Enhancement of phagocytosis and bacterial killing by heterophils from neonatal chicks after administration of Salmonella enteritidis-immune lymphokines

1999 ◽  
Vol 65 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Lacy L Genovese ◽  
Virginia K Lowry ◽  
Kenneth J Genovese ◽  
John R DeLoach ◽  
Michael H Kogut
1995 ◽  
Vol 74 (1) ◽  
pp. 18-25 ◽  
Author(s):  
E.D. MCGRUDER ◽  
G.A. RAMIREZ ◽  
M.H. KOGUT ◽  
R.W. MOORE ◽  
D.E. CORRIER ◽  
...  

Author(s):  
R. B. Moyes ◽  
R. E. Droleskey ◽  
M. H. Kogut ◽  
J. R. DeLoach

Salmonella enteritidis (SE) is of great concern to the poultry industry due to the organism's ability to penetrate the intestinal mucosa of the laying hen and subsequently colonize the ovaries and yolk membrane. The resultant subclinical infection can lead to SE infection of raw eggs and egg products. Interference with the ability of the organism to invade has been linked to the activation and recruitment of inflammatory polymorphonuclear cells, heterophils, to the lamina propria of the intestinal tract.Recently it has been established that heterophil activation and increased resistance to SE organ invasion can be accomplished by the administration of SE-immune lymphokines (SE-ILK) obtained from supernatants of concanavalin-A stimulated SE immune T lymphocytes from SE hyperimmunized hens. Invasion of SE into the lamina propria provides a secondary signal for directing activated heterophils to the site of SE invasion.


2009 ◽  
Vol 8 (9) ◽  
pp. 820-823
Author(s):  
Gabriela V. G- Verduzco ◽  
Guillermo Tellez ◽  
Michael H. Kogut ◽  
Armando Isibasi ◽  
Vianney Ortiz- Navarrete

1995 ◽  
Vol 39 (1) ◽  
pp. 21 ◽  
Author(s):  
Edward D. McGruder ◽  
Michael H. Kogut ◽  
Donald E. Corrier ◽  
John R. DeLoach ◽  
Billy M. Hargis

1996 ◽  
Vol 40 (1) ◽  
pp. 186 ◽  
Author(s):  
Richard L. Ziprin ◽  
Michael H. Kogut ◽  
Edward D. McGruder ◽  
Billy M. Hargis ◽  
John R. DeLoach

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250296
Author(s):  
Anamika Gupta ◽  
Mohit Bansal ◽  
Rohana Liyanage ◽  
Abhinav Upadhyay ◽  
Narayan Rath ◽  
...  

Salmonella Enteritidis is an intracellular foodborne pathogen that has developed multiple mechanisms to alter poultry intestinal physiology and infect the gut. Short chain fatty acid butyrate is derived from microbiota metabolic activities, and it maintains gut homeostasis. There is limited understanding on the interaction between S. Enteritidis infection, butyrate, and host intestinal response. To fill this knowledge gap, chicken macrophages (also known as HTC cells) were infected with S. Enteritidis, treated with sodium butyrate, and proteomic analysis was performed. A growth curve assay was conducted to determine sub-inhibitory concentration (SIC, concentration that do not affect bacterial growth compared to control) of sodium butyrate against S. Enteritidis. HTC cells were infected with S. Enteritidis in the presence and absence of SIC of sodium butyrate. The proteins were extracted and analyzed by tandem mass spectrometry. Our results showed that the SIC was 45 mM. Notably, S. Enteritidis-infected HTC cells upregulated macrophage proteins involved in ATP synthesis through oxidative phosphorylation such as ATP synthase subunit alpha (ATP5A1), ATP synthase subunit d, mitochondrial (ATP5PD) and cellular apoptosis such as Cytochrome-c (CYC). Furthermore, sodium butyrate influenced S. Enteritidis-infected HTC cells by reducing the expression of macrophage proteins mediating actin cytoskeletal rearrangements such as WD repeat-containing protein-1 (WDR1), Alpha actinin-1 (ACTN1), Vinculin (VCL) and Protein disulfide isomerase (P4HB) and intracellular S. Enteritidis growth and replication such as V-type proton ATPase catalytic subunit A (ATPV1A). Interestingly, sodium butyrate increased the expression of infected HTC cell protein involving in bacterial killing such as Vimentin (VIM). In conclusion, sodium butyrate modulates the expression of HTC cell proteins essential for S. Enteritidis invasion.


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