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

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  • Rahul Mittal

    (Division of Infectious Diseases, Department of Pediatrics
    The Saban Research Institute, Children's Hospital Los Angeles)

  • Nemani V. Prasadarao

    (Division of Infectious Diseases, Department of Pediatrics
    The Saban Research Institute, Children's Hospital Los Angeles
    The Saban Research Institute, Children's Hospital Los Angeles
    Keck School of Medicine, University of Southern California)

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.

Suggested Citation

  • Rahul Mittal & Nemani V. Prasadarao, 2011. "gp96 expression in neutrophils is critical for the onset of Escherichia coli K1 (RS218) meningitis," Nature Communications, Nature, vol. 2(1), pages 1-11, September.
    • Handle: RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1554
    DOI: 10.1038/ncomms1554
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