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Concurrent nematode infection and pregnancy induce physiological responses that impair linear growth in the murine foetus

Published online by Cambridge University Press:  23 December 2009

M. R. ODIERE*
Affiliation:
Institute of Parasitology, McGill University (Macdonald Campus), 21 111 Lakeshore Road, Ste-Anne de Bellevue, QC H9X 3V9, Canada
K. G. KOSKI
Affiliation:
School of Dietetics and Human Nutrition, McGill University (Macdonald Campus), 21 111 Lakeshore Road, Ste-Anne de Bellevue, QC H9X 3V9, Canada
H. A. WEILER
Affiliation:
School of Dietetics and Human Nutrition, McGill University (Macdonald Campus), 21 111 Lakeshore Road, Ste-Anne de Bellevue, QC H9X 3V9, Canada
M. E. SCOTT
Affiliation:
Institute of Parasitology, McGill University (Macdonald Campus), 21 111 Lakeshore Road, Ste-Anne de Bellevue, QC H9X 3V9, Canada
*
*Corresponding author: Institute of Parasitology, McGill University (Macdonald Campus), 21 111 Lakeshore Road, Ste-Anne de Bellevue, QC H9X 3V9, Canada. Tel: +514 398 8382. Fax: +514 398 7857. E-mail: [email protected]

Summary

This study examined concurrent stresses of nematode infection and pregnancy using pregnant and non-pregnant CD1 mice infected 3 times with 0, 50 or 100 Heligmosomoides bakeri larvae. Physiological, energetic, immunological and skeletal responses were measured in maternal and foetal compartments. Resting metabolic rate (RMR) was elevated by pregnancy, but not by the trickle infection. Energy demands during pregnancy were met through increased food intake and fat utilization whereas mice lowered their body temperature during infection. Both infection and pregnancy increased visceral organ mass and both altered regional bone area and mineralization. During pregnancy, lumbar mineralization was lower but femur area and mineralization were higher. On the other hand, infection lowered maternal femur bone area and this was associated with higher IFN-γ in maternal serum of heavily infected pregnant mice. Infection also reduced foetal crown-rump length which was associated with higher amniotic fluid IL-1β.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2009

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