DEPRESSED PHAGOCYTOSIS AND OXIDATIVE BURST IN POLYMORPHONUCLEAR LEUKOCYTES FROM INDIVIDUALS WITH PULMONARY TUBERCULOSIS WITH OR WITHOUT HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION
S. Shalekoff et al., DEPRESSED PHAGOCYTOSIS AND OXIDATIVE BURST IN POLYMORPHONUCLEAR LEUKOCYTES FROM INDIVIDUALS WITH PULMONARY TUBERCULOSIS WITH OR WITHOUT HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION, Clinical and diagnostic laboratory immunology, 5(1), 1998, pp. 41-44
Phagocytosis and oxidative burst in whole-blood granulocytes were asse
ssed by flow cytometry with Phagotest and Bursttest kits, respectively
. Seventy individuals were included in this study: 15 healthy, normal
donors, 18 human immunodeficiency virus (HIV) type 1 (HIV-1)-seroposit
ive patients, 19 patients with pulmonary tuberculosis (TB), and 18 pat
ients co-infected with Mycobacterium tuberculosis and HIV-1 (TB-HIV).
Granulocyte phagocytosis was assessed by incubating whole blood with f
luorescence-labelled Escherichia coli and measuring the proportion of
granulocytes with ingested bacteria and the capacity (fluorescence int
ensity) of each cell to phagocytose E. coli. The percentage of granulo
cytes converting nonfluorescent dihydrorhodamine to fluorescent rhodam
ine 123 on production of reactive oxygen intermediates (ROIs) and the
mean channel shift were assessed as a measure of oxidative burst. No d
ifferences in the proportion of granulocytes that were capable of phag
ocytosing or producing ROIs in response to E. coli were observed betwe
en any of the study groups. Phagocytosis was significantly enhanced in
granulocytes from HIV-1-infected individuals. On the other hand, gran
ulocytes from individuals infected with M. tuberculosis alone or in co
mbination with HIV-1 had a significantly reduced capacity to phagocyto
se E. coli and to produce ROIs in response to E. coli as an agonist. T
hese results provide evidence that granulocytes from individuals with
pulmonary TB with or, without concomitant infection with HIV-1 have an
impaired ability to phagocytose and to undergo oxidative burst, possi
bly contributing to the enhanced susceptibility to opportunistic infec
tions in these patients.