Bactericidal activity of a monocytic cell line (THP-1) against common respiratory tract bacterial pathogens is depressed after infection with respiratory syncytial virus
Mw. Raza et al., Bactericidal activity of a monocytic cell line (THP-1) against common respiratory tract bacterial pathogens is depressed after infection with respiratory syncytial virus, J MED MICRO, 49(3), 2000, pp. 227-233
Non-typable Haemophilus influenzae, Streptococcus pneumoniae, Moraxella cat
arrhalis and respiratory syncytial virus (RSV) are commonly isolated from p
atients during the course of chronic obstructive pulmonary disease (COPD).
Earlier studies found that virus infection enhanced binding of bacterial re
spiratory pathogens to epithelial cells in vitro. The objective of the pres
ent study was to assess the effect of RSV infection of a human monocytic ce
ll line on bactericidal activity and cytokine production in response to the
se bacterial respiratory pathogens. The effect of RSV infection on binding,
uptake and intracellular killing of bacteria by a human monocytic leukaemi
a cell line, THP-1, was assessed. Cell culture supernates were examined wit
h a mouse fibroblast cell assay for tumour necrosis factor-alpha (TNF-alpha
) bioactivity. Expression of CD14, CD11a, CD18, CD15 and CD29 on uninfected
and RSV-infected THP-1 cells was assessed by flow cytometry in relation to
differences in bacterial binding. RSV infection of THP-1 cells significant
ly decreased their ability to bind and kill bacteria. Compared with uninfec
ted cells, fewer bacteria bound to RSV-infected THP-1 cells and the surface
antigens that have been reported to bind bacteria were expressed at lower
levels on RSV-infected cells. RSV-infected cells incubated with bacteria ex
hibited less TNF-alpha bioactivity than uninfected cell incubated with bact
eria. The results elucidate some of the mechanisms involved in the increase
d susceptibility of virus-infected patients to secondary bacterial infectio
n. Reduced bacterial killing by virus-infected monocytes might contribute t
o reduced clearance of bacteria from the respiratory tract and damage elici
ted by the bacteria or cytokine response in COPD patients.