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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Psoriasis&#44; psoriatic arthritis&#44; and other spondyloarthropathies such as those associated with inflammatory bowel disease &#40;IBD&#41; and IBD itself &#40;Crohn disease being the paradigm&#41;&#44; share many pathogenic features&#46; The first characteristic to be identified&#44; and one that was key for defining the concept of immune-mediated inflammatory disease &#40;IMID&#41;&#44; was the response of all these conditions to biologic agents that block tumor necrosis factor &#40;TNF&#41;&#46; However&#44; there are subtle differences in the pattern of response that are worthy of comment&#46; Examples include the lack of efficacy of etanercept in Crohn disease<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a> &#40;which has never been satisfactorily explained&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> the fact that ustekinumab is only effective in Crohn disease after prior failure of at least one other anti-TNF agent&#44;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">3</span></a> and clinical worsening in patients treated with interleukin &#40;IL&#41; 17A inhibitors&#44;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">4</span></a> whose spectacular efficacy in psoriasis confirms the fundamental pathogenic role of IL-17A in this disease&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Another feature common to IMIDs is the appearance of paradoxical manifestations during treatment with anti-TNF agents&#46; Explanations have been proposed for this contradictory behaviour&#44; such as the activation of alternative cytokine pathways&#46; For example&#44; TNF blockade through treatment might induce an increased production of interferon alpha by plasmacytoid dendritic cells&#44; which in turn may then activate production of IL-17A &#40;sustained by IL-23&#41; and IL-22 by the corresponding T-cell subpopulations&#44; as well as expression of IL-22 receptors in keratinocytes&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">6</span></a> This would explain the onset of paradoxical psoriasis in some patients &#40;for example patients with Crohn disease&#41; who receive anti-TNF agents&#46; These patients may have a certain genetic predisposition due to uncommon alleles of the IL23R gene and respond to treatment with ustekinumab&#44;<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">7&#44;8</span></a> whereas activation of another feedback circuit in which the cytokines IL-17<span class="elsevierStyleHsp" style=""></span>C and IL-36&#947; participate may go some way towards explaining the activation of keratinocytes in paradoxical psoriasis&#46; These observations may provide a basis for a new therapeutic approach to this disease<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">9</span></a> and perhaps to other pustular dermatoses&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">With regards to the counterproductive effect of IL-17A blockade in Crohn disease&#44; it has been observed that patients with active disease have lower circulating CD45RO<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>CD4&#43;<span class="elsevierStyleHsp" style=""></span>T helper &#40;Th&#41; 17 cell levels than those present when the disease is controlled with adalimumab&#59; the lymphocyte count inversely correlates with mucosal inflammation estimated from the levels of fecal calprotectin&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">10</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">This apparent paradox requires an explanation&#44; given that IL-23 &#40;which in principle can expand Th17 cell populations and is able to activate tissue-resident IL-17A&#8211;producing T&#947;&#948; cells&#41; has a fundamental role in autoimmune intestinal inflammation in murine models of IBD&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">11</span></a> There are probably different types of Th17 cells&#44; able to produce different combinations of cytokines that determine a relatively specific antimicrobial action&#44; and the imbalanced intestinal microflora in Crohn disease&#44; and certain Gram&#43; bacteria in particular&#8212;segmented filamentous bacteria&#8212;may play a key role in differentiation of Th17 cells and induction of colitis in murine models of IBD&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">11</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The levels of IL-22 produced by type 3 innate lymphoid cells in the intestine are critical for maintaining intestinal barrier function&#44; and in absence of IL-22&#44; overgrowth of segmented filamentous bacteria may occur&#44; along with an increase in the number of Th17 cells both in the mucosa and the corresponding lymph nodes&#46;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">12&#44;13</span></a> Inhibition of IL-17A&#44; one of the cytokines produced by Th17 cells&#44; exacerbates intestinal disease in some patients with Crohn disease&#44; thus suggesting a protective role of IL-17A&#44; consistent with the observations in some murine models of