3.2 The lack of MPO expression inecreased greatly
bacterial output and aggravated the shortening of the colon in mice with
bacterial infection and hypoxia exposure.
The bacterial colonies on the faces of the mice were enumerated on the
following day. (Figure 2a). An increase in excretion indicated an
increase in the severity of inflammation (Figure 2b). Compared with that
in the NI, HKI and KI groups, the number of bacteria excreted in the HI
groups was significantly increased. Comparing the WT and
MPO-/- groups, the number of bacteria excreted in the
MPO-/- groups iecreased significantly. The total
number of bacteria excreted in the HKI groups was the largest.We found
that the colon lengths of the mice in the infected groups were
significantly shorter (Figure 3a-b) after the mice were infected withC. rodentium , indicating that after the mice were infected, the
colonic inflammation in the mice was aggravated as a result of colon
shortening. There was a difference between the HI and NI groups
(P= P <0.05), which indicated that the colon shortening
of mice was more obvious under hypoxic conditions. Compared with that of
the HKI group, the colon shortening of the KI group was more obvious,
and there was a significant difference (P <0.05),
indicating that the colon shortening of the MPO-/-mice in the hypoxic environment was not as obvious as that under
normoxia. Comparing the NC with HC groups and the KC and HKC groups, we
found that hypoxic exposure could significantly increase the colon
length in mice (P <0.05). The average length of each
group is NC 7.01cm,NI 6.05cm,HC 8.75cm,HI 6.43cm,KC 7.00cm,KI 5.78cm,HKC
8.35cm,HKI 6.45cm. There were significant differences between the KI and
NI groups and the HKI and HI groups (P <0.05), which
indicated that the deletion of the MPO gene could aggravate the
shortening of the colon in mice.
3.3 Colitis and inflammatory cell infiltration in spleen
was alleviative in MPO-/- mice.
The results of H&E staining of colon tissue showed (Figure 4a) that the
structure of the small intestinal mucosa of the mice in each control
group was clear and complete, the villus crypts were deep, and the villi
were neatly arranged. We found that the pathological damage to colon
tissue was more severe in the HI and KI groups as a result of colon
oedema, thinning, disorganized and variable villi, inflammatory cell
infiltration around crypts, and shallow crypts.
We evaluated the pathological changes in colon tissue in each group of
mice. The results (Figure 4b) showed that the pathological changes of
the mice in the HI group were the most serious,and the normal tissue
structure of part of the mucosa was significantly damaged. Compared with
the control group, the HI group had significant differences in colon
pathological tissue scores after infection. However, comparing the
pathological scores of the HKI group with the KI group and the HI group
with the NI group, the scores were significantly lower
(P <0.05), indicating that MPO could increase the
inflammatory response in mice. Figure 4c shows that the spleens of mice
in the NI and KI groups had a large amount of inflammatory cell
infiltration.