Asthma and natural colds. Inflammatory indices in induced sputum: a feasibility study.
We examined the feasibility of using induced sputum to evaluate the airway inflammatory response to natural acute respiratory virus infections. We recruited eight asthmatics and nine healthy subjects on Day 4 of a cold. Viral infection was confirmed in six of the asthmatics (influenza A or B) and six of the healthy subjects (influenza A, rhinovirus, adenovirus, respiratory syncytial virus, and coronavirus). In the subjects with confirmed virus infection, five of the asthmatics had an objective exacerbation of asthma during the cold. Their sputum on Day 4 showed a high median total cell count of 19.7 x 10(6) cells/ml with a modest neutrophilia (58. 5%) and high levels of interleukin-8 (IL-8) (16,000 pg/ml), eosinophilic cationic protein (ECP) (1,880 microgram/L) and very high levels of fibrinogen (250 mg/L). In contrast, the proportion (1.3%) and absolute number of eosinophils was low. IL-2 levels were within the normal range, whereas IL-5 and interferon gamma were under the limit of detection of the assays. In the healthy subjects with a confirmed virus infection the sputum findings were qualitatively similar but significantly less prominent. Sputum IL-8 on Day 4 was strongly correlated with neutrophils (rs = 0.8, p < 0.001). This correlation was also significant when each group was analyzed separately. On Day 21 there was a fall in the absolute number of neutrophils and in ECP and fibrinogen levels in both groups. Similar results were found in the two asthmatic and three healthy subjects with a cold of comparable severity but in whom viral infection was not confirmed. We conclude that induced sputum examination can be used to study the effects of natural colds and influenza on the airways of the lungs. The results also suggest that natural colds, on Day 4, cause neutrophilic lower airway inflammation that is greater in asthmatics than in healthy subjects. The greater inflammatory response in asthmatics may be due to the changes associated with trivial eosinophilia or to the different viruses involved.
Pizzichini
M M
MM
Asthma Research Group, Departments of Medicine and Paediatrics, St. Joseph's Hospital and McMaster University, Hamilton, Ontario, Canada.
Pizzichini
E
E
Efthimiadis
A
A
Chauhan
A J
AJ
Johnston
S L
SL
Hussack
P
P
Mahony
J
J
Dolovich
J
J
Hargreave
F E
FE
D000208:Acute Disease; D000256:Adenoviridae; D000328:Adult; D001249:Asthma / Q000276:immunology*; D001798:Blood Proteins / Q000032:analysis; D003139:Common Cold / Q000276:immunology* / Q000821:virology; D017934:Coronavirus; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000473:pathology; D005240:Feasibility Studies; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000032:analysis; D009980:Influenza A virus; D009981:Influenza B virus; D007251:Influenza, Human / Q000276:immunology; D007371:Interferon-gamma / Q000032:analysis; D007376:Interleukin-2 / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D012136:Respiratory Syncytial Viruses; D012229:Rhinovirus; D012260:Ribonucleases; D013183:Sputum / Q000737:chemistry / Q000166:cytology / Q000276:immunology*; D013224:Status Asthmaticus / Q000276:immunology / Q000821:virology
D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D007376:Interleukin-2; D015848:Interleukin-5; D016209:Interleukin-8; D007371:Interferon-gamma; D005340:Fibrinogen; D012260:Ribonucleases