Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid.

Sato Kamiya,Yasuo Inoshima,Ayaka Okada,Kaori Shimizu

doi:10.3390/ani11061548

Abstract

Simple SummarySerum amyloid A (SAA) is an acute phase protein present in mammals and birds. Based on the amino acid sequence, SAA has been classified into isoforms SAA1–4 in mice. Previously, it was reported that after the stimulation with bacterial antigens, the expression of the Saa3 mRNA was induced more strongly than that of the Saa1 mRNA in mouse epithelia, including colonic and alveolar epithelial cells, indicating that SAA3 plays a role in the local response. However, the contribution of SAA3 to the local response in mouse mammary epithelium, where mastitis occurs due to bacterial infection, has not been completely determined yet. In this study, to clarify whether mouse SAA3 has a role in the defense against bacterial infection in mouse mammary epithelium, normal murine mammary gland (NMuMG) epithelial cells were stimulated with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). LPS and LTA significantly enhanced mRNA expression level of the Saa3 gene but not that of Saa1. Furthermore, LPS induced SAA3 protein expression more strongly than LTA. Our data indicate that SAA3 expression in mouse mammary epithelial cells was increased by the stimulation with bacterial antigens, suggesting that SAA3 is involved in the defense against bacterial infection in mouse mammary epithelium.In this study, to establish whether serum amyloid A (SAA) 3 plays a role in the defense against bacterial infection in mouse mammary epithelium, normal murine mammary gland (NMuMG) epithelial cells were stimulated with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). LPS and LTA significantly enhanced mRNA expression level of the Saa3 gene, whereas no significant change was observed in the Saa1 mRNA level. Furthermore, LPS induced SAA3 protein expression more strongly than LTA, whereas neither LPS nor LTA significantly affected SAA1 protein expression. These data indicate that the expression of SAA3 in mouse mammary epithelial cells was increased by the stimulation with bacterial antigens. SAA3 has been reported to stimulate neutrophils in the intestinal epithelium and increase interleukin-22 expression, which induces activation of the innate immune system and production of antibacterial proteins, such as antimicrobial peptides. Therefore, collectively, these data suggest that SAA3 is involved in the defense against bacterial infection in mouse mammary epithelium.

Highlights

Systemic amyloid A (AA) amyloidosis is a severe complication of inflammation associated with life-threatening diseases such as rheumatoid arthritis, Crohn’s disease, and gout in humans, but it is observed in other mammalian species and in birds [1,2]
It has been reported that the presence of SAA3 reduces the severity of non-bacterial infectious colitis [12]. These findings suggest that SAA3 plays a role in the prevention of bacterial infections and in the inflammation during local immunity reactions in mouse epithelium
Saa3 and lipoteichoic acid (LTA), respectively,after afterstimulation stimulationfor for 22 hh (Figure (Figure 2)

Summary

Introduction

Systemic amyloid A (AA) amyloidosis is a severe complication of inflammation associated with life-threatening diseases such as rheumatoid arthritis, Crohn’s disease, and gout in humans, but it is observed in other mammalian species and in birds [1,2]. This disease is caused by the conformational conversion of the circulating soluble precursor protein, serum amyloid A (SAA), into insoluble amyloid fibrils [3].

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