colitis&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">14</span></a> Although a pathogenic role has been proposed for IL-17F and IL-25 in IBD&#44;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">15</span></a> treatment with brodalumab has not proved effective&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> On the other hand&#44; it has been postulated that exacerbations observed in patients treated with IL-17A inhibitors may be related to altered intestinal mycological flora&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">16</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Currently&#44; it is accepted that a disturbed immune response to an altered intestinal microbiome at the mucosal interface has a fundamental role in the pathogenesis of Crohn disease and ulcerative colitis in individuals with a certain genetic predisposition&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">17</span></a> The microbiome is the set of commensal bacteria associated with each individual&#44; located in the skin&#44; vagina&#44; oral cavity&#44; and principally &#40;70&#37;&#41;&#44; the gastrointestinal tract&#46; The dominant phyla are <span class="elsevierStyleItalic">Bacteroidetes</span> and <span class="elsevierStyleItalic">Firmicutes</span>&#46; The intestinal microbiome contributes to digestion of fiber and polyphenols&#44; the production of certain vitamins&#44; and maintenance of epithelial barrier integrity&#44; regulating homeostasis of the host immune system&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">18</span></a> Taxonomic alterations or imbalances in the intestinal microbiome &#40;dysbiosis&#41; have been associated with a range of conditions&#44; including obesity&#44; colorectal cancer&#44; liver diseases&#44; irritable colon&#44; IBD&#44; and other IMIDs&#46;<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">19</span></a> Both in IBD and spondyloarthritis&#44; disturbances in the intestinal microbiome have been reported&#44; with a decrease in the number of <span class="elsevierStyleItalic">Firmicutes</span>&#44; which may indicate another common pathogenic mechanism&#44;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">20</span></a> and the existence of analogous disturbances &#40;relative decrease of <span class="elsevierStyleItalic">Coprococcus</span> and other beneficial taxa&#41; in psoriatic arthritis&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">21</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Numerous studies have shown that the intestinal microbiome may have an impact on Th17&#47;Treg balance in the lamina propria&#44; and that intestinal Th17 cells may be responsible for the onset of arthritis in experimental models&#46; The activation of Toll-like receptors plays a key role in the differentiation of Th17 cells in the lamina propria and in the induction of autoimmune arthritis&#59; possible mechanisms include cross-recognition of bacterial and endogenous antigens&#44; migration of Th17 cells of intestinal origin to the joints&#44; and an alteration in the microenvironment of cytokines that may stimulate differentiation of autoreactive Th17 cells&#46;<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">22</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Although this mechanism may provide a plausible explanation for the role of a possible dysbiosis in the pathogenesis of psoriasis and psoriatic arthritis&#44; in the case of psoriasis&#44; more attention has been paid to possible alterations in the skin microbiome&#44; by analogy with atopic dermatitis&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">23</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The pathogenic role of intestinal dysbiosis&#44; that is&#44; disturbed immunologic tolerance of intestinal microflora&#44; would seem an important and common feature of different IMIDs&#46; Some physicians&#44; however&#44; may be reluctant to explore the possible therapeutic implications &#40;fecal transplantation&#41; of this mechanism&#46; They may prefer an alternative explanation involving alteration in the skin microbiome&#44; which may have a similar role &#40;alternative or complementary&#41; to intestinal dysbiosis in psoriasis<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">24</span></a> and psoriatic arthritis&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">25</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In conclusion&#44; psoriasis&#44; psoriatic arthritis&#44; and Crohn disease share common pathogenic features&#44; but they also show differences that may help elucidate the complete inflammatory cycles implicated and so develop new therapeutic approaches&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of Interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">L&#46; Puig has received consultancy and&#47;or speaker fees&#44; and has participated as an investigator in clinical trials sponsored by AbbVie&#44; Amgen&#44; Janssen&#44; Lilly&#44; Novartis&#44; and Pfizer&#46;</p></span></span>"
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Opinion Article
Cytokine Pathways and the Role of Dysbiosis in Psoriasis, Psoriatic Arthritis, and Crohn Disease
