In vitro invasion capacity of Salmonella Typhimurium DT9 isolates sourced from humans and layer hen environments

2017 ◽  
Vol 65 (1) ◽  
pp. e259-e264 ◽  
Author(s):  
A. R. McWhorter ◽  
G. Phan ◽  
H. Hocking ◽  
K. K. Chousalkar
2006 ◽  
Vol 72 (6) ◽  
pp. 3862-3871 ◽  
Author(s):  
Hadewig Werbrouck ◽  
Koen Grijspeerdt ◽  
Nadine Botteldoorn ◽  
Els Van Pamel ◽  
Nancy Rijpens ◽  
...  

ABSTRACT In this study, a number of Listeria monocytogenes strains of different origins were evaluated for in vitro invasion capacity for various human cell types (monocytic THP-1, enterocytic Caco-2, and hepatocytic HepG2 cells) and for expression levels of specific virulence genes. For THP-1 cells, no differences between clinical and nonclinical L. monocytogenes strains in invasion capacity or in production of the proinflammatory cytokine interleukin-8 (IL-8) were observed, whereas for the Caco-2 and HepG2 cells, significant differences in invasion capacity were noticed. On average, the clinical strains showed a significantly lower invasion capacity than the nonclinical L. monocytogenes strains. Furthermore, it was shown that the clinical strains induce lower IL-8 levels in HepG2 cells than do the nonclinical strains. This observation led us to study the mRNA expression levels of inlA, inlB, and ami, important virulence genes mediating adhesion and invasion of eukaryotic cells, by real-time reverse transcription-PCR for 27 clinical and 37 nonclinical L. monocytogenes strains. Significant differences in inlA and inlB expression were observed, with clinical strains showing a lower expression level than nonclinical strains. These observations were in accordance with in vitro invasion of Caco-2 and HepG2 cells, respectively. The results of this study indicate that differential expression levels of inlA and inlB possibly play a role in the virulence capacities of L. monocytogenes strains. The lower capacity of clinical strains to invade HepG2 cells and to induce IL-8 is possibly a mechanism of immune evasion used by specific L. monocytogenes strains.


1998 ◽  
Vol 101 (1) ◽  
pp. 263-272 ◽  
Author(s):  
T Ikawa ◽  
M Ikeda ◽  
A Yamaguchi ◽  
W C Tsai ◽  
N Tamura ◽  
...  

2021 ◽  
Vol 120 (3) ◽  
pp. 74a
Author(s):  
Satoshi Katsube ◽  
Katleen Willibal ◽  
Elena B. Tikhonova ◽  
Hariharan Parameswaran ◽  
Sangama Vemulapally ◽  
...  

2021 ◽  
pp. 109063
Author(s):  
Lin Li ◽  
Rui Li ◽  
Caili Qi ◽  
Haixia Gao ◽  
Qiling Wei ◽  
...  

1993 ◽  
Vol 123 (4) ◽  
pp. 895-907 ◽  
Author(s):  
B A McCormick ◽  
S P Colgan ◽  
C Delp-Archer ◽  
S I Miller ◽  
J L Madara

In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model those interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1- phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium.


1991 ◽  
Vol 54 (7) ◽  
pp. 496-501 ◽  
Author(s):  
ARTHUR HINTON ◽  
GEORGE E. SPATES ◽  
DONALD E. CORRIER ◽  
MICHAEL E. HUME ◽  
JOHN R. DELOACH ◽  
...  

A Veillonella species and Enterococcus durans were isolated from the cecal contents of adult broilers. Mixed cultures of Veillonella and E. durans inhibited the growth of Salmonella typhimurium and Escherichia coli 0157:H7 on media containing 2.5% lactose (w/v). The growth of S. typhimurium or E. coli 0157:H7 was not inhibited by mixed cultures containing Veillonella and E. durans on media containing only 0.25% lactose or by pure cultures of Veillonella or E. durans on media containing either 0.25% or 2.5% lactose. The mixed cultures of Veillonella and E. durans produced significantly (P<0.05) more acetic, propionic, and lactic acids in media containing 2.5% lactose than in media containing 0.25% lactose. The inhibition of the enteropathogens was related to the production of lactic acid from lactose by the E. durans and the production of acetic and propionic acids from lactic acid by the Veillonella.


Sign in / Sign up

Export Citation Format

Share Document