TNF-alpha, IL-6 and IFN-gamma secreted by bronchoalveolar leukocytes isolated from patients with bronchial asthma, complicated by fungal airways infections.
It is widely known that fungal airways infections may deteriorate the course of bronchial asthma. The mechanism of the phenomenon is still unclear. The aim of our study was to assess the effect of fungal infections on the secretion of selected cytokines by bronchoalveolar leukocytes. Five patients (group FA) with bronchial asthma and Candida albicans or Aspergillus fumigatus airways infections (confirmed by bronchoscopy and culture) were included in the study. All of them were on the chronic treatment with corticosteroids (10-20 mg of prednisone per day) and underwent several courses of therapy with antibiotics. The control groups comprised 5 previously untreated asthmatics without bronchial colonization with fungi (group A) as well as 5 healthy volunteers (group H). Leukocytes were isolated from bronchoalveolar lavage fluid (BALF) and cultured in the presence or absence of cytokine inducers such as phytohemagglutin L (PHA), lipo-polysaccharide (LPS) from E. coli. The activity of TNF-alpha, IL-6 and IFN-gamma were measured in the BAL cell culture supernatants by using specific bioassays. In comparison with healthy controls the spontaneous or induced secretion of cytokines were significantly augmented in patients from group A. In contrast the asthmatics who represented group FA demonstrated normal levels of spontaneous cytokine secretion. However, the tendency to increase LPS and PHA-induced production was observed in BAL leukocytes from the patients. The above results support the view that beneficial effect of corticosteroid treatment in bronchial asthma may act, at least in part, by inhibition of the high spontaneous secretion of proinflammatory cytokines. Nevertheless, fungal airways infections may lead to increase of LPS- or PHA-induced production of TNF-alpha, IL-6 or IFN-gamma (despite prednisone therapy) by prestimulation of the BAL cells with fungi.
Cembrzyńska-Nowak
M
M
Institute of Immunology and Experimental Therapy, Polish Academy of Science, Weigla, Wrocław, Poland.
Liebhart
J
J
Banaszek
B
B
Dobek
R
R
Bieńkowska
M
M
Szklarz
E
E
D000328:Adult; D001229:Aspergillosis, Allergic Bronchopulmonary / Q000150:complications* / Q000503:physiopathology; D001232:Aspergillus fumigatus; D001249:Asthma / Q000382:microbiology* / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002177:Candidiasis / Q000150:complications* / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010835:Phytohemagglutinins / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D015850:Interleukin-6; D008070:Lipopolysaccharides; D010835:Phytohemagglutinins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma