Effects of perfluorooctane sulfonate (PFOS) exposure on markers of inflammation in female B6C3F1 mice

Abstract

Perfluorooctane sulfonate (PFOS; 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-1-octanesulfonic acid) has been reported to alter humoral immune functions, but inflammatory processes following PFOS exposure have not been fully characterized. Therefore, the current study, assessed TNF-α and IL-6 concentrations in serum and peritoneal lavage fluid, numbers of splenoctyes expressing intracellular TNF-α, IL-6, IL-10 or IL-1, and ex vivo TNF-α and IL-6 production by peritoneal macrophages following either in vivo or in vitro LPS exposure. Adult female B6C3F1 mice were exposed orally for 28 days to 0, 1, 3, or 300 mg PFOS/kg total administered dose [TAD] (e.g., 0, 0.0331, 0.0993 or 9.93 mg/kg/day). Body and spleen masses were significantly reduced in the highest PFOS treatment group compared to the control group, whereas liver mass was significantly increased. Serum TNF-α levels were significantly decreased following exposure to 1 mg PFOS/kg TAD as compared to controls, while serum IL-6 levels were increased. IL-6 concentrations in peritoneal lavage fluid decreased with increasing dose. PFOS treatment did not alter numbers of splenocytes expressing intracellular levels of TNF-α, IL-10 or IL-1. Numbers of splenocytes expressing intracellular levels of IL-6 were significantly decreased in the 3 mg/kg treatment as compared to controls. Overall, these data suggest that PFOS exposure can alter some inflammatory processes, which could potentially lead to misdirected inflammatory responses.

Keywords:

• PFOS
• inflammation
• IL-6
• TNFα
• cytokines
• immune
• macrophages

Acknowledgments

The authors would like to thank Erin Driscoll, Dr. Gary Gilkeson, and Jackie EuDaly for their assistance. The authors thank Dr. James A. Cook for discussions and inflammation protocols. The authors also thank the following reviewers for their critical review of the manuscript: Drs. Mike Twiner, Malcolm Meaburn, and Natasha Henry. The research described in this paper has not been subject to the U.S. Food and Drug Administration (FDA) peer and administrative review and therefore does not reflect the views of the FDA; nor does the mention of trade names or commercial products constitute endorsement or recommendation of use by FDA.

This publication does not constitute an endorsement of any commercial product or intend to be an opinion beyond scientific or other results obtained by the National Oceanic and Atmospheric Administration (NOAA). No reference shall be made to NOAA, or this publication furnished by NOAA, to any advertising or sales promotion which would indicate or imply that NOAA recommends or endorses any proprietary product mentioned herein, or which has as its purpose an interest to cause the advertised product to be used or purchased because of this publication. The project was funded in part by the National Oceanic and Atmospheric Administration/National Ocean Service/Center for Coastal Environmental Health and Biomolecular Research and internal university funding. The authors have no conflict of interest to declare.