chick kidney
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Development ◽  
2015 ◽  
Vol 142 (15) ◽  
pp. 2686-2695 ◽  
Author(s):  
Jenny Schneider ◽  
Alaa A. Arraf ◽  
Mor Grinstein ◽  
Ronit Yelin ◽  
Thomas M. Schultheiss
Keyword(s):  

2009 ◽  
Vol 2 (4) ◽  
pp. 289-296 ◽  
Author(s):  
John Cunningham ◽  
Daniel D. Bikle ◽  
Louis V. Avioli

Author(s):  
K. Sugiura ◽  
N. Aste ◽  
M. Fujii ◽  
K. Shimada ◽  
N. Saito
Keyword(s):  

Steroids ◽  
2007 ◽  
Vol 72 (2) ◽  
pp. 158-164 ◽  
Author(s):  
R.C. Khanal ◽  
N.M. Smith ◽  
I. Nemere

2005 ◽  
Vol 73 (4) ◽  
pp. 2094-2100 ◽  
Author(s):  
Chris K. Smith ◽  
Pete Kaiser ◽  
Lisa Rothwell ◽  
Tom Humphrey ◽  
Paul A. Barrow ◽  
...  

ABSTRACT Campylobacter jejuni is a major cause of human inflammatory enteritis. During the course of human disease numerous proinflammatory cytokines are produced. Little is known, however, about the cytokine responses produced during the interaction of this bacterium with the avian host. Campylobacter has been considered a commensal of the avian host. Any differences in innate responses to this pathogen between the human and avian hosts should lead to a greater understanding of the disease process in humans. We have demonstrated expression of proinflammatory cytokines and chemokines in response to Campylobacter infection in avian primary chick kidney cells and the avian macrophage cell line HD11. The data indicate that Campylobacter can stimulate the avian host in a proinflammatory manner. The data strongly suggest that the lack of pathology in vivo is not due to an inability of Campylobacter to stimulate a proinflammatory response from avian cells.


2003 ◽  
Vol 8 (4) ◽  
pp. 1161-1166 ◽  
Author(s):  
Xu Bao-hua ◽  
Xu Zi-rong ◽  
Xia Mei-sheng ◽  
Hu Cai-hong ◽  
Deng Yue-song ◽  
...  

2000 ◽  
Vol 98 (1-2) ◽  
pp. 121-125 ◽  
Author(s):  
Michael R. Stark ◽  
Mahendra S. Rao ◽  
Gary C. Schoenwolf ◽  
Guizhi Yang ◽  
Danielle Smith ◽  
...  

1999 ◽  
Vol 67 (7) ◽  
pp. 3580-3586 ◽  
Author(s):  
S. Christine Henderson ◽  
Denise I. Bounous ◽  
Margie D. Lee

ABSTRACT Salmonellae are gastrointestinal pathogens of man and animals. However, strains that are host-specific avian pathogens are often avirulent in mammals, and those which are nonspecific are commensal in poultry. The objective of this study was to determine whether host specificity was exhibited by bacterial abilities to invade epithelial cells or resist leukocyte killing. In this study, leukocytes isolated from humans and chickens were used to kill Salmonella in vitro. Both Salmonella pullorum, an avian-specific serotype, and Salmonella typhimurium, a broad-host-range serotype, were sensitive to killing by polymorphonuclear leukocytes isolated from both species. Both serotypes replicated in cells of the MQ-NCSU avian-macrophage cell line. In contrast, S. pullorum was noninvasive for cultured epithelial Henle 407, chick kidney, chick ovary, and budgerigar abdominal tumor cells. In the bird challenge, however, S. typhimurium rapidly caused inflammation of the intestinal mucosa, but S. pullorumpreferentially targeted the bursa of Fabricius prior to eliciting intestinal inflammation. Salmonella serotypes which cause typhoid fever in mice have been shown to target the gut-associated lymphoid tissue. Observations from this study show that S. pullorum initiated a route of infection in chicks comparable to the route it takes in cases of enteric fever.


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