Enhanced AHR in asthmatic mice with A(H1N1)pdm09
infection
The central airway resistance revealed by the Rrs value
was significantly increased in the A(H1N1)pdm09 mouse group compared to
that in the seasonal H1N1 mouse or control group (Fig. 1 ); this
was particularly prominent after treatment with 48 mg/ml methacholine at
3 and 7 days after infection [3 days post-infection A(H1N1)pdm09vs. seasonal; 4.40 vs. 3.29 s/ml, p < 0.001,vs. control; vs. 3.11 s/ml, p < 0.001; 7 days
post-infection A(H1N1)pdm09 vs. seasonal; 8.60 vs. 3.24 s/ml, p
< 0.001, vs. control; vs. 3.00 s/ml, p
< 0.001]. However, there was no significant difference among
the three groups at 10 days post-infection. In contrast, there were no
significant differences in the Rrs between the seasonal
H1N1 and mock groups at 3, 7, or 10 days post-infection.
Next, peripheral airway resistance as reflected by G was compared among
the three groups (Fig. 2 ). The peripheral airway resistance was
also significantly increased in the A(H1N1)pdm09 group compared to that
in the seasonal H1N1 and control groups; this difference was
particularly prominent after treatment with 48 mg/ml methacholine at 3
and 7 days post-infection [3 days post-infection A(H1N1)pdm09 vs.
seasonal; 25.2 vs. 16.5 s/ml, p < 0.001, vs.control; vs. 15.5 s/ml, p < 0.001; 7 days
post-infection A(H1N1)pdm09 vs. seasonal; 50.0 vs. 16.7 s/ml, p
< 0.001, vs. control; vs. 15.6 s/ml, p
< 0.001]. However, these differences in airway resistance
were not significantly different among the three groups at 10 days
post-infection.
We investigated the changes in AHR of non-asthmatic mice with
A(H1N1)pdm09 infection (Figs. 1, 2 ). Although AHR was enhanced
with A(H1N1)pdm09 infection in non-asthmatic mice, the changes in AHR
were slight compared to the changes observed in asthmatic mice,
suggesting that A(H1N1)pdm09 infection more robustly enhances AHR in
asthmatic animals.
We further evaluated the alternations of AHR in asthmatic mice during
the post-infection period of A(H1N1)pdm09 infection (Fig. 3 ).
Airway resistance was significantly enhanced at 7 days post-infection
compared to at 3- or 10-days post-infection (p < 0.001),
whereas there were no differences in airway resistance between 3 and 10
days post-infection. When the body weight of mice was compared among the
three groups to evaluate the systemic damage caused by A(H1N1)pdm09
infection at 3, 7, or 10 days post-infection, no significant differences
between days were detected (data not shown).