Cigarette smoke modulates PGE₂ and host defence against Moraxella catarrhalis infection in human airway epithelial cells

Abstract

The results suggest that in well-differentiated human bronchial epithelial cells, WCS may impair host defence against Mc in part through inhibiting PGE(2) production.

Impact of cigarette smoke exposure on host–bacterial pathogen interactions

“…It is well known that cigarette smoke induces epithelial cell death, which also amplifies the ongoing inflammatory response [19]. Regarding the effect of cigarette smoke on the production of antimicrobial molecules by airway epithelial cells, the expression of the antimicrobial peptide human b-defensin (hBD)-2 in brushed bronchial epithelial cells from COPD patients has been found to be lower than in tissues from healthy subjects [33]; in addition, significantly decreased levels of SP-A and SP-D have been observed in smokers compared with nonsmokers [34]. Alveolar macrophages activated by cigarette smoke secrete a repertoire of inflammatory mediators, some of which (IL-8, growth-related oncogenea, LTB 4 and monocyte chemoattractant protein-1) are neutrophil chemoattractants [19].…”

“…An independent study detected M. catarrhalis-specific Th1 cells in BAL fluid of COPD-infected patients [97]. Moreover, cigarette smoke has been shown to decrease M. catarrhalis-induced hBD-2 antimicrobial peptide expression and prostaglandin E 2 induction, and increase the bacterial load on the bronchial epithelium of smokers [33].…”

Antibacterial Defense of Human Airway Epithelial Cells from Chronic Obstructive Pulmonary Disease Patients Induced by Acute Exposure to Nontypeable Haemophilus influenzae: Modulation by Cigarette Smoke

“…Moreover, it has been demonstrated that cigarette smoke (CS) exposure attenuated the antibacterial activity and microbialinduced expression of hBD-2 in cultured airway epithelial cells [12][13][14] . This suggests that the inducible antibacterial activity is affected in airway epithelial cells from smokers and COPD patients.…”

Defensins and Other Antimicrobial Peptides and a Role of Neutrophil Protein-Synthesing Function Disorders for Pathogenesis of Respiratory Diseases

“…Особое значение имеет нарушение функции нейт-рофилов при заболеваниях, ассоциированных с ку-рением [52,54,55]. В исследовании концентрации β-HD-2 в смывах из ротоглотки и со слизистой брон-хов у курящих больных внебольничной пневмонией установлено выраженное подавление механизмов врожденного иммунитета, которое было частично нивелировано увеличением концентрации перекиси водорода и каталазной активности.…”

“…Снижение концентрации TLR-4 и молекулы β-HD-2 в бронхиальных смывах у курящих и бросивших курить пациентов выявлено E.Pace et al [52]. При культивировании эпителиоци-тов, полученных методом щеточной биопсии у боль-ных ХОБЛ и здоровых добровольцев, доказано, что при курении снижается продукция β-HD-2 и проста-гландина Е2, что одновременно способствует разви-тию инфекционного процесса, вызванного Moraxella catarrhalis из-за повышения проникновения бактерий в эпителиальные клетки [54].…”