TY - JOUR
T1 - NKT cells play a limited role in the neutrophilic inflammatory responses and host defense to pulmonary infection with Pseudomonas aeruginosa
AU - Kinjo, Takeshi
AU - Nakamatsu, Masashi
AU - Nakasone, Chikara
AU - Yamamoto, Natsuo
AU - Kinjo, Yuki
AU - Miyagi, Kazuya
AU - Uezu, Kaori
AU - Nakamura, Kiwamu
AU - Higa, Futoshi
AU - Tateyama, Masao
AU - Takeda, Kazuyoshi
AU - Nakayama, Toshinori
AU - Taniguchi, Masaru
AU - Kaku, Mitsuo
AU - Fujita, Jiro
AU - Kawakami, Kazuyoshi
N1 - Funding Information:
The authors thank Dr. Luc Van Kaer (Vanderbilt University Graduate School of Medicine, Nashville, TN) for a kind gift of CD1dKO mice. This work was supported in part by a Grant-in-Aid for Science Research (C) (16590366) from the Ministry of Education, Science and Culture and Tohoku University 21 st COE program “CRESCENDO”.
PY - 2006/10
Y1 - 2006/10
N2 - CD1d-restricted NKT cells are reported to play a critical role in the host defense to pulmonary infection with Pseudomonas aeruginosa. However, the contribution of a major subset expressing a Vα14-Jα18 gene segment remains unclear. In the present study, we re-evaluated the role of NKT cells in the neutrophilic inflammatory responses and host defense to this infection using mice genetically lacking Jα18 or CD1d (Jα18KO or CD1dKO mice). These mice cleared the bacteria in lungs at a comparable level to wild-type (WT) mice. There was no significant difference in the local neutrophilic responses, as shown by neutrophil counts and synthesis of MIP-2 and TNF-α, in either KO mice from those in WT mice. Administration of α-galactosylceramide, a specific activator of Vα14+ NKT cells, failed to promote the bacterial clearance and neutrophilic responses, although the same treatment increased the synthesis of IFN-γ, suggesting the involvement of this cytokine downstream of NKT cells. In agreement against this notion, these responses were not further enhanced by administration of recombinant IFN-γ in the infected Jα18KO mice. Our data indicate that NKT cells play a limited role in the development of neutrophilic inflammatory responses and host defense to pulmonary infection with P. aeruginosa.
AB - CD1d-restricted NKT cells are reported to play a critical role in the host defense to pulmonary infection with Pseudomonas aeruginosa. However, the contribution of a major subset expressing a Vα14-Jα18 gene segment remains unclear. In the present study, we re-evaluated the role of NKT cells in the neutrophilic inflammatory responses and host defense to this infection using mice genetically lacking Jα18 or CD1d (Jα18KO or CD1dKO mice). These mice cleared the bacteria in lungs at a comparable level to wild-type (WT) mice. There was no significant difference in the local neutrophilic responses, as shown by neutrophil counts and synthesis of MIP-2 and TNF-α, in either KO mice from those in WT mice. Administration of α-galactosylceramide, a specific activator of Vα14+ NKT cells, failed to promote the bacterial clearance and neutrophilic responses, although the same treatment increased the synthesis of IFN-γ, suggesting the involvement of this cytokine downstream of NKT cells. In agreement against this notion, these responses were not further enhanced by administration of recombinant IFN-γ in the infected Jα18KO mice. Our data indicate that NKT cells play a limited role in the development of neutrophilic inflammatory responses and host defense to pulmonary infection with P. aeruginosa.
KW - Host defense
KW - MIP-2
KW - NKT cells
KW - Neutrophils
KW - Pseudomonas aeruginosa
KW - Streptococcus pneumoniae
KW - TNF-α
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U2 - 10.1016/j.micinf.2006.07.016
DO - 10.1016/j.micinf.2006.07.016
M3 - Article
C2 - 16979364
AN - SCOPUS:33751079376
VL - 8
SP - 2679
EP - 2685
JO - Microbes and Infection
JF - Microbes and Infection
SN - 1286-4579
IS - 12-13
ER -