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a National Heart and
Lung Institute, London, UK, b Osler Chest Unit, Churchill Hospital, Oxford, UK, c Chest Department, Wycombe,
General Hospital, High Wycombe, UK
Correspondence to: Dr S R Durham, Respiratory Medicine, Imperial College School of Medicine at National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, UK.
Received 3 September 1997; Returned to authors 15 October 1997; Revised version received 1 April 1998; Accepted for publication 1 April 1998
BACKGROUND
Bronchiectasis
is a chronic suppurative lung disease characterised by irreversible
dilation of the bronchi and persistent purulent sputum. The
immunopathology of the disease was studied using a quantitative
immunostaining technique with particular reference to T lymphocytes,
macrophages, and granulocytes.
METHODSBronchial
mucosal biopsy specimens were obtained by fibreoptic bronchoscopy from
12 patients with bronchiectasis (six receiving inhaled steroids) and 11 normal healthy controls. Immunostaining (APAAP method) was
performed on frozen cryostat sections with a panel of monoclonal
antibodies to total leucocytes (CD45), T lymphocyte phenotypic markers
(CD3, CD4, CD8), macrophages (CD68), eosinophils (EG2), and neutrophils (elastase).
RESULTSThere was a
mononuclear cell infiltrate in both patients with bronchiectasis and
normal controls, but an overall increase in total leucocyte cell
numbers (CD45+ cells) was identified in those with bronchiectasis
(median values 422 cells/mm2 versus 113 cells/mm2 in control tissue, p<0.001). Intense
infiltration of CD3+ T lymphocytes was observed compared with healthy
controls (292 cells/mm2 and 40 cells/mm2,
respectively, p<0.001). This comprised predominantly CD4+ T cells (118 cells/mm2) rather than CD8+ T cells (47 cells/mm2). CD3+ cell counts were reduced in those subjects
on inhaled steroids compared with those not receiving inhaled steroids
(197 cells/mm2 versus 369 cells/mm2, p<0.05),
as were CD4+ cell counts (82 cells/mm2 versus 190 cells/mm2, p<0.05). Neutrophil and macrophage cell numbers
were also increased in patients with bronchiectasis (114 cells/mm2 and 213 cells/mm2, respectively)
compared with controls (41 neutrophils/mm2 and 40 macrophages/mm2). EG2+ (activated) eosinophil numbers were
much lower than T cells, macrophages, and neutrophils in patients with
bronchiectasis but were increased compared with controls (36 cells/mm2 versus 0 cells/mm2, p<0.001). In
view of the markedly increased neutrophil counts in patients with
bronchiectasis, biopsy specimens were immunostained for interleukin 8 (IL-8) which was highly significantly increased compared with controls
(47 cells/mm2 versus 15 cells/mm2, p<0.01).
IL-8+ cells were less prominent in steroid treated patients than in
patients not receiving treatment (30 cells/mm2 versus 60 cells/mm2, p<0.05). A further characteristic of
bronchiectasis was mucous gland hypertrophy. Gland area comprised up to
40% of the tissue in some bronchiectasis sections while no hypertrophy
was noted in control biopsy specimens (p<0.05).
CONCLUSIONAirway
inflammation in bronchiectasis is characterised by tissue neutrophilia,
a mononuclear cell infiltrate composed mainly of CD4+ T cells and CD68+
macrophages, and increased IL-8 expression. Inhaled corticosteroid
treatment in patients with bronchiectasis is associated with a less
marked infiltration by T cells and IL-8+ cells within the bronchial
mucosa, although this finding requires confirmation in a prospective
placebo controlled trial.
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