scholarly journals Natural Killer Cells Mediate Protection against Yersinia pseudotuberculosis in the Mesenteric Lymph Nodes

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0136290 ◽  
Author(s):  
Maik Rosenheinrich ◽  
Wiebke Heine ◽  
Carina M. Schmühl ◽  
Fabio Pisano ◽  
Petra Dersch
2008 ◽  
Vol 32 (7) ◽  
pp. 773-783 ◽  
Author(s):  
Preben Boysen ◽  
Gjermund Gunnes ◽  
Daniela Pende ◽  
Mette Valheim ◽  
Anne K. Storset

2015 ◽  
Vol 25 (1) ◽  
pp. 22-34 ◽  
Author(s):  
Ana M. Vuletić ◽  
Irena P. Jovanić ◽  
Vladimir B. Jurišić ◽  
Zorka M. Milovanović ◽  
Srđan S. Nikolić ◽  
...  

2009 ◽  
Vol 128 (1-3) ◽  
pp. 312
Author(s):  
Preben Boysen ◽  
Gjermund Gunnes ◽  
Daniela Pende ◽  
Mette Valheim ◽  
Anne K. Storset

2012 ◽  
Vol 8 (8) ◽  
pp. e1002828 ◽  
Author(s):  
Gregory T. Crimmins ◽  
Sina Mohammadi ◽  
Erin R. Green ◽  
Molly A. Bergman ◽  
Ralph R. Isberg ◽  
...  

2011 ◽  
Vol 6 (3) ◽  
pp. 432-438 ◽  
Author(s):  
Thomas Schneider ◽  
Silvia Kimpfler ◽  
Arne Warth ◽  
Philipp A. Schnabel ◽  
Hendrik Dienemann ◽  
...  

2001 ◽  
Vol 69 (5) ◽  
pp. 2779-2787 ◽  
Author(s):  
Joan Mecsas ◽  
Inna Bilis ◽  
Stanley Falkow

ABSTRACT Yersinia pseudotuberculosis localizes to the distal ileum, cecum, and proximal colon of the gastrointestinal tract after oral infection. Using signature-tagged mutagenesis, we isolated 13Y. pseudotuberculosis mutants that failed to survive in the cecum of mice after orogastric inoculation. Twelve of these mutants were also attenuated for replication in the spleen after intraperitoneal infection, whereas one strain, mutated the gene encoding invasin, replicated as well as wild-type bacteria in the spleen. Several mutations were in operons encoding components of the type III secretion system, including components involved in translocating Yop proteins into host cells. This indicates that one or more Yops may be necessary for survival in the gastrointestinal tract. Three mutants were defective in O-antigen biosynthesis; these mutants were also unable to invade epithelial cells as efficiently as wild-typeY. pseudotuberculosis. Several other mutations were in genes that had not previously been associated with growth in a host, including cls, ksgA, and sufl. In addition, using Y. pseudotuberculosis strains marked with signature tags, we counted the number of different bacterial clones that were present in the cecum, mesenteric lymph nodes, and spleen 5 days postinfection. We find barriers in the host animal that limit the number of bacteria that succeed in reaching and/or replicating in the mesenteric lymph nodes and spleen after breaching the gut mucosa.


1983 ◽  
Vol 17 (4) ◽  
pp. 311-320 ◽  
Author(s):  
L. F. Taffs ◽  
Glynis Dunn

A spontaneous outbreak of yersiniosis caused by Yersinia pseudotuberculosis serotype IIB occurred in a small indoor breeding colony of red-bellied tamarins ( Saguinus labiatus) during the winter of 1981. Of 3S monkeys at risk 6 died of an acute or subacute infection over a period of 23 days. Clinical signs were anorexia, weakness, listlessness and depression. The disease was characterized by focal necrosis of the liver, spleen, mesenteric lymph nodes, ulcerative enteritis, and the presence of colonies of Gram-negative bacilli in the lesions. Y. pseudotuberculosis was isolated from the liver, spleen, mesenteric lymph nodes and kidney but not from the blood, lung or intestine. Contaminated food was believed to be the source of infection.


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