To determine the role of GpoA during pneumococcal infection, we constructed the gpoA mutant in the capsulated D39 strain (serotype 2), which is virulent in BALB/c mice using intranasal inoculation [38], and its corresponding revertant strain ( wt gpoA + )
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CO also suppressed the function of early growth response protein 1 (EGR-1), a crucial transcription factor in the inflammatory response initiated by macrophages [60]
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bolus injection into the vena cava through an insulin needle 2 min before injection of GLP-1
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