TY - JOUR
T1 - Elizabethkingia anophelis, an emerging pathogen, inhibits RAW 264.7 macrophage function
AU - Mayura, I. Putu Bayu
AU - Gotoh, Kazuyoshi
AU - Nishimura, Hayato
AU - Nakai, Erina
AU - Mima, Takehiko
AU - Yamamoto, Yumiko
AU - Yokota, Kenji
AU - Matsushita, Osamu
N1 - Funding Information:
We thank Yusuke Takahashi for his helpful comments and discussion. This study did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Publisher Copyright:
© 2021 The Societies and John Wiley & Sons Australia, Ltd.
PY - 2021/8
Y1 - 2021/8
N2 - Elizabethkingia anophelis is a pathogen that can cause a life-threatening infection in immunocompromised patients. The first case of E. anophelis infection was reported in 2013; subsequently, an increase in its incidence has been reported globally. Additionally, a mortality rate of more than 30% was observed in the US outbreak of 2015. To date, the pathogenic mechanisms underlying E. anophelis infection, such as toxin production, remain unclear. Since tissue macrophages act as the first line of defense against pathogens, in the present study the interactions between E. anophelis and a macrophage-like cell line RAW 264.7 were examined. Although E. anophelis showed no cytotoxicity toward RAW 264.7 macrophages, the infection inhibited LPS-induced morphological changes and activation of differentiation markers for the polarization of RAW 264.7 macrophages toward an M1-like phenotype. However, when the cell contact was restricted using Transwell inserts or bacterial culture supernatants were used instead of live bacteria, no such inhibition was observed. Moreover, it was shown that E. anophelis evaded phagocytosis. Overall, the results suggest that E. anophelis infection inhibits the differentiation of RAW 264.7 macrophages to a pro-inflammatory phenotype in a contact-dependent manner.
AB - Elizabethkingia anophelis is a pathogen that can cause a life-threatening infection in immunocompromised patients. The first case of E. anophelis infection was reported in 2013; subsequently, an increase in its incidence has been reported globally. Additionally, a mortality rate of more than 30% was observed in the US outbreak of 2015. To date, the pathogenic mechanisms underlying E. anophelis infection, such as toxin production, remain unclear. Since tissue macrophages act as the first line of defense against pathogens, in the present study the interactions between E. anophelis and a macrophage-like cell line RAW 264.7 were examined. Although E. anophelis showed no cytotoxicity toward RAW 264.7 macrophages, the infection inhibited LPS-induced morphological changes and activation of differentiation markers for the polarization of RAW 264.7 macrophages toward an M1-like phenotype. However, when the cell contact was restricted using Transwell inserts or bacterial culture supernatants were used instead of live bacteria, no such inhibition was observed. Moreover, it was shown that E. anophelis evaded phagocytosis. Overall, the results suggest that E. anophelis infection inhibits the differentiation of RAW 264.7 macrophages to a pro-inflammatory phenotype in a contact-dependent manner.
KW - Elizabethkingia anophelis
KW - RAW 264.7
KW - differentiation
KW - phagocytosis
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U2 - 10.1111/1348-0421.12888
DO - 10.1111/1348-0421.12888
M3 - Article
C2 - 33913521
AN - SCOPUS:85110235433
SN - 0385-5600
VL - 65
SP - 317
EP - 324
JO - Microbiology and Immunology
JF - Microbiology and Immunology
IS - 8
ER -