OBJECTIVE: Myeloid-derived suppressor cells (MDSCs) have recently been implicated in the pathogenesis of @entity565 through inhibiting T cell response. However, the issue of whether Lipopolysaccharide (LPS)-derived MDSCs regulate the immune response in an @entity565 environment is currently unclear. We sought to characterize the pathogenic function of various subtypes of MDSCs in @entity565 mediated by @entity10328 in @entity19 model, in order to show that LPS-induced MDSCs can shift the balance back to normal in a @entity61 -dominant asthmatic environment. MATERIALS AND METHODS: Subgroups of MDSCs with @entity19347 + @entity17775 +, @entity19347 - @entity17775 +, @entity19347 + @entity17775 - or @entity19347 - @entity17775 - expression were isolated by flow cytometry and were co-cultured with spleen lymphocytes. The proportion of @entity630 , @entity61 , or Treg cells in the treated spleen lymphocytes were analyzed by flow cytometry. In an @entity10328 (OVA)-induced @entity19 @entity565 model, @entity19 were intravenously injected (tail vein) by MDSCs with specific marker, then the lung function and tissue pathology, @entity58 content in bronchoalveolar lavage fluid (BALF) and peripheral blood, and proportion of @entity630 , @entity61 , or Treg cells in peripheral blood were analyzed. RESULTS: @entity19347 + @entity17775 + MDSCs transferred into asthmatic @entity19 via intravenous injection suppressed the infiltration of inflammatory cells into the lung and @entity61 cytokine in BALF and blood. We observed a significant increase of Treg cells in the spleen lymphocytes co-cultured with @entity19347 + @entity17775 +, @entity19347 - @entity17775 +, @entity19347 + @entity17775 -, @entity19347 - @entity17775 - or @entity3804 + MDSCs. The adoptive transfer of @entity19347 + @entity17775 +, @entity19347 - @entity17775 +, @entity3804 + MDSCs resulted in decrease of Penh, total cell number, eosinophil and neutrophil percentage in BALF, and concentration of @entity58 in BALF and serum, thus improving the inflammatory injury, histopathology and lung function in the @entity19 with @entity565 . The up-regulation of the @entity630 / @entity61 ratio and Treg frequency were observed after adoptive transfer of @entity19347 + @entity17775 +, @entity19347 - @entity17775 +, @entity19347 + @entity17775 -, @entity19347 - @entity17775 - and @entity3804 + MDSCs. CONCLUSIONS: The LPS-derived MDSCs with specific markers were able to suppress natural inflammatory response and improve inflammatory injury through reversing @entity630 / @entity61 ratio, increasing Treg proportion and decreasing @entity58 concentration. These findings imply that LPS-derived MDSCs inhibit @entity61 cell-medicated response against allergen. We propose that @entity565 may be effectively targeted using a novel MDSC-based cell therapy approach.

Passive transfer of lipopolysaccharide-derived myeloid-derived suppressor cells inhibits XXXX -related airway inflammation.

@entity10328 :: ('282665(Tax:10090)', 'Gene') :: ['ovalbumin'] @entity17775 :: ('546644(Tax:10090)', 'Gene') :: ['Ly6G'] @entity19347 :: ('17067(Tax:10090)', 'Gene') :: ['Ly6C'] @entity19 :: ('10090', 'Species') :: ['mice', 'mouse'] @entity565 :: ('MESH:D001249', 'Disease') :: ['asthma'] @entity61 :: ('15111(Tax:10090)', 'Gene') :: ['Th2'] @entity58 :: ('16189(Tax:10090)', 'Gene') :: ['IL-4'] @entity3804 :: ('16409(Tax:10090)', 'Gene') :: ['CD11b'] @entity630 :: ('57314(Tax:10090)', 'Gene') :: ['Th1']
@entity565 :: (MESH:D001249,Disease) :: ['asthma']
