Abstract
In human pathological conditions, the acidification of local environment is a frequent feature, such as tumor and inflammation. As the pH of microenvironment alters, the functions of immune cells are about to change. It makes the extracellular acidification a key modulator of innate immunity. Here we detected the impact of extracellular acidification on neutrophil apoptosis and functions, including cell death, respiratory burst, migration and phagocytosis. As a result, we found that under the acid environment, neutrophil apoptosis delayed, respiratory burst inhibited, polarization augmented, chemotaxis differed, endocytosis enhanced and bacteria killing suppressed. These findings suggested that extracellular acidification acts as a key regulator of neutrophil apoptosis and functions.
MeSH terms
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Actins / genetics
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Actins / immunology
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Apoptosis / drug effects
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Apoptosis / immunology*
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Caspase 3 / genetics
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Caspase 3 / immunology
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Chemotaxis / drug effects
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Chemotaxis / immunology*
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Escherichia coli / immunology
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Gene Expression Regulation
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Humans
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Hydrogen-Ion Concentration
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Immunity, Innate
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N-Formylmethionine Leucyl-Phenylalanine / pharmacology
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Neutrophils / cytology
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Neutrophils / drug effects
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Neutrophils / immunology*
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Phagocytosis / drug effects
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Phosphorylation
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Primary Cell Culture
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / immunology
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Reactive Oxygen Species / immunology
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Reactive Oxygen Species / metabolism
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Respiratory Burst / drug effects
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Respiratory Burst / immunology*
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Signal Transduction
Substances
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Actins
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Reactive Oxygen Species
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N-Formylmethionine Leucyl-Phenylalanine
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Proto-Oncogene Proteins c-akt
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Caspase 3
Grants and funding
The authors have no support or funding to report.