Cigarette smoke alters the ability of human dendritic cells to promote anti-Streptococcus pneumoniae Th17 response

Chenivesse, Cécile; Koné, B.; Kluza, Jérôme; Marchetti, Philippe; Hennegrave, Florence; Olivier, Cecile; Kervoaze, Gwenola; Vilain, Eva; Mordacq, C.; Just, N.; Pérez, Thierry; Bautin, N.; Pichavant, Muriel; Gosset, Philippe

doi:10.1186/s12931-016-0408-6

Cited by 23 publications

(27 citation statements)

References 35 publications

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“…This cytokine is particularly central to lung immunity because it has been demonstrated that innate host defenses to respiratory pathogens are compromised in mice lacking this proinflammatory cytokine or its receptor (IL-17RA), leading to reduced neutrophil activation, differentiation and recruitment and increased bacterial proliferation. 61 Le Rouzic et al 62 in their study showed that chronic exposure to cigarette smoke extract (CSE) inhibits S. pneumoniaeinduced monocyte-derived dendritic cells (MDDC) maturation and secretion of cytokines involved in Th1 and Th17 T cell differentiation, among which are IL-1β, IL-6, IL-12 and IL-23 (which is necessary to Th17 polarization). These events can contribute to colonization of pathogens capable of generating exacerbations.…”

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confidence: 99%

“…A chronic exposure to CSE has been related to a deficiency in the phagolysosome trafficking in DC, secondary to low expression of maturation markers such as CD83, which leads to a deficient antigenic presentation and, consequently, an inadequate response against bacteria such as S. pneumoniae. 62 van der Sluijs et al 64 reported in their study that inhibiting the production of IL-10 (inhibitory cytokine) by Tregs decreases the likelihood of secondary S. pneumoniae infection.…”

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confidence: 99%

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Th17 profile in COPD exacerbations

Ponce-Gallegos¹,

Ramírez‐Venegas²,

Falfán-Valencia³

2017

COPD

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COPD is characterized by an ongoing inflammatory process of the airways that leads to obstruction or limitation of airflow. It is mainly associated with exposure to cigarette smoke. In addition, it is considered, at present, a serious public health problem, ranking fourth in mortality worldwide. Many cells participate in the pathophysiology of COPD, the most important are neutrophils, macrophages and CD4+ and CD8+ T cells. Neutrophil migration to the inflammation area could be mediated largely by cytokines related to CD4+ Th17 lymphocytes, because it has been shown that IL-17A, IL-17F and IL-22 act as inducers for CXCL8, CXCL1, CXCL5, G-CSF, and GM-CSF secretion by epithelial cells of the airways. The aims of these molecules are differentiation, proliferation and recruitment of neutrophils. Furthermore, it is believed that CD4+ lymphocytes Th17 may be involved in protection against pathogens for which Th1 and Th2 are not prepared to fight. In COPD exacerbations, there is an increased cellularity in the lung region and respiratory tract. Therefore, the increase in the number of neutrophils and macrophages in the airways and the increase in proinflammatory cytokines are directly related to the severity of exacerbations and that is the importance of the functions of Th17 profile in this entity.

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confidence: 99%

mentioning

confidence: 99%

Th17 profile in COPD exacerbations

Ponce-Gallegos¹,

Ramírez‐Venegas²,

Falfán-Valencia³

2017

COPD

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“…In mice chronically exposed to cigarette smoke, we reported a defective IL-17A and IL-22 response to S. pneumoniae, which was related to reduced production of IL-1β and IL-23 by alveolar macrophages and dendritic cells [85]. In addition, we observed that in vitro exposure to cigarette smoke altered the response of dendritic cells to S. pneumoniae, leading to a decreased ability to promote Th17 differentiation of T-cells [86]. Ex vivo exposure to S. pneumoniae of peripheral blood mononuclear cells from COPD patients does not increase IL-17A and IL-22 production, in contrast to healthy nonsmokers and healthy smokers [85].…”

