Background & Aims: Cellular infiltrates are present already in early stages
of chronic pancreatitis. The mechanisms responsible for their recruitment
are unknown. Hence, we determined the differential expression of chemokine
genes and their cellular sources in normal and affected pancreatic tissues.
Methods: Pancreatic tissues from 23 patients with chronic pancreatitis and
from 4 normal controls were subjected to in situ hybridization for detecti
ng messenger RNA (mRNA) of the chemokine genes interleukin 8, ENA-78, MIG,
MCP-1, and 1-309. Results: Normal pancreatic tissues lack cells expressing;
mRNA for IL-8, ENA-78, MIG, and MCP-1. In contrast, pancreatic lobuli with
mild to moderate signs of tissue alterations strongly expressed MCP-1 mRNA
in centroacinar ducts, endothelia, fibroblasts, macrophages, T cells, and
occasionally in nerves. Interleukin 8 and ENA-78 mRNA is preferentially det
ected in centroacinar ducts of pancreatic lobuli with more advanced alterat
ions. Variable numbers of pancreas-infiltrating T cells express MIG mRNA. 1
-309 mRNA, however, is consistently observed in normal acini and in tissue
with mild to moderate signs of tissue alterations. Conclusions: The observe
d differential expression of distinct chemokine genes in pancreatic parench
yma and infiltrates from patients with chronic pancreatitis strongly sugges
ts an involvement of distinct chemokines in the initiation and perpetuation
of disease.