Immunological functions of the pulmonary epithelium

Thompson, Austin B.; Robbins, Richard; Romberger, Debra J.; Sisson, Joseph H.; Spurzem, John R.; Teschler, Helmut; Rennard, Stephen I.

doi:10.1183/09031936.95.08010127

Cited by 145 publications

(104 citation statements)

References 232 publications

(227 reference statements)

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“…These cells provide a barrier and innate immunity that protect the airway from environmental stressors, pollutants and pathogens (34)(35)(36). Cigarette smoking is associated with disordering of the differentiation of the SAE basal cells, with consequent disordered function of the airway mucociliary barrier (34,35). The ability of the SAE to alter gene expression in response to external stimuli is critical to airway defense and repair mechanisms (30,31,34,36).…”

Section: Introductionmentioning

confidence: 99%

“…In humans, the SAE consists of four major cell types: ciliated, secretory, columnar and basal cells (30,33). These cells provide a barrier and innate immunity that protect the airway from environmental stressors, pollutants and pathogens (34)(35)(36). Cigarette smoking is associated with disordering of the differentiation of the SAE basal cells, with consequent disordered function of the airway mucociliary barrier (34,35).…”

Section: Introductionmentioning

confidence: 99%

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Cigarette smoking induces small airway epithelial epigenetic changes with corresponding modulation of gene expression

Buro-Auriemma

Salit

Hackett

et al. 2013

Human Molecular Genetics

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The small airway epithelium (SAE), the first site of smoking-induced lung pathology, exhibits genome-wide changes in gene expression in response to cigarette smoking. Based on the increasing evidence that the epigenome can respond to external stimuli in a rapid manner, we assessed the SAE of smokers for genome-wide DNA methylation changes compared with nonsmokers, and whether changes in SAE DNA methylation were linked to the transcriptional output of these cells. Using genome-wide methylation analysis of SAE DNA of nonsmokers and smokers, the data identified 204 unique genes differentially methylated in SAE DNA of smokers compared with nonsmokers, with 67% of the regions with differential methylation occurring within 2 kb of the transcriptional start site. Among the genes with differential methylation were those related to metabolism, transcription, signal transduction and transport. For the differentially methylated genes, 35 exhibited a correlation with gene expression, 54% with an inverse correlation of DNA methylation with gene expression and 46% a direct correlation. These observations provide evidence that cigarette smoking alters the DNA methylation patterning of the SAE and that, for some genes, these changes are associated with the smoking-related changes in gene expression.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cigarette smoking induces small airway epithelial epigenetic changes with corresponding modulation of gene expression

Buro-Auriemma

Salit

Hackett

et al. 2013

Human Molecular Genetics

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“…Until recently, the bronchial epithelium was considered to be a passive barrier between the environment and the internal milieu of the lung [1]. In addition to this barrier function, bronchial epithelial cells are now also known to produce various inflammatory mediators upon exposure to immunologic and nonimmunologic stimuli [1].…”

mentioning

confidence: 99%

“…In addition to this barrier function, bronchial epithelial cells are now also known to produce various inflammatory mediators upon exposure to immunologic and nonimmunologic stimuli [1]. Cultures of human bronchial epithelial cells exposed to toluene diisocyanate or to stimuli such as acetylcholine and phorbol-12-myristate-13-acetate, release chemotactic arachidonic acid metabolites, such as 15-hydroxyeicosatetraenoic acid (15-HETE), prostaglandin E 2 (PGE 2 ) and prostaglandin F 2α (PGF 2α ) [1,2].…”

mentioning

confidence: 99%

Modulation of glucocorticoid receptor expression in human bronchial epithelial cell lines by IL-1 beta, TNF-alpha and LPS

Verheggen¹,

Hal²,

Adriaansen-Soeting³

et al. 1996

Eur Respir J

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M Mo od du ul la at ti io on n o of f g gl lu uc co oc co or rt ti ic co oi id d r re ec ce ep pt to or r e ex xp pr re es ss si io on n i in n h hu um ma an n b br ro on nc ch hi ia al l e ep pi it th he el li ia al l c ce el ll l l li in ne es s b by y I IL L--1 1β, , T TN NF F--α a an nd d L LP PS S nM, respectively. Using electrophoretic mobility shift assays we demonstrated the binding of nuclear translocated GR to specific sites on deoxyribonucleic acid (DNA), named glucocorticoid responsive elements (GRE).Lipopolysaccharide (LPS) and interleukin-1β (IL-1β) significantly increased the number of GR per cell (median=312% and 171% of control, respectively; p<0.05), but significantly reduced the ligand affinity of these receptors, i.e. increased the Kd (median=410% and 145% of control, respectively; p<0.05) in BEAS 2B cells.These results indicate that the bronchial epithelium may be an actual target for glucocorticoid therapy. Inflammatory mediators, such as IL-1β and LPS, modulate the number and ligand affinity of these GR. Therefore, the response of bronchial epithelium to glucocorticoid therapy may be modulated by airway diseases associated with inflammation. Eur Respir J., 1996Respir J., , 9, 2036Respir J., -2043

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“…Il s'agit de facteurs dérivés du mésenchyme pulmonaire capables d'induire la prolifération de l'épithélium bronchique et alvéolaire [19]. En particulier, le KGF accélère la réparation de l'épithélium alvéolaire, du derme et du côlon en augmentant la prolifération et la migration cellulaire [20,21].…”

Section: Rôle Des Facteurs De Croissanceunclassified

Le remodelage bronchique dans l’asthme : mécanismes et enjeux thérapeutiques

Benayoun

Pretolani

2003

Med Sci (Paris)

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Immunological functions of the pulmonary epithelium

Abstract: I Im mm mu un no ol lo og gi ic ca al l f fu un nc ct ti io on ns s o of f t th he e p pu ul lm mo on na ar ry y e ep pi it th he el li iu um m

Cited by 145 publications

References 232 publications

Cigarette smoking induces small airway epithelial epigenetic changes with corresponding modulation of gene expression

Cigarette smoking induces small airway epithelial epigenetic changes with corresponding modulation of gene expression

Modulation of glucocorticoid receptor expression in human bronchial epithelial cell lines by IL-1 beta, TNF-alpha and LPS

Le remodelage bronchique dans l’asthme : mécanismes et enjeux thérapeutiques

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