Recombinant Brugia malayi pepsin inhibitor (rBm33) induced monocyte function and absence of apoptotic cell death: an in vitro study
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Updated: May 23, 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
Kirthika Sreenivas1, Kamalakannan Vijayan, Subash Babu
1Centre for Biotechnology, Anna University, S.P road, Guindy, Chennai, Tamil Nadu 600025, India.
Abstract:
The effect of recombinant Brugia malayi pepsin inhibitor (rBm33) on human monocytes/macrophages has been examined using THP-1 cells. THP-1 cells stimulated with rBm33 showed enhanced levels of expression of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and diminished levels of IL-12, iNOS and anti-inflammatory cytokine (IL-10) expression suggesting the predominant features of Th1 response. Phorbol-12-myristate-13-acetate (PMA) treated THP-1 cells stimulated with rBm33 and subsequent incubation with GFP expressing Escherichia coli (E. coli) for 2 h enhanced the uptake of E. coli. Nitric oxide (NO) levels measured in the supernatants of these cultures did not show significant changes. Apoptotic studies with Peripheral Blood Mononuclear Cells (PBMCs) from normal individuals stimulated with rBm33 did not induce apoptosis of monocytes or lymphocytes. These observations suggest that rBm33 stimulates macrophages to induce Th1 response and does not promote apoptosis.
Insights
Recombinant Brugia malayi pepsin inhibitor (rBm33) stimulates human macrophages to promote a Th1 immune response. This immune modulator enhances cytokine expression and bacterial uptake without inducing apoptosis in immune cells.
Area of Science:
- Immunology
- Molecular Biology
Background:
- The Brugia malayi pepsin inhibitor (Bm33) is a potential target for filariasis treatment.
- Understanding the immunomodulatory effects of Bm33 on host immune cells is crucial for vaccine development.
Purpose of the Study:
- To investigate the effect of recombinant Bm33 (rBm33) on human monocyte/macrophage immune responses.
- To assess the impact of rBm33 on cytokine production, phagocytosis, and apoptosis.
Main Methods:
- THP-1 cells were stimulated with rBm33.
- Cytokine expression (IL-1β, TNF-α, IL-6, IL-12, IL-10) and inducible nitric oxide synthase (iNOS) levels were measured.
- Phagocytosis of GFP-expressing Escherichia coli was assessed.
- Apoptosis assays were performed on Peripheral Blood Mononuclear Cells (PBMCs).
Main Results:
- rBm33 stimulation led to increased pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and decreased IL-12, iNOS, and IL-10 expression, indicating a Th1-biased response.
- rBm33 enhanced the uptake of E. coli by macrophages.
- No significant changes in nitric oxide (NO) levels were observed.
- rBm33 did not induce apoptosis in monocytes or lymphocytes from normal PBMCs.
Conclusions:
- rBm33 acts as an immunomodulator, stimulating macrophages to induce a Th1 immune response.
- rBm33 promotes phagocytosis and does not trigger apoptosis, suggesting its potential as a therapeutic or vaccine adjuvant.
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