Analysis of Virulence and Inflammatory Potential of Shigella flexneri Purine Biosynthesis Mutants

Delivery of Biologically Active Anti-Inflammatory Cytokines IL-10 and IL-1ra In Vivo by the Shigella Type III Secretion Apparatus

“…This is consistent with our previous studies with the rabbit ligated-loop model of infection, in which we observed that neutralization of TNF-␣ by specific Ab decreased tissue injury (5). Indeed, elevated levels of TNF-␣ were associated with increased severity of inflammation in shigellosis (5,(41)(42)(43). Notably, there was no significant difference in IL-1␤ mRNA synthesis after infection with wild-type or IL-10-expressing strains.…”

Emergence of a Novel Shigella flexneri Serotype 4s Strain That Evolved from a Serotype X Variant in China

“…The set1A, set1B, sen, ial, ipaH, and virF virulence genes were detected using multiplex PCR assays described previously (2,5,10,11). A plasmid purification kit (Qiagen, Germany) was used to isolate the bacterial plasmids in accordance with the manufacturer's recommendations.…”

Role of Toll-Like Receptor 4 in the Proinflammatory Response to Vibrio cholerae O1 El Tor Strains Deficient in Production of Cholera Toxin and Accessory Toxins

“…Although adult mice are resistant to intestinal colonization by V. cholerae (12), we found that acute inflammation develops in the lung tissue after intranasal inoculation with V. cholerae, providing a model for the assessment of the toxic action on inflammation of a mucosal epithelial layer (8). This model is based on experiments using Shigella flexneri dependent on the premise that the bronchial tree is composed of a mucosal lining with relevant characteristics similar to those of the intestine, including simple cubodial-to-columnar epithelial cells, lymphoid aggregates, bronchiole-associated lymphoid tissue similar to Peyer's patches, and the presence of several varieties of antigen-presenting cells (5,19,23,28).Using this new murine model, we previously found that wild-type CT-producing strains of V. cholerae induce a rapid cell death due to fluid accumulation in the lung but that a strain deleted of the genes for CT stimulates proinflammatory cytokine and chemokine production, leading to development of a lethal pneumonia characterized by infiltration of neutrophils, hemorrhages, and bacteremia (8). When mice were inoculated with a multitoxin mutant strain with deletions of genes for the accessory toxins hemagglutinin/protease (hapA), hemolysin (hlyA), and the actin cross-linking RTX toxin (rtxA), in addition to deletions of genes for CT (ctxAB), the mice did not develop severe pneumonia and cleared the infection.…”

“…Although adult mice are resistant to intestinal colonization by V. cholerae (12), we found that acute inflammation develops in the lung tissue after intranasal inoculation with V. cholerae, providing a model for the assessment of the toxic action on inflammation of a mucosal epithelial layer (8). This model is based on experiments using Shigella flexneri dependent on the premise that the bronchial tree is composed of a mucosal lining with relevant characteristics similar to those of the intestine, including simple cubodial-to-columnar epithelial cells, lymphoid aggregates, bronchiole-associated lymphoid tissue similar to Peyer's patches, and the presence of several varieties of antigen-presenting cells (5,19,23,28).…”