Lv. Kendall et al., Antibody and cytokine responses to the cilium-associated respiratory bacillus in BALB/c and C57BL/6 mice, INFEC IMMUN, 68(9), 2000, pp. 4961-4967
The cilium-associated respiratory (CAR) bacillus is a gram-negative, glidin
g bacterium that causes persistent respiratory tract infections in rodents
despite histologic and serologic evidence of a marked immune response. To a
ssess humoral immunity and cytokine responses in CAR bacillus disease, 6-we
ek-old female BALB/c and C57BL/6 mice were inoculated intratracheally with
10(5) CAR bacillus organisms. CAR bacillus-specific serum immunoglobulins (
immunoglobulin M [IgM], IgG1, IgG2a, IgG2b, IgG3, and IgA) and local pulmon
ary cytokines (tumor necrosis factor alpha [TNF-alpha], gamma interferon [I
FN-gamma], and interleukin-4 [IL-4]) were evaluated by enzyme-linked immuno
sorbent assay every 7 days for 49 days. BALB/c mice developed CAR bacillus-
induced lesions early in the course of disease that became more severe with
time, Correlating with increasing disease severity, BALB/c mice had elevat
ions in all antibody isotypes tested, and elevations in pulmonary TNF-alpha
, IFN-gamma, and IL-4. C57BL/6 mice developed mild lesions with mild increa
ses in serum IgM, IgG1, IgG2b, and IgG3 levels and minimally detectable IgG
2a and IgA, Cytokine perturbations were not detected in C57BL/6 mice. The p
ersistence of infection in BALB/c mice with vigorous serum antibody respons
es and increased IFN-gamma and IL-4 responses suggests that humoral immunit
y and T-cell responses are ineffective at preventing CAR bacillus disease.
Furthermore, the lackluster antibody responses and undetectable cytokine re
sponses in C57BL/6 mice suggest that humoral immunity and T-cell responses
are not critical in resistance to CAR bacillus-induced disease.