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10.1152/ajplung.00280.2001 http://scihub22266oqcxt.onion/10.1152/ajplung.00280.2001 11839553!ä!11839553 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Lung+Cell+Mol+Physiol 2002 ; 282 (3): L563-72 Nephropedia Template TP {{tp|p=11839553|t=2002. Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection |pdf=|usr=}}{{11839553}} gab.com Text Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=11839553 #FOAvip Mice lacking surfactant protein SP-A [SP-A(-/-)] and wild type SP-A(+/+) mice were infected with influenza A virus (IAV) by intranasal instillation. Decreased clearance of IAV was observed in SP-A(-/-) mice and was associated with increased pulmonary inflammation. Treatment of SP-A(-/-) mice with exogenous SP-A enhanced viral clearance and decreased lung inflammation. Uptake of IAV by alveolar macrophages was similar in SP-A(-/-) and SP-A(+/+) mice. Myeloperoxidase activity was reduced in isolated bronchoalveolar lavage neutrophils from SP-A(-/-) mice. B lymphocytes and activated T lymphocytes were increased in the lung and spleen, whereas T helper (Th) 1 responses were increased [interferon-gamma, interleukin (IL)-2, and IgG(2a)] and Th2 responses were decreased (IL-4, and IL-10, and IgG(1)) in the lungs of SP-A(-/-) mice 7 days after IAV infection. In the absence of SP-A, impaired viral clearance was associated with increased lung inflammation, decreased neutrophil myeloperoxidase activity, and increased Th1 responses. Because the airway is the usual portal of entry for IAV and other respiratory pathogens, SP-A is likely to play a role in innate defense and adaptive immune responses to IAV. Twit Text FOAVip Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=11839553 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=11839553 #FOAvip English Wikipedia <ref>{{Cite pmid|11839553}}</ref> Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection #MMPMID11839553 LeVine AM; Hartshorn K; Elliott J; Whitsett J; Korfhagen T Am J Physiol Lung Cell Mol Physiol 2002[Mar]; 282 (3): L563-72 PMID11839553show ga Mice lacking surfactant protein SP-A [SP-A(-/-)] and wild type SP-A(+/+) mice were infected with influenza A virus (IAV) by intranasal instillation. Decreased clearance of IAV was observed in SP-A(-/-) mice and was associated with increased pulmonary inflammation. Treatment of SP-A(-/-) mice with exogenous SP-A enhanced viral clearance and decreased lung inflammation. Uptake of IAV by alveolar macrophages was similar in SP-A(-/-) and SP-A(+/+) mice. Myeloperoxidase activity was reduced in isolated bronchoalveolar lavage neutrophils from SP-A(-/-) mice. B lymphocytes and activated T lymphocytes were increased in the lung and spleen, whereas T helper (Th) 1 responses were increased [interferon-gamma, interleukin (IL)-2, and IgG(2a)] and Th2 responses were decreased (IL-4, and IL-10, and IgG(1)) in the lungs of SP-A(-/-) mice 7 days after IAV infection. In the absence of SP-A, impaired viral clearance was associated with increased lung inflammation, decreased neutrophil myeloperoxidase activity, and increased Th1 responses. Because the airway is the usual portal of entry for IAV and other respiratory pathogens, SP-A is likely to play a role in innate defense and adaptive immune responses to IAV. |*Alphainfluenzavirus/drug effects/pathogenicity[MESH] |Adaptation, Physiological/*physiology[MESH] |Animals[MESH] |Bronchoalveolar Lavage Fluid/cytology[MESH] |CD4 Lymphocyte Count[MESH] |CD8-Positive T-Lymphocytes/pathology[MESH] |Cytokines/metabolism[MESH] |Hemagglutination/drug effects[MESH] |Immunoglobulins/blood[MESH] |Lung Diseases/pathology/*physiopathology[MESH] |Lung/metabolism/pathology/virology[MESH] |Lymphocyte Count[MESH] |Lymphocytes/pathology[MESH] |Macrophages/physiology[MESH] |Mice[MESH] |Mice, Knockout/genetics[MESH] |Neutrophils/metabolism[MESH] |Orthomyxoviridae Infections/pathology/*physiopathology[MESH] |Peroxidase/metabolism[MESH] |Phagocytosis/physiology[MESH] |Proteolipids/genetics/*physiology[MESH] |Pulmonary Surfactant-Associated Protein A[MESH] |Pulmonary Surfactant-Associated Proteins[MESH] |Pulmonary Surfactants/genetics/*physiology[MESH] |Spleen/pathology[MESH]Absence of SP-A modulates innate and adaptive defense responses to pul(epmc).pdf DeepDyve Pubget Overpricing