Antibodies from chlamydia-infected individuals facilitate phagocytosis via Fc receptors

Author:

Hybiske Kevin1ORCID,Paktinat Shahrokh2,Newman Katherine1,Patton Dorothy2,Khosropour Christine3,Roxby Alison C.45,Mugo Nelly R.56,Oluoch Lynda6,Ngure Kenneth57,Suchland Robert4,Hladik Florian28ORCID,Vojtech Lucia2ORCID

Affiliation:

1. Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington, USA

2. Department of Obstetrics and Gynecology, University of Washington, Seattle, Washington, USA

3. Department of Epidemiology, University of Washington, Seattle, Washington, USA

4. Department of Medicine, University of Washington, Seattle, Washington, USA

5. Department of Global Health, University of Washington, Seattle, Washington, USA

6. Centre for Clinical Research, Kenya Medical Research Institute, Nairobi, Kenya

7. School of Public Health, Jomo Kenyatta University of Agriculture and Technology, Nairobi, Kenya

8. Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA

Abstract

ABSTRACT Non-neutralizing functions of antibodies, including phagocytosis, may play a role in Chlamydia trachomatis (CT) infection, but these functions have not been studied and assays are lacking. We utilized a flow-cytometry-based assay to determine whether serum samples from a well-characterized cohort of CT-infected and naïve control individuals enhanced phagocytosis via Fc-receptor-expressing THP-1 cells, and whether this activity correlated with antibody titers. Fc-receptor-mediated phagocytosis was detected only in CT+ donors. Phagocytosis generally did not correlate well with antibody titer. In addition, we found that complement from both CT+ and negative individuals enhanced phagocytosis of CT into primary neutrophils. These results suggest that anti-CT antibodies can have functions that are not reflected by titer. This method could be used to quantitively measure Fc-receptor-mediated function of anti-CT antibodies or complement activity and could reveal new immune correlates of protection.

Funder

University of Washington Royalty Research Fund

HHS | NIH | National Institute of Allergy and Infectious Diseases

HHS | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development

UW | Center for AIDS Research, University of Washington

Publisher

American Society for Microbiology

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