Inflammation is a common finding in benign prostatic hyperplasia (BPH)
and may be classified as acute, chronic active or chronic inactive pr
ostatitis. The aim of the present study was to localise the different
types of inflammatory cells in prostatic lesions to determine the sequ
ence of events in the cellular reaction. We have carried out immunohis
tological characterisation of the inflammatory cells, using CD45RO and
CD3 antibodies to detect T-lymphocytes, CD20 antibodies to detect B-I
ymphocytes, CD68 to detect macrophages, kappa and lambda immunoglobuli
n light chains, and antibodies against prostate specific antigen (PSA)
and prostate specific acid phosphatase (PSAP). Macrophages accumulate
d in the lumen and glandular epithelial layers of damaged prostatic gl
ands and were found in the periglandular cuff of inflammatory cells in
acute and chronic active prostatitis. Lymphocytes also accumulated in
large numbers in the glandular epithelial layers and around the, glan
ds, indicating an association with macrophages. B-lymphocytes were sca
nty, if at all present, in acute and chronic. active prostatitis, but
were prominent within well-organised follicle centres in chronic activ
e prostatitis. Cells positive for light chains were few and scattered
in prostatic tissue. PSA and PSAP activity was lost in recently damage
d prostatic glandular epithelium and reappeared only in regenerating s
ecretory epithelium, indicating leakage as a result of damage. We sugg
est that the initial response to prostatic injury is cellular, and pro
bably related to leakage into the periglandular tissues of PSA, PSAP a
nd other antigenic molecules normally present in prostatic secretion.
Macrophages respond, followed by recruitment of T-lymphocytes which pa
rticipate in the inflammatory response and accumulate around the damag
ed glands. B-cell activity appears to be a late event.