Lm. Maglova et al., HUMAN CYTOMEGALOVIRUS-INFECTION STIMULATES CL- HCO3- EXCHANGER ACTIVITY IN HUMAN FIBROBLASTS/, American journal of physiology. Cell physiology, 44(2), 1998, pp. 515-526
The effects of human cytomegalovirus (HCMV) infection on Cl-/HCO3- exc
hanger activity in human lung fibroblasts (MRC-5 cells) were studied u
sing fluorescent, ion-sensitive dyes. The intracellular pH (pH(i)) of
mock- and HCMV-infected cells bathed in a solution containing 5% CO2-2
5 mM HCO3- were nearly the same. However, replacement of external Cl-
with gluconate caused an H2DIDS-inhibitable (100 mu M) increase in the
pH(i) of HCMV-infected cells but not in mock-infected cells. Continuo
us exposure to hyperosmotic external media containing CO2/HCO3- caused
the pH(i) of both cell types to increase. The pH(i) remained elevated
in mock-infected cells. However, in HCMV-infected cells, the pH(i) pe
aked and then recovered toward control values. This pH(i) recovery pha
se was completely blocked by 100 mu M H2DIDS. In the presence of CO2/H
CO3-, there was an H2DIDS-sensitive component of net Cl- efflux (exter
nal Cl- was substituted with gluconate) that was less in mock- than in
HCMV-infected cells. When nitrate was substituted for external Cl- (i
n the nominal absence of CO2/HCO3-), the H2DIDS-sensitive net Cl- effl
ux was much greater from HCMV- than from mock-infected cells. In mock-
infected cells, H2DIDS-sensitive, net Cl- efflux decreased as pH(i) in
creased, whereas for HCMV-infected cells, efflux increased as pH(i) in
creased. All these results are consistent with an HCMV-induced enhance
ment of Cl-/HCO3- exchanger activity.