Abstract
Background: The pathogenic mechanisms underlying influenza A(H1N1)pdm09-associated central nervous system (CNS) manifestations and pneumonia remain unclear. This study examined A(H1N1)pdm09 host responses using gene expression profiles of patients' peripheral blood. Methods: Sixteen A(H1N1)pdm09-infected children in three groups were examined: a CNS group, with convulsion and altered consciousness (n = 6); a pneumonia (Pneu) group (n = 5); and a group of infected control patients (n = 5). The signal ratios of the acute to recovery phases in CNS or Pneu were analyzed versus those of the control. Results: The CNS (619 transcripts) and Pneu (656 transcripts) groups had significantly increased signal ratios compared to the control group. Regarding the increased ratios of transcripts shown by multiple probes, contactin-associated protein-like 3 transcripts, oleoyl-ACP hydrolase transcripts, and interleukin 1 type 1 receptor were observed in CNS and Pneu. Increased ratios of prostaglandin-endoperoxide synthase 2 and α-synuclein were characteristic of CNS. Alkaline phosphatase and the Fc fragment of IgA receptor were characteristic of Pneu. Regarding enriched gene ontology terms, 'response to lipopolysaccharide', 'innate immune response', and 'intrinsic to membrane' were observed commonly in CNS and Pneu. Enriched gene ontology terms related to 'hemoglobin' and 'hemostasis' were, respectively, characteristic of CNS and Pneu. Conclusion: These symptom-associated transcripts might be some clues to the pathogenesis of the A(H1N1)pdm09 infection.
| Original language | English |
|---|---|
| Pages (from-to) | 572-577 |
| Number of pages | 6 |
| Journal | Pediatrics International |
| Volume | 55 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - Oct 2013 |
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Keywords
- central nervous system manifestations
- gene expression profile
- influenza A(H1N1)pdm09
- pneumonia
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health
Cite this
Pathogenic mechanisms of influenza A(H1N1)pdm09 infection elucidated on gene expression profiling. / Yamashita, Nobuko; Tsukahara, Hirokazu; Tsuge, Mitsuru; Nagaoka, Yoshiharu; Yashiro, Masato; Saito, Yukie; Fujii, Yosuke; Oka, Takashi; Morishima, Tsuneo.
In: Pediatrics International, Vol. 55, No. 5, 10.2013, p. 572-577.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Pathogenic mechanisms of influenza A(H1N1)pdm09 infection elucidated on gene expression profiling
AU - Yamashita, Nobuko
AU - Tsukahara, Hirokazu
AU - Tsuge, Mitsuru
AU - Nagaoka, Yoshiharu
AU - Yashiro, Masato
AU - Saito, Yukie
AU - Fujii, Yosuke
AU - Oka, Takashi
AU - Morishima, Tsuneo
PY - 2013/10
Y1 - 2013/10
N2 - Background: The pathogenic mechanisms underlying influenza A(H1N1)pdm09-associated central nervous system (CNS) manifestations and pneumonia remain unclear. This study examined A(H1N1)pdm09 host responses using gene expression profiles of patients' peripheral blood. Methods: Sixteen A(H1N1)pdm09-infected children in three groups were examined: a CNS group, with convulsion and altered consciousness (n = 6); a pneumonia (Pneu) group (n = 5); and a group of infected control patients (n = 5). The signal ratios of the acute to recovery phases in CNS or Pneu were analyzed versus those of the control. Results: The CNS (619 transcripts) and Pneu (656 transcripts) groups had significantly increased signal ratios compared to the control group. Regarding the increased ratios of transcripts shown by multiple probes, contactin-associated protein-like 3 transcripts, oleoyl-ACP hydrolase transcripts, and interleukin 1 type 1 receptor were observed in CNS and Pneu. Increased ratios of prostaglandin-endoperoxide synthase 2 and α-synuclein were characteristic of CNS. Alkaline phosphatase and the Fc fragment of IgA receptor were characteristic of Pneu. Regarding enriched gene ontology terms, 'response to lipopolysaccharide', 'innate immune response', and 'intrinsic to membrane' were observed commonly in CNS and Pneu. Enriched gene ontology terms related to 'hemoglobin' and 'hemostasis' were, respectively, characteristic of CNS and Pneu. Conclusion: These symptom-associated transcripts might be some clues to the pathogenesis of the A(H1N1)pdm09 infection.
AB - Background: The pathogenic mechanisms underlying influenza A(H1N1)pdm09-associated central nervous system (CNS) manifestations and pneumonia remain unclear. This study examined A(H1N1)pdm09 host responses using gene expression profiles of patients' peripheral blood. Methods: Sixteen A(H1N1)pdm09-infected children in three groups were examined: a CNS group, with convulsion and altered consciousness (n = 6); a pneumonia (Pneu) group (n = 5); and a group of infected control patients (n = 5). The signal ratios of the acute to recovery phases in CNS or Pneu were analyzed versus those of the control. Results: The CNS (619 transcripts) and Pneu (656 transcripts) groups had significantly increased signal ratios compared to the control group. Regarding the increased ratios of transcripts shown by multiple probes, contactin-associated protein-like 3 transcripts, oleoyl-ACP hydrolase transcripts, and interleukin 1 type 1 receptor were observed in CNS and Pneu. Increased ratios of prostaglandin-endoperoxide synthase 2 and α-synuclein were characteristic of CNS. Alkaline phosphatase and the Fc fragment of IgA receptor were characteristic of Pneu. Regarding enriched gene ontology terms, 'response to lipopolysaccharide', 'innate immune response', and 'intrinsic to membrane' were observed commonly in CNS and Pneu. Enriched gene ontology terms related to 'hemoglobin' and 'hemostasis' were, respectively, characteristic of CNS and Pneu. Conclusion: These symptom-associated transcripts might be some clues to the pathogenesis of the A(H1N1)pdm09 infection.
KW - central nervous system manifestations
KW - gene expression profile
KW - influenza A(H1N1)pdm09
KW - pneumonia
UR - http://www.scopus.com/inward/record.url?scp=84886093564&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84886093564&partnerID=8YFLogxK
U2 - 10.1111/ped.12139
DO - 10.1111/ped.12139
M3 - Article
C2 - 23701225
AN - SCOPUS:84886093564
VL - 55
SP - 572
EP - 577
JO - Pediatrics International
JF - Pediatrics International
SN - 1328-8067
IS - 5
ER -