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15] we propose a model in which SP-A regulates host defense function by both indirect and direct mechanisms. The indirect effects, as documented in this study, comprise a broad-based regulation of levels of expression of a number of BAL proteins important for innate immunity and host defense function. In the K. pneumoniae model employed here these deficits were rapidly reversed by the infectious c
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15] we propose a model in which SP-A regulates host defense function by both indirect and direct mechanisms. The indirect effects, as documented in this study, comprise a broad-based regulation of levels of expression of a number of BAL proteins important for innate immunity and host defense function. In the K. pneumoniae model employed here these deficits were rapidly reversed by the infectious c
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Tatistically significant in WT mice, but did not achieve significance in the SP-A-/- mice. These proteins appear to play a role in asthma, chronic obstructive pulmonary disease, and other inflammatory lung diseases [37-39] although their exact action in these conditions is not known. Annexin A1 had a similar pattern, increasing with infection in both strains, but only reaching significance in the
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- mice appear to be rapidly compensated for with the induction of infection, but without a corresponding improvement in clinical status (i.e. survival). This lack of improvement indicates that the direct effects of SP-A on host defense against K. pneumoniae (i.e. enhancement of phagocytosis [12,15] or bacterial killing) may be moreBaselineWT >> SP-A-/WT > SP-A-/SP-A-/- >> WT SP-A-/- > WTFigure 3 N
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- mice appear to be rapidly compensated for with the induction of infection, but without a corresponding improvement in clinical status (i.e. survival). This lack of improvement indicates that the direct effects of SP-A on host defense against K. pneumoniae (i.e. enhancement of phagocytosis [12,15] or bacterial killing) may be moreBaselineWT >> SP-A-/WT > SP-A-/SP-A-/- >> WT SP-A-/- > WTFigure 3 N
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- mice appear to be rapidly compensated for with the induction of infection, but without a corresponding improvement in clinical status (i.e. survival). This lack of improvement indicates that the direct effects of SP-A on host defense against K. pneumoniae (i.e. enhancement of phagocytosis [12,15] or bacterial killing) may be moreBaselineWT >> SP-A-/WT > SP-A-/SP-A-/- >> WT SP-A-/- > WTFigure 3 N
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Change for both proteins was greater in the SP-A-/- mice than in WT. It should be pointed out that we did not observe corresponding increases in other serum proteins including albumin, ceruloplasmin, and haptoglobin indicating that these increases in hemoglobin are probably not due to serum protein leakage into the alveolar spaces. Hemoglobin expression has been shown to occur in alveolar epitheli
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Ot detectable (ND) in SP-A-/- mice.lower than at 4 hr (40/19 = 2.1), although the increases continue to predominate. However, most of this change is due to the PMM group, which has reverted at the 24 hr point post-infection to having more than twice as many proteins (9 of 13) at reduced levels in the SP-A-/- mice, as was the case in control (baseline) SP-A-/- mice. The overall numbers of increased