Induction of polymorphonuclear leukocyte response by human cytomegalovirus
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Updated: Aug 8, 2026
An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Petra Jerström Skarman1, Afsar Rahbar, Xun Xie
1Department of Medicine, Center for Molecular Medicine, L8:03, Karolinska Institutet, Karolinska University Hospital, SE-171 76 Stockholm, Sweden.
Abstract:
Neutrophils are important in the defense against bacterial infections, by ingesting and killing invading microorganisms. Because of the higher incidence of bacterial infections in patients with active human cytomegalovirus (HCMV) infections, we hypothesized that HCMV-infected neutrophils were inefficient in eliminating the bacteria. Therefore, we mock infected or infected neutrophils with HCMV by contact with HCMV-infected human pulmonary artery endothelial cells. We found that HCMV infection without N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation increased the surface expression of CD11b to the same extent as fMLP stimulation of mock infected cells. Also, HCMV-infected neutrophils became more efficient in phagocytosing serum opsonized yeast particles than mock infected cells. Furthermore, we observed an increase in intracellular free calcium and chemiluminescence in HCMV-infected cells, in response to fMLP compared to fMLP-treated mock cells. We also found that apoptosis was significantly inhibited in HCMV-infected neutrophils. In conclusion, our results suggest that neutrophils become more effective in performing their effector functions when infected with HCMV. Thus, the higher incidence of bacterial infections in HCMV patients might not be due directly to a dysfunction in the neutrophils. Instead, the fact that apoptosis is inhibited may cause over-reactive neutrophils to remain in the tissues, where they will start leaking their contents, damaging the tissues and contributing to inflammatory processes.
Insights
Human cytomegalovirus (HCMV) infection enhances neutrophil functions like bacterial killing and phagocytosis. However, inhibited apoptosis in infected neutrophils may lead to tissue damage and inflammation.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Neutrophils are critical for combating bacterial infections.
- Patients with active human cytomegalovirus (HCMV) infections exhibit increased susceptibility to bacterial infections.
- The functional status of neutrophils during HCMV infection is not fully understood.
Purpose of the Study:
- To investigate the effect of HCMV infection on neutrophil functions, including bacterial phagocytosis and killing.
- To determine if HCMV infection alters neutrophil responses to stimuli like N-formyl-methionyl-leucyl-phenylalanine (fMLP).
- To assess the impact of HCMV infection on neutrophil apoptosis.
Main Methods:
- Neutrophils were mock-infected or infected with HCMV via co-culture with infected endothelial cells.
- Surface expression of CD11b was measured.
- Phagocytosis of opsonized yeast particles was assessed.
- Intracellular calcium levels and chemiluminescence were measured following fMLP stimulation.
- Apoptosis rates were determined in mock-infected and HCMV-infected neutrophils.
Main Results:
- HCMV infection increased CD11b surface expression on neutrophils, similar to fMLP stimulation.
- HCMV-infected neutrophils demonstrated enhanced phagocytosis of yeast particles.
- HCMV-infected neutrophils exhibited increased intracellular calcium and chemiluminescence responses to fMLP.
- Apoptosis was significantly inhibited in neutrophils infected with HCMV.
Conclusions:
- HCMV infection enhances neutrophil effector functions, including phagocytosis and response to stimuli.
- The increased incidence of bacterial infections in HCMV patients may not stem from neutrophil dysfunction.
- Inhibition of neutrophil apoptosis during HCMV infection could lead to prolonged neutrophil lifespan, potentially contributing to tissue damage and inflammation.
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