Section: Il-17 and Il-22 In Copd Exacerbationsmentioning

confidence: 80%

“…Deciphering the mechanism responsible for the altered production and function of IL-22 seems essential in order to propose a therapeutic approach in this context. Since alteration of the function of dendritic cells by cigarette smoke is not mainly dependent on oxidative stress, we suspect that exposure to cigarette smoke alters phagolysosome trafficking, which secondarily impacts the signalling pathways triggered by bacteria [86]. In addition, dysregulation of miRNA expression after cigarette smoke exposure is implicated in dendritic cell dysfunction, although their role during exacerbations has not yet been evaluated [75].…”

Section: Future Directionsmentioning

confidence: 99%

Th17 cytokines: novel potential therapeutic targets for COPD pathogenesis and exacerbations

et al. 2017

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Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airways caused mainly by cigarette smoke exposure. COPD progression is marked by exacerbations of the disease, often associated with infections. Recent data show the involvement in COPD pathophysiology of interleukin (IL)-17 and IL-22, two cytokines that are important in the control of lung inflammation and infection. During the initiation and progression of the disease, increased IL-17 secretion causes neutrophil recruitment, leading to chronic inflammation, airways obstruction and emphysema. In the established phase of COPD, a defective IL-22 response facilitates pathogen-associated infections and disease exacerbations. Altered production of these cytokines involves a complex network of immune cells and dysfunction of antigen-presenting cells. In this review, we describe current knowledge on the involvement of IL-17 and IL-22 in COPD pathophysiology at steady state and during exacerbations, and discuss implications for COPD management and future therapeutic approaches.

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“…In this context, Le Rouzic and colleagues [ 38 ] recently reported that cigarette smoke might alter the ability to activate the antigen specific T-cell response of the human immune system against Streptococcus pneumoniae .…”

Section: Discussionmentioning

confidence: 99%

Pneumococcal Colonization in the Familial Context and Implications for Anti-Pneumococcal Immunization in Adults: Results from the BINOCOLO Project in Sicily

Tramuto

Amodio

Calamusa

et al. 2017

IJMS

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The spread of Streptococcus pneumoniae within families has been scarcely investigated so far. This feasibility study aimed to estimate the prevalence of pneumococcal carriage in school-aged children and co-habiting relatives and to explore the potential link between the family environment and the sharing of pneumococcal serotypes covered by the vaccine. Oropharyngeal samples of 146 subjects belonging to 36 different family groups were molecularly tested for pneumococcal detection and serotyping. The overall prevalence of pneumococcal carriage was 65.8% (n = 96/146), whereas it was higher among schoolchildren (77.8%, n = 28/36); subjects of seven years of age had the highest odds of being colonized (odds ratio, OR = 5.176; p = 0.145). Pneumococcal serotypes included in the 13-valent conjugate vaccine formulation were largely detected in the study population and multiple serotypes colonization was considerable. Factors relating to a close proximity among people at the family level were statistically associated with pneumococcal carriage (OR = 2.121; p = 0.049), as well as active smoking habit with a clear dose-response effect (ORs = 1.017–3.326). About half of family clusters evidenced similar patterns of carried pneumococcal serotypes and the odds of sustaining a high level of intrafamilial sharing increased with household size (ORs = 1.083–5.000). This study highlighted the potential role played by the family environment in sustaining both the circulation and horizontal transmission of pneumococcus.

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Cigarette smoke alters the ability of human dendritic cells to promote anti-Streptococcus pneumoniae Th17 response

Cited by 23 publications

References 35 publications

Th17 profile in COPD exacerbations

Th17 profile in COPD exacerbations

Th17 cytokines: novel potential therapeutic targets for COPD pathogenesis and exacerbations

Pneumococcal Colonization in the Familial Context and Implications for Anti-Pneumococcal Immunization in Adults: Results from the BINOCOLO Project in Sicily

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