Enhanced influenza-induced lung inflammation in Cd59a mice is mediated by complement-dependent and-independent mechanisms

(A) MAC deposition was analysed by C9 staining on lung sections. Representative views of mouse lungs (×40original magnification) from WT (top) or Cd59a (bottom) mice infected with influenza are shown. Arrowheads indicate lung airway epithelium staining. (B,C) Complement was inhibited by administration of sCR1 (i.v.) daily and mice were infected with influenza virus. After 3days, lungs were harvested and total numbers of lung-infiltrating neutrophils (B) and CD4 T cells (C) were determined by flow cytometry. Each symbol represents an individual mouse (=5/group). Means are represented in all graphs. Statistical significance was evaluated using Student's -test.<p><b>Copyright information:</b></p><p>Taken from "CD59a deficiency exacerbates influenza-induced lung inflammation through complement-dependent and-independent mechanisms"</p><p></p><p>European Journal of Immunology 2007;37(5):1266-1274.</p><p>Published online Jan 2007</p><p>PMCID:PMC2435422.</p><p>Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</p

Increased immune cell recruitment in the lungs of influenza-infected Cd59a mice

Cd59a and WT mice (=5/group) were infected i.n. with influenza virus. Lungs were harvested at the times indicated and lung-infiltrating neutrophils (A) CD8 (B) and CD4 T cells (C) were enumerated by flow cytometry. Neutrophils were identified as SSC CD11b Gr1 F4/80. Each symbol represents an individual mouse. Means are represented in all graphs. Statistical significance was evaluated using Student's -test.<p><b>Copyright information:</b></p><p>Taken from "CD59a deficiency exacerbates influenza-induced lung inflammation through complement-dependent and-independent mechanisms"</p><p></p><p>European Journal of Immunology 2007;37(5):1266-1274.</p><p>Published online Jan 2007</p><p>PMCID:PMC2435422.</p><p>Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</p

(A–C) Histological analysis of lung sections taken from Cd59a, WT and age-matched WT controls

Lung histology (H&E stain) demonstrating pulmonary injury 8days after infection with influenza virus (=9/group). Representative views of mouse lungs (×20original magnification) from WT(A) or Cd59a (B) mice infected with influenza are shown. A representative section from an uninfected WT control (C) is also included. In Cd59a mice there is mild hyperplasia of alveolar type-II cells and an extensive infiltrate of mononuclear cells into the interstitium (arrows). The alveolar walls contained dilated capillaries filled with RBC, with mild fibrotic changes (f) and perivascular lymphocytic infiltrates (g). In the healthy lung (C), the alveoli (a), alveolar septa (s) and alveolar duct (d) are marked for comparison. (D) Mice on the Balb/c background were infected with influenza virus and weight was monitored daily. Results represent mean values ± SEM of five mice per group. Statistical significance was evaluated using the Student's -test. value was <p><b>Copyright information:</b></p><p>Taken from "CD59a deficiency exacerbates influenza-induced lung inflammation through complement-dependent and-independent mechanisms"</p><p></p><p>European Journal of Immunology 2007;37(5):1266-1274.</p><p>Published online Jan 2007</p><p>PMCID:PMC2435422.</p><p>Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</p

Leftover Chicken Products Collected from Case-Patient Homes, Multistate Outbreak of Multidrug-Resistant <i>Salmonella</i> Heidelberg Infections Linked to a Single Poultry Company, 2013–2014.

<p>Leftover Chicken Products Collected from Case-Patient Homes, Multistate Outbreak of Multidrug-Resistant <i>Salmonella</i> Heidelberg Infections Linked to a Single Poultry Company, 2013–2014.</p

Persons Infected with the Outbreak Strains of <i>Salmonella</i> Heidelberg by State, n = 634, 2013–2014.

<p>Persons Infected with the Outbreak Strains of <i>Salmonella</i> Heidelberg by State, n = 634, 2013–2014.</p

Persons Infected with the Outbreak Strains of <i>Salmonella</i> Heidelberg, by Week of Illness Onset, March 2013-July 2014.

<p>Persons Infected with the Outbreak Strains of <i>Salmonella</i> Heidelberg, by Week of Illness Onset, March 2013-July 2014.</p

Case-patient Characteristics in Multistate Outbreak of Multidrug-Resistant <i>Salmonella</i> Heidelberg Infections Linked to a Single Poultry Company, by Pulsed-Field Gel Electrophoresis Pattern, 2013–2014.

<p>Case-patient Characteristics in Multistate Outbreak of Multidrug-Resistant <i>Salmonella</i> Heidelberg Infections Linked to a Single Poultry Company, by Pulsed-Field Gel Electrophoresis Pattern, 2013–2014.</p

Antimicrobial Susceptibility Testing Results, Multistate Outbreak of Multidrug-Resistant (MDR)^† <i>Salmonella</i> Heidelberg Infections Linked to a Single Poultry Company, 2013–2014.

<p>Antimicrobial Susceptibility Testing Results, Multistate Outbreak of Multidrug-Resistant (MDR)<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0162369#t003fn002" target="_blank">^†</a> <i>Salmonella</i> Heidelberg Infections Linked to a Single Poultry Company, 2013–2014.</p