrantSponsor" id="gs2">SEPAR</span><span class="elsevierStyleGrantNumber" refid="gs2">2018-562</span>&#44; <span class="elsevierStyleGrantNumber" refid="gs2">2019-792</span>&#44; <span class="elsevierStyleGrantSponsor" id="gs3">SOCAP</span><span class="elsevierStyleGrantNumber" refid="gs3">2017</span>&#44; <span class="elsevierStyleGrantSponsor" id="gs4">FUCAP</span><span class="elsevierStyleGrantNumber" refid="gs4">2018</span>&#46;</p></span></span>"
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ISSN: 15792129
Original language: English
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