Psoriasis, artritis psoriásica y enfermedad de Crohn: circuitos de citocinas y papel de la disbiosis
L. Puig
Servicio de Dermatología, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Psoriasis&#44; psoriatic arthritis&#44; and other spondyloarthropathies such as those associated with inflammatory bowel disease &#40;IBD&#41; and IBD itself &#40;Crohn disease being the paradigm&#41;&#44; share many pathogenic features&#46; The first characteristic to be identified&#44; and one that was key for defining the concept of immune-mediated inflammatory disease &#40;IMID&#41;&#44; was the response of all these conditions to biologic agents that block tumor necrosis factor &#40;TNF&#41;&#46; However&#44; there are subtle differences in the pattern of response that are worthy of comment&#46; Examples include the lack of efficacy of etanercept in Crohn disease<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a> &#40;which has never been satisfactorily explained&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> the fact that ustekinumab is only effective in Crohn disease after prior failure of at least one other anti-TNF agent&#44;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">3</span></a> and clinical worsening in patients treated with interleukin &#40;IL&#41; 17A inhibitors&#44;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">4</span></a> whose spectacular efficacy in psoriasis confirms the fundamental pathogenic role of IL-17A in this disease&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Another feature common to IMIDs is the appearance of paradoxical manifestations during treatment with anti-TNF agents&#46; Explanations have been proposed for this contradictory behaviour&#44; such as the activation of alternative cytokine pathways&#46; For example&#44; TNF blockade through treatment might induce an increased production of interferon alpha by plasmacytoid dendritic cells&#44; which in turn may then activate production of IL-17A &#40;sustained by IL-23&#41; and IL-22 by the corresponding T-cell subpopulations&#44; as well as expression of IL-22 receptors in keratinocytes&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">6</span></a> This would explain the onset of paradoxical psoriasis in some patients &#40;for example patients with Crohn disease&#41; who receive anti-TNF agents&#46; These patients may have a certain genetic predisposition due to uncommon alleles of the IL23R gene and respond to treatment with ustekinumab&#44;<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">7&#44;8</span></a> whereas activation of another feedback circuit in which the cytokines IL-17<span class="elsevierStyleHsp" style=""></span>C and IL-36&#947; participate may go some way towards explaining the activation of keratinocytes in paradoxical psoriasis&#46; These observations may provide a basis for a new therapeutic approach to this disease<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">9</span></a> and perhaps to other pustular dermatoses&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">With regards to the counterproductive effect of IL-17A blockade in Crohn disease&#44; it has been observed that patients with active disease have lower circulating CD45RO<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>CD4&#43;<span class="elsevierStyleHsp" style=""></span>T helper &#40;Th&#41; 17 cell levels than those present when the disease is controlled with adalimumab&#59; the lymphocyte count inversely correlates with mucosal inflammation estimated from the levels of fecal calprotectin&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">10</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">This apparent paradox requires an explanation&#44; given that IL-23 &#40;which in principle can expand Th17 cell populations and is able to activate tissue-resident IL-17A&#8211;producing T&#947;&#948; cells&#41; has a fundamental role in autoimmune intestinal inflammation in murine models of IBD&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">11</span></a> There are probably different types of Th17 cells&#44; able to produce different combinations of cytokines that determine a relatively specific antimicrobial action&#44; and the imbalanced intestinal microflora in Crohn disease&#44; and certain Gram&#43; bacteria in particular&#8212;segmented filamentous bacteria&#8212;may play a key role in differentiation of Th17 cells and induction of colitis in murine models of IBD&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">11</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The levels of IL-22 produced by type 3 innate lymphoid cells in the intestine are critical for maintaining intestinal barrier function&#44; and in absence of IL-22&#44; overgrowth of segmented filamentous bacteria may occur&#44; along with an increase in the number of Th17 cells both in the mucosa and the corresponding lymph nodes&#46;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">12&#44;13</span></a> Inhibition of IL-17A&#44; one of the cytokines produced by Th17 cells&#44; exacerbates intestinal disease in some patients with Crohn disease&#44; thus suggesting a protective role