Inflammatory biomarker, neopterin, suppresses B lymphopoiesis for possible facilitation of granulocyte responses, which is severely altered in age-related stromal-cell-impaired mice, SCI/SAM.

摘要: Neopterin is produced by monocytes and a useful biomarker of inflammatory activation. We found that neopterin enhanced in vivo vitro granulopoiesis triggered the stromal-cell production cytokines mice. The effects on B lymphopoiesis during enhancement were determined using mouse model senescent impairment (SCI), subline senescence-accelerated mice (SAM). In non-SCI (a less stage SCI mice), treatment with decreased number colonies, semisolid medium, colony-forming units pre-B-cell progenitors (CFU-preB) from unfractionated bone marrow (BM) cells, but not population rich pro-B pre-B cells without stromal cells. upregulated expression genes for negative regulators such as tumor necrosis factor-alpha (TNF-alpha ), interleukin-6 (IL-6), transforming growth factor-beta (TGF-beta) cultured implying suppressed CFU-preB colony formation inducing intraperitoneal injection into resulted marked decrease femoral within 1 day, along increases TNF-alpha IL-6 levels. However, mice, responses to upregulation after than those These results suggest predominantly resulting selective suppression lymphopoiesis. also facilitated BM suppressing lymphopoiesis, thereby contributing potentiation process; interestingly, function became impaired senescence because attenuated function, downmodulation host-defense mechanism aged.