Lipoolygosaccharide indirectly enhances inflammatory lesions in lungs as aprimary infection site by non-encapsulated and type B Haemophilus influenzae through production of cytokines
S. Miyazaki et al., Lipoolygosaccharide indirectly enhances inflammatory lesions in lungs as aprimary infection site by non-encapsulated and type B Haemophilus influenzae through production of cytokines, CYTOKINE, 15(3), 2001, pp. 171-174
We investigated the role of cytokines in differences in histopathologic cha
nges in the lung between bronchopneumonia caused by non-encapsulated Haemop
hilus influenzae strain 770235f(0)b(0) and systemic disease caused by type
b H. influenzae strain 770235f(0)b(+). Tumour necrosis factor-alpha (TNF-al
pha), interleukin-(IL)-6 and IL-1 beta levels in bronchoalveolar lavage flu
id (BALF) samples of mice infected with strain 770235f(0)b(0) were higher t
han in those infected with strain 770235f(0)b(0) until 24 h post-infection.
Serum IL-6 rapidly increased in strain 770235f(0)b(0) infection after 72 h
post-infection. Serum TNF-alpha level in strain 770235f(0)b(0) infection a
ppeared earlier than in strain 770235f(0)b(0) infection. IL-1 beta producti
on in strain 770235f(0)b(+) infection was later than in strain 770235f(0)b(
0) infection. Moreover, a biphasic concentration pattern of TNF-alpha and I
L-6 was noted in BALF of mice with strain 770235f(0)b(0) infection. (C) 200
1 Academic Press.