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Suppressive effects of neutrophil by S alp16‐like salivary gland proteins from I xodes persulcatus S chulze tick
Author(s) -
Hidano A.,
Konnai S.,
Yamada S.,
Githaka N.,
Isezaki M.,
Higuchi H.,
Nagahata H.,
Ito T.,
Takano A.,
Ando S.,
Kawabata H.,
Murata S.,
Ohahsi K.
Publication year - 2014
Publication title -
insect molecular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.955
H-Index - 93
eISSN - 1365-2583
pISSN - 0962-1075
DOI - 10.1111/imb.12101
Subject(s) - anaplasma phagocytophilum , ixodes persulcatus , biology , tick , ixodes scapularis , innate immune system , microbiology and biotechnology , virology , saliva , tick borne disease , pathogen , immunology , immune system , antibody , ixodidae , borrelia burgdorferi , biochemistry
Salp16, a 16‐kDa tick salivary gland protein, is known to be the molecule involved in the transmission of A naplasma phagocytophilum , an obligate intracellular pathogen causing zoonotic anaplasmosis, from its mammalian hosts to I xodes scapularis. Recently, the presence of A . phagocytophilum was documented in J apan and I xodes persulcatus was identified as one of its vectors. The purpose of this study was to identify S alp16 genes in I . persulcatus and characterize their function. Two cDNA clones encoding the S alp16 ‐like sequences were obtained from the salivary glands of fed female I . persulcatus ticks and designated S alp16 I per1 and I per2 . Gene expression analyses showed that the S alp16 I per genes were expressed specifically in the salivary glands and were up‐regulated by blood feeding. These proteins attenuated the oxidative burst of activated bovine neutrophils and inhibited their migration induced by the chemoattractant interleukin‐8 ( IL ‐8). These results demonstrate that S alp16 I per proteins contribute to the establishment of blood feeding as an immunosuppressant of neutrophil, an essential factor in innate host immunity. Further examination of the role of S alp16 I per in the transmission of pathogens, including A . phagocytophilum , will increase our understanding of the tick–host–pathogen interface.