scholarly journals SspA Is Required for Lethal Salmonella enterica Serovar Typhimurium Infections in Calves but Is Not Essential for Diarrhea

2000 ◽  
Vol 68 (6) ◽  
pp. 3158-3163 ◽  
Author(s):  
Renée M. Tsolis ◽  
L. Garry Adams ◽  
Michael J. Hantman ◽  
Christina A. Scherer ◽  
Tyler Kimbrough ◽  
...  

ABSTRACT Salmonella pathogenicity island 1 (SPI-1) encodes virulence determinants, which are important for enteropathogenicity in calves. To determine whether the Salmonella entericaserovar Typhimurium SPI-1 effector proteins SspA and SptP are important for enteropathogenicity, strains lacking these proteins were tested during oral infection of calves. Calves infected with asptP mutant or its isogenic parent developed diarrhea and lethal morbidity. In contrast, calves infected with an sspAmutant developed diarrhea, which resolved within 10 days but did not result in mortality. The sspA mutant was recovered from bovine intestinal tissues at numbers similar to those obtained for its isogenic parent and caused marked intestinal lesions. Thus, the severity of pathological changes caused by serovar Typhimurium strains or their ability to cause diarrhea were not predictive of their ability to cause lethal morbidity in calves. We conclude that factors other than or in addition to bacterial colonization, intestinal lesions, or electrolyte loss contribute to lethal morbidity in calves infected with serovar Typhimurium.

2003 ◽  
Vol 71 (7) ◽  
pp. 4052-4058 ◽  
Author(s):  
Andrea Haraga ◽  
Samuel I. Miller

ABSTRACT Nontyphoidal salmonellae are enteric pathogens that cause acute gastroenteritis and colonize the intestinal tract for prolonged periods. In the intestinal epithelia, these bacteria induce secretion of proinflammatory cytokines, such as interleukin-8 (IL-8), which leads to a profound inflammatory response through recruitment of polymorphonuclear leukocytes. Production of IL-8 induced by Salmonella spp. is due to the activation of the transcription factors nuclear factor κB (NF-κB) and activator protein-1 (AP-1). This work demonstrates that Salmonella enterica serovar Typhimurium can downmodulate IL-8 production after invasion of intestinal epithelial cells. The Salmonella translocated effector proteins SspH1 and SptP participate in this process. SspH1 is a member of the bacterial LPX repeat protein family that localizes to the mammalian nucleus and inhibits NF-κB-dependent gene expression. A Shigella flexneri translocated effector, IpaH9.8, which has a similar structure and subcellular localization in mammalian cells, also inhibits NF-κB-dependent gene expression. We propose that suppression of inflammatory responses by intracellular S. enterica serovar Typhimurium, and perhaps Shigella flexneri, contributes to bacterial colonization of host tissues and pathogenesis.


Microbiology ◽  
2007 ◽  
Vol 153 (4) ◽  
pp. 1221-1228 ◽  
Author(s):  
M. N Giacomodonato ◽  
S Uzzau ◽  
D Bacciu ◽  
R Caccuri ◽  
S. H Sarnacki ◽  
...  

2010 ◽  
Vol 6 (12) ◽  
pp. 2448 ◽  
Author(s):  
Garry W. Buchko ◽  
George Niemann ◽  
Erin S. Baker ◽  
Mikhail E. Belov ◽  
Richard D. Smith ◽  
...  

2006 ◽  
Vol 74 (9) ◽  
pp. 5221-5226 ◽  
Author(s):  
Pu Feng ◽  
Allan L. Truant ◽  
Joseph J. Meissler ◽  
John P. Gaughan ◽  
Martin W. Adler ◽  
...  

ABSTRACT Understanding the consequences of drug withdrawal on immune function and host defense to infection is important. We, and others, previously demonstrated that morphine withdrawal results in immunosuppression and sensitizes to lipopolysaccharide-induced septic shock. In the present study, the effect of morphine withdrawal on spontaneous sepsis and on oral infection with Salmonella enterica serovar Typhimurium was examined. Mice were chronically exposed to morphine for 96 h by implantation of a slow-release morphine pellet. Abrupt withdrawal was induced by removal of the pellet. In the sepsis model, bacterial colonization was examined and bacterial species were identified by necropsy of various tissues. It was found that at 48 h postwithdrawal, morphine-treated mice had enteric bacteria that were detected in the Peyer's patches (4/5), mesenteric lymph nodes (4/5), spleens (4/10), livers (6/10), and peritoneal cavities (8/10). In placebo pellet-withdrawn mice, only 2/40 cultures were positive. The most frequently detected organisms in tissues of morphine-withdrawn mice were Enterococcus faecium followed by Klebsiella pneumoniae. Both organisms are part of the normal gastrointestinal flora. In the infection model, mice were orally inoculated with S. enterica 24 h post-initiation of abrupt withdrawal from morphine. Withdrawal significantly decreased the mean survival time and significantly increased the Salmonella burden in various tissues of infected mice compared to placebo-withdrawn animals. Elevated levels of the proinflammatory cytokines were observed in spleens of morphine-withdrawn mice, compared to placebo-withdrawn mice. These findings demonstrate that morphine withdrawal sensitizes to oral infection with a bacterial pathogen and predisposes mice to bacterial sepsis.


