Premium
Changes in Brainstem Inflammatory Gene Expression Following Systemic LPS Injections During a Critical Period of Neonatal Development
Author(s) -
Mayer Catherine,
Valerio Dana,
Hodges Craig,
MacFarlane Peter
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.861.10
Subject(s) - saline , intraperitoneal injection , medicine , hypoxia (environmental) , endocrinology , gene expression , period (music) , inflammation , brainstem , tumor necrosis factor alpha , systemic inflammation , respiratory system , lipopolysaccharide , sepsis , andrology , biology , chemistry , gene , physics , acoustics , biochemistry , organic chemistry , oxygen
We showed previously the respiratory neural control system exhibits a lethal vulnerability to pro‐inflammatory challenges (sustained hypoxia exposure and systemic LPS injections) during the second postnatal week of life (~10 days of postnatal age, P10). In the current study, we investigated brainstem pro‐inflammatory (TNFα and iNOS) mRNA expression following LPS treatment at various postnatal ages. Rat pups received an intraperitoneal injection of LPS (0.1mg/kg) at either P5, P10, or P20; the brainstems were removed 2 hours later for determining changes in TNFα and iNOS mRNA expression using qRTPCR. In control (saline injected) rats there was a developmental increase in constitutive iNOS expression that peaked at P10; TNFα expression followed a similar profile. iNOS mRNA expression increased in all 3 age groups following LPS treatment compared to saline treated rats, but the increase was attenuated at P10. The transient peak in iNOS mRNA and attenuated response to LPS at P10 was associated with a high incidence of mortality compared to younger (P5) or older (P20) animals. We propose the postnatal development of inflammatory gene expression and the unique changes observed at P10 may play a vital role in determining the heightened vulnerability of the neonate and its ability (or lack thereof) to mount appropriate responses to defend against potentially lethal pro‐inflammatory challenges.