scholarly journals THE NATURE & ROLE OF MUCOSAL DAMAGE IN RELATION TO SALMONELLA TYPHIMURIUM-INDUCED FLUID SECRETION IN THE RABBIT ILEUM

1986 ◽  
Vol 20 (7) ◽  
pp. 691-691 ◽  
Author(s):  
T S Wallis ◽  
W G Starkey ◽  
J Stephen ◽  
S J Haddon ◽  
M P Osborne ◽  
...  
1986 ◽  
Vol 22 (1) ◽  
pp. 39-49 ◽  
Author(s):  
T. S. Wallis ◽  
W. G. Starkey ◽  
J. Stephen ◽  
S. J. Haddon ◽  
M. P. Osborne ◽  
...  

1990 ◽  
Vol 31 (1) ◽  
pp. 27-35 ◽  
Author(s):  
T. S. Wallis ◽  
A. T. M. Vaughan ◽  
G. J. Clarke ◽  
G.-M. Qi ◽  
K. J. Worton ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2554
Author(s):  
Marc Micó-Carnero ◽  
Araní Casillas-Ramírez ◽  
Albert Caballeria-Casals ◽  
Carlos Rojano-Alfonso ◽  
Alfredo Sánchez-González ◽  
...  

Herein, we investigate whether: (1) the administration of glucose or a lipid emulsion is useful in liver transplantation (LT) using steatotic (induced genetically or nutritionally) or non-steatotic livers from donors after brain death (DBDs); and (2) any such benefits are due to reductions in intestinal damage and consequently to gut microbiota preservation. In recipients from DBDs, we show increased hepatic damage and failure in the maintenance of ATP, glycogen, phospholipid and growth factor (HGF, IGF1 and VEGFA) levels, compared to recipients from non-DBDs. In recipients of non-steatotic grafts from DBDs, the administration of glucose or lipids did not protect against hepatic damage. This was associated with unchanged ATP, glycogen, phospholipid and growth factor levels. However, the administration of lipids in steatotic grafts from DBDs protected against damage and ATP and glycogen drop and increased phospholipid levels. This was associated with increases in growth factors. In all recipients from DBDs, intestinal inflammation and damage (evaluated by LPS, vascular permeability, mucosal damage, TLR4, TNF, IL1, IL-10, MPO, MDA and edema formation) was not shown. In such cases, potential changes in gut microbiota would not be relevant since neither inflammation nor damage was evidenced in the intestine following LT in any of the groups evaluated. In conclusion, lipid treatment is the preferable nutritional support to protect against hepatic damage in steatotic LT from DBDs; the benefits were independent of alterations in the recipient intestine.


1978 ◽  
Vol 74 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Paul B. Weisberg ◽  
Gerald M. Carlson ◽  
Sidney Cohen

Pharmacology ◽  
2009 ◽  
Vol 84 (5) ◽  
pp. 294-299 ◽  
Author(s):  
Brigitta M. Peskar ◽  
Karlheinz Ehrlich ◽  
Rufina Schuligoi ◽  
Bernhard A. Peskar

1991 ◽  
Vol 5 (2) ◽  
pp. 401-407 ◽  
Author(s):  
K. Johnson ◽  
I. Charles ◽  
G. Dougan ◽  
D. Pickard ◽  
P. O'Gaora ◽  
...  

2021 ◽  
Vol 368 (18) ◽  
Author(s):  
Jing Li ◽  
Na Li ◽  
Chengcheng Ning ◽  
Yun Guo ◽  
Chunhui Ji ◽  
...  

ABSTRACT Small RNAs (sRNAs) are essential virulent regulators in Salmonella typhimurium (STM). To explore the role of sRNA STnc150 in regulating STM virulence, we constructed a STnc150 deletion strain (ΔSTnc150) and its complementary strain (ΔSTnc150/C). Then, we compared their characteristics to their original parent strain experimentally, identified the target genes of STnc150 and determined the expression levels of target genes. The results showed that the ΔSTnc150 strain exhibited delayed biofilm formation, enhanced adhesion to macrophages, significantly reduced LD50, increased liver and spleen viral loads and more vital pathological damaging ability than its parent and complementary strains. Further, bioinformatics combined with the bacterial dual plasmid reporter system confirmed that the bases 72–88 of STnc150 locating at the secondary stem-loop structure of the STnc150 are complementary with the bases 1–19 in the 5′-terminal of fimA mRNA of the type 1 fimbriae subunit. Western blot analysis showed that fimA protein level was increased in STnc150 strain compared with its parent and complementary strains. Together, this study suggested that STnc150 can down-regulate STM fimA expression at the translation level, which provided insights into the regulatory mechanisms of sRNAs in virulence of STM.


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