2008 ◽  
Vol 77 (1) ◽  
pp. 60-69 ◽  
Author(s):  
Kim Thien Ly ◽  
James E. Casanova

ABSTRACT The intracellular gram-negative bacterial pathogen Salmonella enterica serovar Typhimurium gains entry into nonphagocytic cells by manipulating the assembly of the host actin cytoskeleton. S. enterica serovar Typhimurium entry requires a functional type III secretion system, a conduit through which bacterial effector proteins are directly translocated into the host cytosol. We and others have previously reported the enhancement of tyrosine kinase activities during Salmonella serovar Typhimurium infection; however, neither specific kinases nor their targets have been well characterized. In this study, we investigated the roles of the cellular Abelson tyrosine kinase (c-Abl) and the related protein Arg in the context of serovar Typhimurium infection. We found that bacterial internalization was inhibited by more than 70% in cells lacking both c-Abl and Arg and that treatment of wild-type cells with a pharmaceutical inhibitor of the c-Abl kinase, STI571 (imatinib), reduced serovar Typhimurium invasion efficiency to a similar extent. Bacterial infection led to enhanced phosphorylation of two previously identified c-Abl substrates, the adaptor protein CT10 regulator of kinase (CrkII) and the Abelson-interacting protein Abi1, a component of the WAVE2 complex. Furthermore, overexpression of the nonphosphorylatable form of CrkII resulted in decreased invasion. Taken together, these findings indicate that c-Abl is activated during S. enterica serovar Typhimurium infection and that its phosphorylation of multiple downstream targets is functionally important in bacterial internalization.


2007 ◽  
Vol 76 (1) ◽  
pp. 403-416 ◽  
Author(s):  
Trevor D. Lawley ◽  
Donna M. Bouley ◽  
Yana E. Hoy ◽  
Christine Gerke ◽  
David A. Relman ◽  
...  

ABSTRACT Transmission is an essential stage of a pathogen's life cycle and remains poorly understood. We describe here a model in which persistently infected 129X1/SvJ mice provide a natural model of Salmonella enterica serovar Typhimurium transmission. In this model only a subset of the infected mice, termed supershedders, shed high levels (>108 CFU/g) of Salmonella serovar Typhimurium in their feces and, as a result, rapidly transmit infection. While most Salmonella serovar Typhimurium-infected mice show signs of intestinal inflammation, only supershedder mice develop colitis. Development of the supershedder phenotype depends on the virulence determinants Salmonella pathogenicity islands 1 and 2, and it is characterized by mucosal invasion and, importantly, high luminal abundance of Salmonella serovar Typhimurium within the colon. Immunosuppression of infected mice does not induce the supershedder phenotype, demonstrating that the immune response is not the main determinant of Salmonella serovar Typhimurium levels within the colon. In contrast, treatment of mice with antibiotics that alter the health-associated indigenous intestinal microbiota rapidly induces the supershedder phenotype in infected mice and predisposes uninfected mice to the supershedder phenotype for several days. These results demonstrate that the intestinal microbiota plays a critical role in controlling Salmonella serovar Typhimurium infection, disease, and transmissibility. This novel model should facilitate the study of host, pathogen, and intestinal microbiota factors that contribute to infectious disease transmission.


2008 ◽  
Vol 52 (12) ◽  
pp. 4514-4517 ◽  
Author(s):  
Ana Herrero ◽  
M. Carmen Mendoza ◽  
Rosaura Rodicio ◽  
M. Rosario Rodicio

ABSTRACT pUO-StVR2 is a virulence-resistance plasmid which originated from pSLT of Salmonella enterica serovar Typhimurium through acquisition of a complex resistance island, flanked by regions that provide a toxin-antitoxin system and an iron uptake system. The presence of resistance and virulence determinants on the same plasmid allows coselection of both properties, potentially increasing health risks.


2013 ◽  
Vol 15 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Niladri Bhusan Pati ◽  
Vikalp Vishwakarma ◽  
Sangeeta Jaiswal ◽  
Balamurugan Periaswamy ◽  
Wolf-Dietrich Hardt ◽  
...  

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