Macrolides Attenuate Phorbol Ester-Induced Tumor Necrosis Factor-α and Mucin Production from Human Airway Epithelial Cells

Poachanukoon, Orapan; Koontongkaew, Sittichai; Monthanapisut, Paopanga; Pattanacharoenchai, Napaporn

doi:10.1159/000358366

Cited by 16 publications

(14 citation statements)

References 24 publications

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“…EMT could be inhibited by muscarinic antagonists . Macrolides, evaluated in COPD for their anti‐inflammatory properties, are able to reduce goblet cell hyperplasia and to inhibit EMT in vitro . This could be consistent with the observation that long‐term macrolide treatment could decrease the exacerbation rate in a subgroup of COPD patients with a frequent exacerbation phenotype, refractory to standard care .…”

Section: The Epithelium As Therapeutic Target In Chronic Airway Diseasessupporting

confidence: 79%

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Gohy

Hupin

Pilette

et al. 2016

Clin Experimental Allergy

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The respiratory epithelium plays a critical role for the maintenance of airway integrity and defense against inhaled particles. Physical barrier provided by apical junctions and mucociliary clearance clears inhaled pathogens, allergens or toxics, to prevent continuous stimulation of adaptive immune responses. The "chemical barrier", consisting of several anti-microbial factors such as lysozyme and lactoferrin, constitutes another protective mechanism of the mucosae against external aggressions before adaptive immune response starts. The reconstruction of damaged respiratory epithelium is crucial to restore this barrier. This review examines the role of the airway epithelium through recent advances in health and chronic inflammatory diseases in the lower conducting airways (in asthma and chronic obstructive pulmonary disease). Better understanding of normal and altered epithelial functions continuously provides new insights into the physiopathology of chronic airway diseases and should help to identify new epithelial-targeted therapies.

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Section: The Epithelium As Therapeutic Target In Chronic Airway Diseasessupporting

confidence: 79%

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Gohy

Hupin

Pilette

et al. 2016

Clin Experimental Allergy

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“…PMA was reported to stimulate the endogenenous activator of protein kinase C (PKC), diacylglycerol, 24 and it can induce MUC2 and MUC5AC production from NCI-H292 cells. 13,25 Our findings have demonstrated that CEZE obviously inhibits PMA-induced mucin gene and protein expression. It is known that the downstream effectors of the PKC pathway are MAPKs.…”

Section: Discussionmentioning

confidence: 68%

“…9 Phorbol 12myristate 13-acetate (PMA) is a well-known stimulant for secretion and gene expression of airway mucin, especially MUC2 and MUC5AC. 13 Therefore, the aim of this study was to investigate whether Z. cassumunar suppresses PMA-induced mucin synthesis in human airway epithelial cells and, if so, to examine whether the suppression operates via the MAPK signal transduction pathway.…”

Section: Introductionmentioning

confidence: 99%

Crude ethanolic extracts of Zingiber cassumunar ROXB. inhibit PMA-induced MUC2 and MUC5AC expression via ERK inhibition in human airway epithelial cells

2014

Asian Pac J Allergy Immunol

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“…Azithromycin is a macrolide antibiotic which has anti-inflammatory and immunomodulatory properties via inhibition of the transcription factor Nuclear Factor Kappa-B [25]. Azithromycin has been reported in vitro to suppress T-cell proliferation and activation and to reduce the expression of mucins and pro-inflammatory cytokines [26–28]. As a result azithromycin is found to be beneficial in the treatment of diseases characterised by pathological inflammation [29].…”

Section: Introductionmentioning

confidence: 99%

Ocular immune responses, Chlamydia trachomatis infection and clinical signs of trachoma before and after azithromycin mass drug administration in a treatment naïve trachoma-endemic Tanzanian community

et al. 2019

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Background Trachoma, caused by Chlamydia trachomatis , remains the leading infectious cause of blindness worldwide. Persistence and progression of the resulting clinical disease appears to be an immunologically mediated process. Azithromycin, which is distributed at the community level for trachoma control, has immunomodulatory properties. We investigated the impact of one round of oral azithromycin on conjunctival immune responses, C . trachomatis infection and clinical signs three- and six- months post treatment relative to three pre-treatment time-points. Methodology A cohort of children aged 6 to 10 years were recruited from a trachoma endemic region of northern Tanzania and were visited five times in a 12-month period. They were examined for clinical signs of trachoma and conjunctival swabs were collected for laboratory analysis. C . trachomatis infection was detected and the expression of 46 host genes was quantified using quantitative PCR. All community members were offered azithromycin treatment immediately after the six-month timepoint according to international guidelines. Findings The prevalence of C . trachomatis infection and inflammatory disease signs were significantly reduced three- and six- months post-mass drug administration (MDA). C . trachomatis infection was strongly associated with clinical signs at all five time-points. A profound anti-inflammatory effect on conjunctival gene expression was observed 3 months post-MDA, however, gene expression had largely returned to pre-treatment levels of variation by 6 months. This effect was less marked, but still observed, after adjusting for C . trachomatis infection and when the analysis was restricted to individuals who were free from both infection and clinical disease at all five time-points. Interestingly, a modest effect was also observed in individuals who did not receive treatment. Conclusion Conjunctival inflammation is the major clinical risk factor for progressive scarring trachoma, therefore, the reduction in inflammation associated with azithromycin treatment may be beneficial in limiting the development of potentially blinding disease sequelae. Future work should seek to determine whether this effect is mediated directly through inhibition of pro-inflammatory intracellular signalling molecules, through reductions in concurrent, sub-clinical infections, and/or through reduction of infection exposure.

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Macrolides Attenuate Phorbol Ester-Induced Tumor Necrosis Factor-α and Mucin Production from Human Airway Epithelial Cells

Cited by 16 publications

References 24 publications

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Crude ethanolic extracts of Zingiber cassumunar ROXB. inhibit PMA-induced MUC2 and MUC5AC expression via ERK inhibition in human airway epithelial cells

Ocular immune responses, Chlamydia trachomatis infection and clinical signs of trachoma before and after azithromycin mass drug administration in a treatment naïve trachoma-endemic Tanzanian community

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