Pathogenicity of heat-killed K. pneumoniae in
experimental AIP
The association between reduced colonization by Klebsiella spp.and induction of remission led us to examine the pathogenicity of this
bacterium in AIP. Therefore, we employed a well-established murine model
of AIP in MRL/MpJ mice [14, 16, 19, 20]. Repeated IP injections of
poly (I:C) into MRL/MpJ mice at a higher dose of 100 µg triggered severe
AIP, characterized by massive infiltration of immune cells, destruction
of acinar architecture, and fibrosis; whereas, repeated IP injections at
a lower dose of 10 µg caused mild AIP with infiltration of immune cells
[14, 16, 19, 20]. We hypothesized that immune responses againstKlebsiella spp. increase the sensitivity to experimental AIP. To
test this hypothesis, MRL/MpJ mice received combined treatment with
orally administered heat-killed K. pneumoniae and IP injections
of poly (I:C) (10 µg) twice a week, for a total of 16 times.
As expected, infiltration of immune cells was seen in the pancreas of
MRL/MpJ mice that received IP injections of 10 µg of poly (I:C) alone
(Fig. 5A). Interestingly, this infiltration was accompanied by the
destruction of acinar architecture in the pancreas of MRL/MpJ mice
following combined treatment with orally administered heat-killedK. pneumoniae and IP injections of poly (I:C) (Fig. 5A).
Quantitative assessment of pathological scores confirmed that oral
administration of heat-killed K. pneumoniae promoted the
development of pancreatitis (Fig. 5B).