Effect of Lipopolysaccharide and Muramyl Dipeptide on Apoptosis of Bovine Mammary Gland Lymphocytes.

Petr Slama,Shubhadeep Roychoudhury,Kazuhiro Kimura,Yoshio Kiku,Eliska Kabourkova,Jong-Young Kwak,Andrea Roztocilova,Lucie Kratochvilova,Vladimir Tancin,Zbysek Sladek,Michal Uhrincat,Roman Konecny,Ales Pavlik,Monika Zouharova,Kristina Kharkevich,Atsushi Watanabe,Terezie Zavadilova

doi:10.3390/ani10060990

Abstract

The aim of this study was to evaluate whether apoptosis of lymphocytes is modulated by stimulation by lipopolysaccharide (LPS) of Escherichia coli or muramyl dipeptide (MDP). Cell populations were obtained by lavaging of the mammary glands 24, 48, 72, and 168 hours following intramammary induced inflammation. The portion of apoptotic lymphocytes peaked at 48 hours after treatment with LPS or MDP. The analysis of CD44 expression of the same cell populations showed a higher percentage of CD44-positive lymphocytes 24- and 48-hours following induction of inflammation by LPS or MDP. The results demonstrate that during both experimental infection of bovine mammary glands with LPS or MDP, apoptosis of lymphocytes was induced in the initial phase of the inflammatory response and CD44 was also overexpressed at the beginning of inflammation. These data suggest a connection of lymphocyte apoptosis with the expression of CD44 receptors.

Highlights

Bacteria are the most important pathogens which are able to cause inflammation of the mammary gland
The inflammatory response was induced by LPS or muramyl dipeptide (MDP)
We noticed that LPS elicited an influx of leukocytes, especially neutrophils (Table 2), more intensively than MDP

Summary

Introduction

Bacteria are the most important pathogens which are able to cause inflammation of the mammary gland (mastitis). In the group of major Gram-positive bacteria, which are able to cause bovine mastitis, there are two important pathogens causing a lot of inflammation of mammary glands: Staphylococcus aureus and Streptococcus uberis [6]. Their pathogenicity is given by their special mechanisms to avoid direct elimination by immune cells. Str. uberis very “cleverly” use the Streptococcus uberis adhesion molecule (SUAM) to internalize into epithelial cells [8,9,10,11,12] These bacteria are hidden inside epithelial cells without causing any other physiological problem. The specific immune response has to play a role of eradication of these antigens

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