Free markets and dead mothers: the social ecology of maternal mortality in post-socialist Mongolia

Beginning in 1990, Mongolia, a former client state of what was then the Soviet Union, undertook liberal economic reforms. These came as a great shock to Mongolia and Mongolians, and resulted in food shortages, reports of famine, widespread unemployment, and a collapse of public health and health care. Although economic conditions have stabilized in recent years, unemployment and poverty are still at disturbingly high levels. One important consequence of the transition has been the transformation of the rural, primarily pastoral, economy. With de-collectivization, herding households have been thrown into a highly insecure subsistence mode of production, and, as a consequence, have become vulnerable to local fluctuations in rainfall and availability and quality of forage, and many now lack access to traded staples and essential commodities. Household food insecurity, malnutrition, and migration of impoverished households to provincial centers and the capital of Ulaanbaatar are one result. Reductions to investments in the health sector have also eroded the quality of services in rural areas, and restricted access to those services still functioning. Evidence suggests that women are particularly vulnerable to these political-ecological changes, and that this vulnerability is manifested in increasing rates of poor reproductive health and maternal mortality. Drawing on case-study ethnographic and epidemiological data, this article explores the links between neoliberal economic reform and maternal mortality in Mongolia.     

Type II-Activated Murine Macrophages Produce IL-4

Background

Type II activation of macrophages is known to support Th2 responses development; however, the role of Th2 cytokines (esp. IL-4) on type II activation is unknown. To assess whether the central Th2 cytokine IL-4 can alter type II activation of macrophages, we compared the ability of bone marrow-derived macrophages from wild type (WT) and IL-4Rα-deficient mice to be classically or type II-activated in vitro.

Results

We found that although both WT and IL-4Rα-deficient macrophages could be classically activated by LPS or type II activated by immune complexes plus LPS, IL-4Rα-deficient macrophages consistently produced much higher levels of IL-12p40 and IL-10 than WT macrophages. Additionally, we discovered that type II macrophages from both strains were capable of producing IL-4; however, this IL-4 was not responsible for the reduced IL-12p40 and IL-10 levels produced by WT mice. Instead, we found that derivation culture conditions (GM-CSF plus IL-3 versus M-CSF) could explain the different responses of BALB/c and IL-4Rα−/− macrophages, and these cytokines shaped the ensuing macrophage such that GM-CSF plus IL-3 promoted more IL-12 and IL-4 while M-CSF led to higher IL-10 production. Finally, we found that enhanced IL-4 production is characteristic of the type II activation state as other type II-activating products showed similar results.

Conclusions

Taken together, these results implicate type II activated macrophages as an important innate immune source of IL-4 that may play an important role in shaping adaptive immune responses.