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Elizabethkingia anophelis , an emerging pathogen, inhibits RAW 264.7 macrophage function
Author(s) -
Mayura I. Putu Bayu,
Gotoh Kazuyoshi,
Nishimura Hayato,
Nakai Erina,
Mima Takehiko,
Yamamoto Yumiko,
Yokota Kenji,
Matsushita Osamu
Publication year - 2021
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12888
Subject(s) - biology , microbiology and biotechnology , phagocytosis , macrophage , pathogen , phenotype , cell culture , cytotoxicity , gene , genetics , in vitro
Abstract 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.