Acidosis Improves Uptake of Antigens and MHC Class I-Restricted Presentation by Dendritic Cells

Vermeulen, Mónica; Giordano, Mirta; Trevani, Analía Silvina; Sedlik, Christine; Gamberale, Romina; Fernández-Calotti, Paula; Salamone, Gabriela; Raiden, Silvina; Sanjurjo, Julieta; Geffner, Jorge

doi:10.4049/jimmunol.172.5.3196

Cited by 115 publications

(99 citation statements)

References 66 publications

(92 reference statements)

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“…We have reported previously that extracellular acidosis induces the activation of both neutrophils (20) and dendritic cells (21,22), supporting the idea that low pH values can be recognized by immune cells as a danger signal favoring the initiation of innate and adaptive immune response. Interestingly, previous studies have also shown that acidosis activates the alternative pathway of complement (23)(24)(25), supporting the hypothesis that two of the most important pathways of innate immunity are activated by protons.…”

mentioning

confidence: 77%

“…Surprisingly, there are few studies directed at analyzing the effect of extracellular acidosis on the immune response. We have reported previously that extracellular acidosis induces the activation of neutrophils (20) and dendritic cells (21), suggesting that acidosis acts FIGURE 6. Acidosis improves the acquisition of OVA by neutrophils for MHC class I-restricted presentation.…”

Section: Discussionmentioning

confidence: 99%

“…We have shown previously that extracellular acidosis not only increases endocytosis but also improves acquisition of extracellular Ags by dendritic cells for MHC class I-restricted presentation (21). This pathway, called cross-presentation, allows the display of exogenous Ags in the context of MHC class I molecules (43,44).…”

Section: Extracellular Acidosis Improves Mhc Class I-restricted Ag Prmentioning

confidence: 99%

“…We have shown previously that acidosis improves the endocytic capacity of mouse dendritic cells (21). Taking this finding into account, to further characterize the impact of extracellular acidosis on neutrophil function we performed another set of experiments to establish whether acidosis was also able to stimulate endocytosis by human neutrophils.…”

Section: Extracellular Acidosis Increases Endocytosis By Human Neutromentioning

confidence: 99%

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Extracellular Acidosis Induces Neutrophil Activation by a Mechanism Dependent on Activation of Phosphatidylinositol 3-Kinase/Akt and ERK Pathways

Martínez

Vermeulen

Trevani

et al. 2006

The Journal of Immunology

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128

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Inflammation in peripheral tissues is usually associated with the development of local acidosis; however, there are few studies aimed at analyzing the influence of acidosis on immune cells. We have shown previously that extracellular acidosis triggers human neutrophil activation, inducing a transient increase in intracellular Ca2+ concentration, a shape change response, the up-regulation of CD18 expression, and a delay of apoptosis. In this study, we analyzed the signaling pathways responsible for neutrophil activation. We found that acidosis triggers the phosphorylation of Akt (the main downstream target of PI3K) and ERK MAPK, but not that of p38 and JNK MAPK. No degradation of IκB was observed, supporting the hypothesis that NF-κB is not activated under acidosis. Inhibition of PI3K by wortmannin or LY294002 markedly decreased the shape change response and the induction of Ca2+ transients triggered by acidosis, whereas the inhibition of MEK by PD98059 or U0126 significantly inhibited the shape change response without affecting the induction of Ca2+ transients. We also found that acidosis not only induces a shape change response and the induction of Ca2+ transients in human neutrophils but also stimulates the endocytosis of FITC-OVA and FITC-dextran. Stimulation of endocytosis was partially prevented by inhibitors of PI3K and MEK. Together, our results support the notion that the stimulation of human neutrophils by extracellular acidosis is dependent on the activation of PI3K/Akt and ERK pathways. Of note, using mouse peritoneal neutrophils we observed that the enhancement of endocytosis induced by acidosis was associated with an improved ability to present extracellular Ags through a MHC class I-restricted pathway.

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mentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Extracellular Acidosis Improves Mhc Class I-restricted Ag Prmentioning

confidence: 99%

Section: Extracellular Acidosis Increases Endocytosis By Human Neutromentioning

confidence: 99%

See 2 more Smart Citations

Extracellular Acidosis Induces Neutrophil Activation by a Mechanism Dependent on Activation of Phosphatidylinositol 3-Kinase/Akt and ERK Pathways

Martínez

Vermeulen

Trevani

et al. 2006

The Journal of Immunology

Self Cite

128

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“…The study sought understanding of the molecular mechanisms by which DCs detect changes in extracellular pH in a sensitive manner (2,3).…”

mentioning

confidence: 99%

Comment on “Acid-Sensing Ion Channels Contribute to the Effect of Acidosis on the Function of Dendritic Cells”

Yuan

Zhao

et al. 2011

The Journal of Immunology

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Preparation and evaluation of parathyroid hormone incorporated CaP coating via a biomimetic method

Wei

2011

J Biomed Mater Res

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Parathyroid hormone (PTH) is a potent bone growth stimulator used for osteoporosis treatment. However, the inconvenience of daily administration and side effect of systemic exposure severely limit its use in clinical applications. Local, controlled delivery is a promising approach which can maintain therapeutic concentration locally for a long period. In this study, PTH was incorporated into a biomimetic calcium phosphate (CaP) coating via a coprecipitation process in a modified simulated body fluid (m-SBF). It was found that PTH was successfully incorporated into biomimetic CaP coating on titanium surface with a high incorporation efficiency. The incorporation of PTH into coatings had significantly changed the coating morphology, but the composition of the coating remained unchanged. Localized release of PTH had occurred in vitro, and was accompanied with partial dissolution of CaP coatings. Cell culture study demonstrated that the PTH released from CaP coatings fully retained its bioactivity. It had improved substantially MC3T3-E1 cell proliferation but slightly delayed the expression of alkaline phosphatase (ALP) of the cells. In summary, our results have shown that CaP coatings incorporated with PTH may be a promising approach for osteoporosis and other bone-related disease treatment in the future.

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Acidosis Improves Uptake of Antigens and MHC Class I-Restricted Presentation by Dendritic Cells

Cited by 115 publications

References 66 publications

Extracellular Acidosis Induces Neutrophil Activation by a Mechanism Dependent on Activation of Phosphatidylinositol 3-Kinase/Akt and ERK Pathways

Extracellular Acidosis Induces Neutrophil Activation by a Mechanism Dependent on Activation of Phosphatidylinositol 3-Kinase/Akt and ERK Pathways

Comment on “Acid-Sensing Ion Channels Contribute to the Effect of Acidosis on the Function of Dendritic Cells”

Preparation and evaluation of parathyroid hormone incorporated CaP coating via a biomimetic method

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