Effects of pH on killing of Staphylococcus aureus and Escherichia coli by constituents of the neutrophil phagolysosome

Styrt, Barbara; Klempner, Mark S.

doi:10.1099/00222615-25-2-101

Cited by 12 publications

(7 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It also suggests that internalization of acute strains of E. coli into bovine mammary epithelial cells occurred mainly through RME. These results are in agreement with other studies (Styrt and Klempner 1988;Sreenivasan et al 1993, Almeida and.…”

Section: Discussionsupporting

confidence: 94%

Intracellular fate of strains of Escherichia coli isolated from dairy cows with acute or chronic mastitis

et al. 2011

View full text Add to dashboard Cite

Research on mastitis in dairy cows caused by Escherichia coli has reported the emergence of strains capable of inducing chronic mastitis and that these strains adhered to and internalized into bovine mammary epithelial cells better than strains of E. coli isolated from acute mastitis. To understand mechanisms and strategies used by chronic E. coli strains to survive intracellularly internalization studies using bovine mammary epithelial cells treated with inhibitors of caveolae-mediated endocytosis (CME) and receptor-mediated endocytosis (RME), double immunofluorescence labeling confocal laser and fluorescence microscopy were conducted. Internalization studies showed that strains chronic E. coli strains persisted intracellularly longer than acute E. coli strains. Treatment of bovine mammary epithelial cells CME or RME inhibitors resulted in lower numbers of intracellular E. coli strains associated with chronic or acute mastitis than untreated controls. In addition, when selective CME inhibitors were used significantly fewer chronic E. coli were detected intracellularly than acute E. coli or untreated controls. Confocal laser microscopy showed that chronic E. coli strains colocalized preferentially with caveolae whereas acute strains did so with early endosomes, an early step of RME. These results suggest that strains of E. coli associated with chronic mastitis exploit lipid rafts/CME to internalize into and move through mammary epithelial cells. By exploiting this endocytosis pathway, chronic E. coli strains avoid bactericidal mechanisms such as endosome acidification and endosome-lysosome fusion, thus allowing intracellular survival. Data from this study helps to explain how these strains are capable of causing chronic E. coli mastitis.

show abstract

Section: Discussionsupporting

confidence: 94%

Intracellular fate of strains of Escherichia coli isolated from dairy cows with acute or chronic mastitis

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Leishmania parasites are rapidly killed by a H 2 O 2 -dependent process (33). Acid pH activates a number of acid hydrolases and promotes conversion of superoxide anion to H 2 O 2 (34). We have previously found, by subcellular fractionation assays, that the ATP-dependent acidification capacity, required for phagosome acidification, and FIGURE 9.…”

Section: Discussionmentioning

confidence: 99%

Selective Fusion of Azurophilic Granules with Leishmania-containing Phagosomes in Human Neutrophils

Mollinedo

Janssen

Iglesia-Vicente

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

Leishmania parasites use polymorphonuclear neutrophils as intermediate hosts before their ultimate delivery to macrophages following engulfment of parasite-infected neutrophils. This leads to a silent and unrecognized entry of Leishmania into the macrophage host cell. Neutrophil function depends on its cytoplasmic granules, but their mobilization and role in how Leishmania parasites evade intracellular killing in neutrophils remain undetermined. Here, we have found by ultrastructural approaches that neutrophils ingested Leishmania major promastigotes, and azurophilic granules fused in a preferential way with parasite-containing phagosomes, without promoting parasite killing. Azurophilic granules, identified by the granule marker myeloperoxidase, also fused with Leishmania donovaniengulfed vacuoles in human neutrophils. In addition, the azurophilic membrane marker CD63 was also detected in the vacuole surrounding the parasite, and in the fusion of azurophilic granules with the parasite-engulfed phagosome. Tertiary and specific granules, involved in vacuole acidification and superoxide anion generation, hardly fused with Leishmania-containing phagosomes. L. major interaction with neutrophils did not elicit production of reactive oxygen species or mobilization of tertiary and specific granules. By using immunogold electron microscopy approaches in the engulfment of L. major and L. donovani by human neutrophils, we did not find a significant contribution of endoplasmic reticulum to the formation of Leishmania-containing vacuoles. Live Leishmania parasites were required to be optimally internalized by neutrophils. Our data suggest that Leishmania promastigotes modulate their uptake by neutrophils, and regulate granule fusion processes in a rather selective way to favor parasite survival in human neutrophils.

show abstract

“…Phagosomal acidification has a key role in degradation of phagocytosed bacterial cells by mammalian macrophages (Downey et al 1999;Styrt and Klempner 1988). This process can be inhibited by neutralising agents such as ammonium chloride as well as inhibitors such as bafilomycin A and monensin.…”

Section: Discussionmentioning

confidence: 99%

Mechanism involved in phagocytosis and killing of Listeria monocytogenes by Acanthamoeba polyphaga

2009

View full text Add to dashboard Cite

Intra-cellular pathogen, Listeria monocytogenes, is capable of invasion and survival within mammalian cells. However, Acanthamoeba polyphaga trophozoites phagocytose and rapidly degrade Listeria cells. In order to provide more information on amoeba phagocytosis and killing mechanisms, this study used several inhibitor agents known to affect the phagocytosis and killing of bacteria by eukaryotes. Amoebae were pre-treated with mannose, cytochalasin D, wortmannin, suramin, ammonium chloride, bafilomycin A and monensin followed by co-culture with bacteria. Phagocytosis and killing of bacterial cells by amoeba trophozoites was assessed using plate counting methods and microscopy. The data presented indicates that actin polymerisation and cytoskeletal rearrangement are involved in phagocytosis of L. monocytogenes cells by A. polyphaga trophozoites. Further, both phagosomal acidification and phagosome-lysosome fusion are involved in killing and degradation of L. monocytogenes cells by A. polyphaga. However, the mannose-binding protein receptor does not play an important role in uptake of bacteria by amoeba trophozoites. In conclusion, this data reveals the similar principles of molecular mechanisms used by different types of eukaryotes in uptake and killing of bacteria.

show abstract

Effects of pH on killing of Staphylococcus aureus and Escherichia coli by constituents of the neutrophil phagolysosome

Cited by 12 publications

References 15 publications

Intracellular fate of strains of Escherichia coli isolated from dairy cows with acute or chronic mastitis

Intracellular fate of strains of Escherichia coli isolated from dairy cows with acute or chronic mastitis

Selective Fusion of Azurophilic Granules with Leishmania-containing Phagosomes in Human Neutrophils

Mechanism involved in phagocytosis and killing of Listeria monocytogenes by Acanthamoeba polyphaga

Contact Info

Product

Resources

About