Monocytes maintain central nervous system homeostasis following helminth-induced inflammation.

Neuroimmune interactions are crucial for regulating immunity and inflammation. Recent studies have revealed that the central nervous system (CNS) senses peripheral inflammation and responds by releasing molecules that limit immune cell activation, thereby promoting tolerance and tissue integrity. However, the extent to which this is a bidirectional process, and whether peripheral immune cells also promote tolerance mechanisms in the CNS remains poorly defined. Here we report that helminth-induced type 2 inflammation promotes monocyte responses in the brain that are required to inhibit excessive microglial activation and host death. Mechanistically, infection-induced monocytes express YM1 that is sufficient to inhibit tumor necrosis factor production from activated microglia. Importantly, neuroprotective monocytes persist in the brain, and infected mice are protected from subsequent lipopolysaccharide-induced neuroinflammation months after infection-induced inflammation has resolved. These studies demonstrate that infiltrating monocytes promote CNS homeostasis in response to inflammation in the periphery and demonstrate that a peripheral infection can alter the immunologic landscape of the host brain.

The effect of iron deficiency anemia on experimental dental caries in mice.

OBJECTIVE: The objective of this study was to examine the relationship between iron deficiency and caries susceptibility in a mouse model. MATERIALS AND METHODS: Three-week-old C57BL/J6 mice were fed a cariogenic diet containing either standard iron (48 ppm Fe) or low iron (4 ppm Fe) levels. Concurrently, groups of mice with both diets were orally inoculated with Streptococcus mutans (1 × 108) cells on three consecutive days. At the end of the 5th week after infection, mice were sacrificed and jaws were collected for caries scoring, rating the number and severity of lesions using a modified Keyes method applicable to mice. RESULTS: Blood analysis by the end of the 5th week revealed marked reduction in the hemoglobin and hematocrit levels of the mice fed the iron deficient diet (IDA and IDA-S. mutans). Anemic mice in both groups lacked the incisor enamel pigmentation observed in mice fed an iron deficient diet. Anemic infected mice had the highest caries severity scores reflecting extensive deep lesions (P < 0.05). S. mutans infected mice fed a standard iron diet had similar numbers of lesions and severity scores as un-infected IDA animals (p < 0.05). IDA did not alter S. mutans CFU counts in infected animals (P < 0.05). CONCLUSION: These results demonstrated that IDA mice are at a higher risk of developing deep dental caries compared to non-anemic mice; highlighting the protective role of iron against dental caries.