Regulation of cytoplasmic pH in phagocytic cell function and dysfunction.

Abstract:

:To ensure effective antimicrobial or tumouricidal function, phagocytic cells must maintain their cytoplasmic pH (pHi) at a level conductive to optimal intracellular enzyme activity. The mechanisms by which neutrophils and macrophages regulate their cytoplasmic pH include bicarbonate-independent ion transport systems, most notably the Na+/H+ exchanger, and bicarbonate-dependent ion transport systems, which can be subdivided into the cation-independent and Na(+)-dependent forms of chloride/bicarbonate exchange. In addition, macrophages have been shown to recover from intracellular acid loading by means of an ATP-dependent proton extrusion mechanism, which has the characteristics of a vacuolar-type H+ ATPase. In the microenvironment typically associated with abscesses, the low extracellular pH and the presence of short chain fatty acid by-products of bacterial metabolism tend to induce cytoplasmic acid loading. In this setting, the ability of the various pHi regulatory mechanisms to protect pHi may be overcome, leading to cytoplasmic acidification. Several investigators have shown that cytoplasmic acidification impairs the ability of neutrophils to migrate in response to chemotactic stimuli, and also impairs their ability to generate a respiratory burst, thus inhibiting the release of toxic oxygen radicals. This may result in the inability of phagocytes to effect complete abscess resolution.

journal_name

Clin Biochem

journal_title

Clinical biochemistry

authors

Grinstein S,Swallow CJ,Rotstein OD

doi

10.1016/0009-9120(91)80014-t

subject

Has Abstract

pub_date

1991-06-01 00:00:00

pages

241-7

issue

3

eissn

0009-9120

issn

1873-2933

pii

0009-9120(91)80014-T

journal_volume

24

pub_type

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