gp96 expression in neutrophils is critical for the onset of Escherichia coli K1 (RS218) meningitis

Rahul Mittal and Nemani V. Prasadarao ()
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Rahul Mittal: Division of Infectious Diseases, Department of Pediatrics
Nemani V. Prasadarao: Division of Infectious Diseases, Department of Pediatrics

Nature Communications, 2011, vol. 2, issue 1, 1-11

Abstract: Abstract Despite the fundamental function of neutrophils (polymorphonuclear leukocytes (PMNs)) in innate immunity, their role in Escherichia coli K1 (EC-K1) -induced meningitis is unexplored. Here we show that PMN-depleted mice are resistant to EC-K1 (RS218) meningitis. EC-K1 survives and multiplies in PMNs for which outer membrane protein A (OmpA) expression is essential. EC-K1 infection of PMNs increases the cell surface expression of gp96, which acts as a receptor for bacterial entry. Suppression of gp96 expression in newborn mice prevents the onset of EC-K1 meningitis. Infection of PMNs with EC-K1 suppresses oxidative burst by downregulating rac1, rac2 and gp91phox transcription both in vitro and in vivo. The interaction of loop 2 of OmpA with gp96 is essential for EC-K1-mediated inhibition of oxidative burst. These results reveal that EC-K1 exploits surface-expressed gp96 in PMNs to prevent oxidative burst for the onset of neonatal meningitis.

Date: 2011
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DOI: 10.1038/ncomms1554

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