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Viral induction of a chronic asthma phenotype and genetic segregation from the acute response
Michael J. Walter, Jeffrey D. Morton, Naohiro Kajiwara, Eugene Agapov, Michael J. Holtzman
Michael J. Walter, Jeffrey D. Morton, Naohiro Kajiwara, Eugene Agapov, Michael J. Holtzman
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Article Immunology

Viral induction of a chronic asthma phenotype and genetic segregation from the acute response

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Abstract

Research Article

Authors

Michael J. Walter, Jeffrey D. Morton, Naohiro Kajiwara, Eugene Agapov, Michael J. Holtzman

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Figure 2

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ICAM-1 deficiency protects against weight loss after viral infection wit...
ICAM-1 deficiency protects against weight loss after viral infection without changing viral clearance. Wild-type and ICAM-1–null mice were inoculated with SeV (5,000 EID50) and analyzed as follows. (a) Body weights relative to initial values were determined as mean ± SEM of eight mice. *Significant increase compared with the wild-type cohort. (b) Lungs were subjected to Western blotting against anti-SeV Ab, and bands corresponding to SeV nucleocapsid protein (NP) and the Sp1 control were quantified by densitometry as mean ± SEM of three mice. (c and d) Lungs were also assayed for SeV plaque-forming units (c) and SeV copy number (d). Values for viral plaque-forming units and viral RNA copy number represent mean ± SEM for 1 g of lung tissue and 100 ng of total lung RNA, respectively (three mice/genotype). Viral RNA copy number was determined by real-time RT-PCR for SeV nucleocapsid protein and corrected for GAPDH control. For a–d, values obtained from +/+ and –/– cohorts inoculated with PBS or UV-inactivated SeV were no different from preinoculation values (data not shown).

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