- Introduction
- Materials and Methods
- Results
- Levels of CIC.
- Levels of classical pathway–specific complement activation fragments.
- Activation of classical and MBL pathways in patent filarial infections.
- Effect of PEG-precipitated IC from patients with filarial infection function on release of granular proteins from normal granulocytes.
- Effect of PEG-precipitated IC from patients with filariasis on production of pro-inflammatory cytokines.
- Effect of PEG-precipitated IC from patients with filariasis on PGDF, IL-8, and CXCL1/GROα.
- Discussion
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Heightened Measures of Immune Complex and Complement Function and Immune Complex–Mediated Granulocyte Activation in Human Lymphatic Filariasis
The presence of circulating immune complexes (CICs) is a characteristic feature of human lymphatic filariasis. However, the role of CICs in modulating granulocyte function and complement functional activity in filarial infection is unknown. The levels of CICs in association with complement activation in clinically asymptomatic, filarial-infected patients (INF); filarial-infected patients with overt lymphatic pathologic changes (CPDT); and uninfected controls (EN) were examined. Significantly increased levels of CICs and enhanced functional efficiency of the classical and mannose-binding lectin pathways of the complement system was observed in INF compared with CPDT and EN. Polyethylene glycol–precipitated CICs from INF and CPDT induced significantly increased granulocyte activation compared with those from EN, determined by the increased production of neutrophil granular proteins and a variety of pro-inflammatory cytokines. Thus, CIC-mediated enhanced granulocyte activation and modulation of complement function are important features of filarial infection and disease.
Author Notes
Financial support: This study was supported by the Intramural Research Program of the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health.
Disclosure: Thomas B. Nutman, and Subash Babu are government employees. This study is a government work and is in the public domain in the United States. Notwithstanding any other agreements, the National Institutes of Health reserves the right to provide the work to PubMed Central for display and use by the public, and PubMed Central may tag or modify the work consistent with its customary practices. You can establish rights outside the United States subject to a government use license. The authors have reported no conflicts of interest.
Authors' addresses: Prakash Senbagavalli and Rajamanickam Anuradha, National Institutes of Health–International Centre for Excellence in Research Facility Tuberculosis Research Centre (Indian Council of Medical Research), Chetput Chennai 600031 India, E-mails: sen.valli@gmail.com and anuradhar@trcchennai. Vadakkuppattu D. Ramanathan, Department of Clinical Pathology, Tuberculosis Research Centre (Indian Council of Medical Research), Chetput Chennai 600031, India, E-mail: vdramanathan@trcchennai.in. Vasanthapuram Kumaraswami, Department of Immunology, Tuberculosis Research Centre, (Indian Council of Medical Research), Chetput Chennai 600031 India, E-mail: kumaraswami@gmail.com. Thomas B. Nutman, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville Pike, Bethesda, MD, E-mail: tnutman@niaid.nih.gov. Subash Babu, Tuberculosis Research Centre–International Center for Excellence in Research, Clinical Monitoring Research Program, SAIC-Frederick Inc., National Institute of Allergy and Infectious Diseases, Chetpet, Chennai, India, E-mail: sbabu@mail.nih.gov.