The response of adipose tissues to <i>Mycoplasma pulmonis</i> and Sendai virus infection in C57BL/6 and DBA/2 mice

Abstract

Adipose tissues in mammals are categorized into white and brown adipose tissues in which cellular morphology, cell functions, and tissue distribution are different. White adipose tissue (WAT) plays a major role in energy reservation, while brown adipose tissue (BAT) mainly relates to the thermoregulation of the body. One interesting function of adipose tissue is the response to the infection, especially the pathogens that cause pneumonia. We have previously reported that DBA/2 (D2) mice are susceptible to pathogens causing pneumonia, Mycoplasma ( M .) pulmonis and Sendai virus (SeV), whereas C57BL/6 (B6) mice are resistant to them. Furthermore, morphological alteration of mediastinal fat tissue (MFT) was seen after infection of M. pulmonis in D2 mice but not in B6 mice. In this study, we aimed to exhibit the difference in adipose tissue response in other areas, including interscapular brown adipose tissue (iBAT), inguinal white adipose tissue (ingWAT), and perigonadal WAT (perigoWAT) between resistant strain, B6 and susceptible strain, D2 after challenging them with M. pulmonis and SeV. Compared with B6 mice, D2 mice showed an increase in fat-associated lymphoid cluster in MFT, an increase in BAT in both iBAT and ingWAT after M. pulmonis and SeV infection. The results of this study indicate that pneumonia caused by M. pulmonis and SeV infection induces browning of adipocyte, suggesting that BAT plays a role in pathogen infection and inflammation.

Adipose Tissues from Human and Bat-Derived Cell Lines Support Ebola Virus Infection

“…It is also possible that the decrease in size of the lipid droplets may have resulted from lipolysis following EBOV infection, although this would less likely cause the increase in number of lipid droplets that were seen. Similar metabolic changes have been previously documented during influenza virus and Trypanosoma cruzi infection [ 16 , 39 ]. At present we do not know the mechanism by which this increase number of smaller lipid droplets from these cells occurs following EBOV infection, but is an active investigation in our lab.…”