of IL-17A&#44; consistent with the observations in some murine models of colitis&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">14</span></a> Although a pathogenic role has been proposed for IL-17F and IL-25 in IBD&#44;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">15</span></a> treatment with brodalumab has not proved effective&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> On the other hand&#44; it has been postulated that exacerbations observed in patients treated with IL-17A inhibitors may be related to altered intestinal mycological flora&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">16</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Currently&#44; it is accepted that a disturbed immune response to an altered intestinal microbiome at the mucosal interface has a fundamental role in the pathogenesis of Crohn disease and ulcerative colitis in individuals with a certain genetic predisposition&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">17</span></a> The microbiome is the set of commensal bacteria associated with each individual&#44; located in the skin&#44; vagina&#44; oral cavity&#44; and principally &#40;70&#37;&#41;&#44; the gastrointestinal tract&#46; The dominant phyla are <span class="elsevierStyleItalic">Bacteroidetes</span> and <span class="elsevierStyleItalic">Firmicutes</span>&#46; The intestinal microbiome contributes to digestion of fiber and polyphenols&#44; the production of certain vitamins&#44; and maintenance of epithelial barrier integrity&#44; regulating homeostasis of the host immune system&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">18</span></a> Taxonomic alterations or imbalances in the intestinal microbiome &#40;dysbiosis&#41; have been associated with a range of conditions&#44; including obesity&#44; colorectal cancer&#44; liver diseases&#44; irritable colon&#44; IBD&#44; and other IMIDs&#46;<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">19</span></a> Both in IBD and spondyloarthritis&#44; disturbances in the intestinal microbiome have been reported&#44; with a decrease in the number of <span class="elsevierStyleItalic">Firmicutes</span>&#44; which may indicate another common pathogenic mechanism&#44;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">20</span></a> and the existence of analogous disturbances &#40;relative decrease of <span class="elsevierStyleItalic">Coprococcus</span> and other beneficial taxa&#41; in psoriatic arthritis&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">21</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Numerous studies have shown that the intestinal microbiome may have an impact on Th17&#47;Treg balance in the lamina propria&#44; and that intestinal Th17 cells may be responsible for the onset of arthritis in experimental models&#46; The activation of Toll-like receptors plays a key role in the differentiation of Th17 cells in the lamina propria and in the induction of autoimmune arthritis&#59; possible mechanisms include cross-recognition of bacterial and endogenous antigens&#44; migration of Th17 cells of intestinal origin to the joints&#44; and an alteration in the microenvironment of cytokines that may stimulate differentiation of autoreactive Th17 cells&#46;<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">22</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Although this mechanism may provide a plausible explanation for the role of a possible dysbiosis in the pathogenesis of psoriasis and psoriatic arthritis&#44; in the case of psoriasis&#44; more attention has been paid to possible alterations in the skin microbiome&#44; by analogy with atopic dermatitis&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">23</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The pathogenic role of intestinal dysbiosis&#44; that is&#44; disturbed immunologic tolerance of intestinal microflora&#44; would seem an important and common feature of different IMIDs&#46; Some physicians&#44; however&#44; may be reluctant to explore the possible therapeutic implications &#40;fecal transplantation&#41; of this mechanism&#46; They may prefer an alternative explanation involving alteration in the skin microbiome&#44; which may have a similar role &#40;alternative or complementary&#41; to intestinal dysbiosis in psoriasis<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">24</span></a> and psoriatic arthritis&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">25</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In conclusion&#44; psoriasis&#44; psoriatic arthritis&#44; and Crohn disease share common pathogenic features&#44; but they also show differences that may help elucidate the complete inflammatory cycles implicated and so develop new therapeutic approaches&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of Interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">L&#46; Puig has received consultancy and&#47;or speaker fees&#44; and has participated as an investigator in clinical trials sponsored by AbbVie&#44; Amgen&#44; Janssen&#44; Lilly&#44; Novartis&#44; and Pfizer&#46;</p></span></span>"
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