Impact of cagPAI and T4SS on the Inflammatory Response of Human Neutrophils to Helicobacter pylori Infection

Sánchez-Zauco, Norma; Torres, Javier; Pérez-Figueroa, Gloria Erandi; Álvarez-Arellano, Lourdes; Camorlinga‐Ponce, Margarita; Gómez, Alejandro; Cerezo, Silvia Giono; Maldonado‐Bernal, Carmen

doi:10.1371/journal.pone.0064623

Cited by 26 publications

(19 citation statements)

References 43 publications

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“…Results from these studies indicate that zinc homeostasis plays an important role in regulating the cag T4SS in H. pylori . Previous reports have shown that when H. pylori interacts with gastric epithelial cells, the cag T4SS translocates CagA into host cells leading to activation of c-Src and changes in the cytoskeleton [34] – [36] . A functional cag T4SS also increases the activation of NOD and NFkB [33] , which ultimately results in the production of IL-8 and the recruitment of neutrophils [34] – [36] .…”

Section: Discussionmentioning

confidence: 99%

The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration

et al. 2014

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Transition metals are necessary for all forms of life including microorganisms, evidenced by the fact that 30% of all proteins are predicted to interact with a metal cofactor. Through a process termed nutritional immunity, the host actively sequesters essential nutrient metals away from invading pathogenic bacteria. Neutrophils participate in this process by producing several metal chelating proteins, including lactoferrin and calprotectin (CP). As neutrophils are an important component of the inflammatory response directed against the bacterium Helicobacter pylori, a major risk factor for gastric cancer, it was hypothesized that CP plays a role in the host response to H. pylori. Utilizing a murine model of H. pylori infection and gastric epithelial cell co-cultures, the role CP plays in modifying H. pylori -host interactions and the function of the cag Type IV Secretion System (cag T4SS) was investigated. This study indicates elevated gastric levels of CP are associated with the infiltration of neutrophils to the H. pylori-infected tissue. When infected with an H. pylori strain harboring a functional cag T4SS, calprotectin-deficient mice exhibited decreased bacterial burdens and a trend toward increased cag T4SS -dependent inflammation compared to wild-type mice. In vitro data demonstrate that culturing H. pylori with sub-inhibitory doses of CP reduces the activity of the cag T4SS and the biogenesis of cag T4SS-associated pili in a zinc-dependent fashion. Taken together, these data indicate that zinc homeostasis plays a role in regulating the proinflammatory activity of the cag T4SS.

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Section: Discussionmentioning

confidence: 99%

The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration

et al. 2014

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“…Sánchez‐Zauco et al. elegantly demonstrated that the cag PAI and the type IV secretion system (T4SS) have a great impact on the inflammatory response of neutrophils to H. pylori . They observed that H. pylori downregulates neutrophil expression of TLRs 2 and 5 but upregulates TLR9 expression in a cag PAI and T4SS‐independent manner.…”

Section: Innate Immunitymentioning

confidence: 99%

Immunity, Inflammation, and Vaccines for Helicobacter pylori

D’Elios

Czinn

2014

Helicobacter

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Helicobacter pylori colonizes mucosa, activates Toll-like and Nod-like receptors, and usually elicits a gastric T-helper 1/17 (Th1/Th17) type of immune response. Among several bacterial factors, the secreted peptidyl prolyl cis, trans-isomerase of H. pylori represents a key factor driving Th17 inflammation. A complex and fascinating balance between H. pylori and host factors takes part in the gastric niche and is responsible for the chronicity of the infection. Novel insights into the innate and adaptive responses against H. pylori, dealing with gastric epithelial cells, cytokines, and immune evasion have been elucidated over the past year and are discussed for the development of an effective vaccine.Helicobacter pylori chronically infects the stomach of more than half of the human population and represents the major cause of gastroduodenal diseases. However, only 15-20% of H. pylori-infected patients develop severe pathologies, such as gastric cancer, gastric B-cell lymphoma, peptic ulcer, or gastric autoimmunity, during their lifetime. This fact suggests that the type of immunity elicited by H. pylori may represent an important factor that is able to influence the outcome of the infection toward protection, evasion, or pathology. Here, we present an overview of the major findings on the host response to H. pylori published over the past year.

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“…H. pylori contains many virulence factors, including the cag pathogenicity island ( cag PAI), that are involved in the pathogenesis of several diseases 1, 23, 4.…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori with East Asian-type cag PAI genes is more virulent than strains with Western-type in some cag PAI genes

Yuan

Yan

Yang

et al. 2017

Brazilian Journal of Microbiology

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The severity of Helicobacter pylori-related disease is correlated with the presence and integrity of a cag pathogenicity island (cagPAI). cagPAI genotype may have a modifying effect on the pathogenic potential of the infecting strain. After analyzing the sequences of cagPAI genes, some strains with the East Asian-type cagPAI genes were selected for further analysis to examine the association between the diversity of the cagPAI genes and the virulence of H. pylori. The results showed that gastric mucosal inflammatory cell infiltration was significantly higher in patients with East Asian-type cagPAI genes H. pylori strain compared with mosaicism cagPAI genes H. pylori strain (p < 0.05). H. pylori strains with the East Asian-type cagPAI genes were closely associated with IL-8 secretion in vitro and in vivo compared with H. pylori strains with the mosaicism cagPAI genes (p < 0.01). H. pylori strains with East Asian-type cagPAI genes are able to strongly translocate CagA to host cells. These results suggest that H. pylori strains with East Asian-type cagPAI genes are more virulent than the strains of cagPAI gene/genes that are Western type.

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Impact of cagPAI and T4SS on the Inflammatory Response of Human Neutrophils to Helicobacter pylori Infection

Cited by 26 publications

References 43 publications

The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration

The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration

Immunity, Inflammation, and Vaccines for Helicobacter pylori

Helicobacter pylori with East Asian-type cag PAI genes is more virulent than strains with Western-type in some cag PAI genes

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