Modifying Mycoplasma-infected lung immune cells through an intriguing interplay of BCG priming and peritoneal inflammation

Abstract

Inflammation is a redistribution of immune cells, providing a more efficient elimination of the inflammatory offense. However, it is not limited to local microenvironment. In this study, the interaction of the effect of BCG priming and peritoneal inflammation on the remote inflammatory milieu of infected lung was investigated. Young male AO rats infected with Mycoplasma spp. were s.c. injected with BCG (3x105 CFU) or saline, and 7 days later received an i.p. injection of 7ml of thioglycollate (TG) or saline. Up to 7 days after TG injection, a broncho-alveolar lavage (BAL) was performed, and cells were analysed for their surface marker expression and NO production. Infected rats had a high percentage of HIS48HiCD11bHi neutrophils. BCG priming didn’t alter BAL cells phenotype, while TG injection increased the proportion of MHCII+CD11blow activated alveolar macrophages (aAMFs) on day 7. However, the BCG+TG group showed significant changes – percentage of HIS48HiCD11bHi neutrophils decreased from day 3, the share of aAMFs increased from day 5 and the share of MHCII+CD11b-AMFs increased on days 3-5. However, the percentage of B220+FSClow B lymphocytes were increased from day 1. Production of NO from BAL fluid cells was low in all groups. We conclude that BCG vaccination likely increased the number of circulating B lymphocytes, while TG-induced peritoneal inflammation potentially prevented their entry into the peritoneal cavity, forcing them into permissive tissues, such as lungs.