Airway inflammation in subjects with gastro-oesophageal reflux and gastro-oesophageal reflux-related asthma.
OBJECTIVE
Asthma and gastro-oesophageal reflux (GER) are both characterized by airway inflammation.


METHODS
The purposes of this work were (i) to study airway inflammation in patients troubled by gastro-oesophageal reflux (GER) and GER associated with asthma, (ii) to ascertain whether GER can aggravate asthma by exacerbating the pre-existing airway inflammation and oxidative stress and (iii) to establish the validity of analysing breath condensate and induced sputum when studying the airways of subjects affected by GER. PATIENT S AND METHODS: We enrolled 14 patients affected by mild asthma associated with GER (40 +/-12 years), nine with mild but persistent asthma (39 +/- 13 years), eight with GER (35 +/- 11 years) and 17 healthy subjects (37 +/- 9 years). Sputum cell counts and concentrations of interleukin-4 (IL-4), IL-6 and 8-isoprostane were measured in breath condensate and supernatant.


RESULTS
GER-related asthma is characterized by an eosinophilic inflammation, as determined by elevated concentrations of IL-4 in breath condensate and sputum supernatant, and by sputum cell analysis. GER alone presents a neutrophilic pattern of inflammation when determined by elevated concentrations of IL-6 in sputum cell analysis. A concomitant increase has been found in 8-isoprostane in GER associated (or not associated) with asthma.


CONCLUSIONS
We conclude that GER is characterized by a neutrophilic airway inflammation and by increased oxidative stress. GER does not however aggravate pre-existing airway inflammation in asthma patients. Determinations of inflammatory and oxidant markers in the breath condensate of subjects with GER reflect these measured in the induced sputum.
Carpagnano
G E
GE
Institute of Respiratory Diseases, University of Foggia, Foggia, Italy. ge.carpagnano@unifg.it
Resta
O
O
Ventura
M T
MT
Amoruso
A C
AC
Di Gioia
G
G
Giliberti
T
T
Refolo
L
L
Foschino-Barbaro
M P
MP
D000328:Adult; D001249:Asthma / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D015415:Biomarkers / Q000032:analysis; D001944:Breath Tests; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000032:analysis; D005260:Female; D005541:Forced Expiratory Volume; D005764:Gastroesophageal Reflux / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D018836:Inflammation Mediators / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D013183:Sputum / Q000737:chemistry / Q000166:cytology; D014797:Vital Capacity
D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D015847:Interleukin-4; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost