Marked up-regulation of T lymphocytes and expression of interleukin-9 in bronchial biopsies from patients With chronic bronchitis with obstruction.
OBJECTIVE
To examine the differences in the inflammatory cell and cytokine profile between patients with chronic bronchitis (CB) with and without airway obstruction compared to control subjects.


METHODS
We used bronchial biopsy samples from the patients and control subjects and analyzed them for the presence of CD3 T cells, CD68, major basic protein (MBP), elastase, and tryptase, as well as expression of messenger RNA (mRNA) coding for interleukin (IL)-4, IL-5, interferon (IFN)-gamma, IL-9, eotaxin, and IFN-gamma-inducible protein (IP)-10. The techniques of immunocytochemistry and in situ hybridization were used. Results were expressed as the number of immunoreactive and mRNA-positive cells per field.


RESULTS
Increased number of elastase, CD68, and MBP-positive cells (n = 9, p < 0.01) was demonstrated in both groups of patients with CB compared to control subjects. In patients with CB and obstruction, the number of elastase, CD68, and the number of CD3-positive cells was significantly increased compared to patients with CB without obstruction (n = 9, p < 0.01). IFN-gamma mRNA expression was increased in both groups of patients with CB compared to control subjects (n = 9, p < 0.01). IL-9 mRNA was significantly increased only in patients with CB and obstruction (n = 9, p < 0.01). Co-localization studies demonstrated > 80% of all IL-9-positive cells to be CD3-positive T cells. IP-10 mRNA was significantly increased in both groups of patients with CB compared to control subjects (n = 9, p < 0.01).


CONCLUSIONS
These results indicate a differential expression of inflammatory markers and cytokine mRNA in patients with obstructive CB. Increased presence of T lymphocytes and up-regulation of IL-9 and IP-10 mRNA expression in the bronchial biopsy samples may contribute to the airway obstruction in these patients.
Panzner
Petr
P
Department of Immunology and Allergology, Medical Faculty of the Charles University, Plzen, Czech Republic.
Lafitte
Jean-Jacques
JJ
Tsicopoulos
Anne
A
Hamid
Qutayba
Q
Tulic
Meri K
MK
D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001707:Biopsy, Needle; D001798:Blood Proteins / Q000378:metabolism; D001980:Bronchi / Q000473:pathology*; D029481:Bronchitis, Chronic / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D017252:CD3 Complex / Q000032:analysis; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007249:Inflammation; D016906:Interleukin-9 / Q000096:biosynthesis*; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D010196:Pancreatic Elastase / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D012260:Ribonucleases / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism*; D015854:Up-Regulation; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001798:Blood Proteins; D017252:CD3 Complex; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D016906:Interleukin-9; D010196:Pancreatic Elastase; D012260:Ribonucleases; C515456:CCL11 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule