- Increased susceptibility against Cryptococcus neoformans of lupus mouse models (pristane-induction and FcGRIIb deficiency) is associated with activated macrophage, regardless of genetic background
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Saowapha Surawut , Jiradej Makjaroen , Arthid Thim-uam , Jutamas Wongphoom , Tanapat Palaga , Prapaporn Pisitkun , Ariya Chindamporn , Asada Leelahavanichkul
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J. Microbiol. 2019;57(1):45-53. Published online November 19, 2018
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DOI: https://doi.org/10.1007/s12275-019-8311-8
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The severity of cryptococcosis in lupus from varying geneticbackgrounds
might be different due to the heterogeneity of
lupus-pathogenesis. This study explored cryptococcosis in
lupus mouse models of pristane-induction (normal geneticbackground)
and FcGRIIb deficiency (genetic defect). Because
the severity of lupus nephritis, as determined by proteinuria
and serum creatinine, between pristane and FcGRIIb-/- mice
were similar at 6-month-old, Cryptococcus neoformans was
intravenously administered in 6-month-old mice and were
age-matched with wild-type. Indeed, the cryptococcosis disease
severity, as evaluated by mortality rate, internal-organ
fungal burdens and serum cytokines, between pristane and
FcGRIIb-/- mice was not different. However, the severity of
cryptococcosis in wild-type was less severe than the lupus
mice. On the other hand, phagocytosis activity of peritoneal
macrophages from lupus mice (pristane and FcGRIIb-/-)
was more predominant than the wild-type without the difference
in macrophage killing-activity among these groups.
In addition, the number of active T helper cells (Th-cell) in
the spleen, including Th-cells with intracellular IFN-γ, from
lupus mice (pristane and FcGRIIb-/-) was higher than wildtype.
Moreover, these active Th-cells were even higher after
2 weeks of cryptococcal infection. These data support enhanced
macrophage activation through prominent Th-cells
in both lupus models. In conclusion, an increased susceptibility
of cryptococcosis in both lupus models was independent
to genetic background. This might due to Th-cell enhanced
macrophage phagocytosis with the interference of macrophage
killing activity from Cryptococcal immune-evasion
properties.
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