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Mycoplasma pneumoniae stimulates cPLA2 activation and eicosanoid production in human alveolar macrophages and mouse‐RAW264.7 macrophages
Author(s) -
Kandasamy Pitchaimani,
Chan Ed,
Leslie Christina C.,
Zarini Simona,
Murphy Robert C.,
Voelker Dennis R.
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.21.6.a977-c
Mycoplasma pneumoniae (Mpn) is a human pathogen causing pneumonia and serious exacerbations of asthma. The mechanisms of asthma exacerbations are unknown but could involve induction of prostaglandin and leukotriene formation, as well as other inflammatory mediators by host cells. We examined the mobilization of arachidonic acid (AA) by Mpn in the mouse RAW 264.7 cell line, and primary cultures of human alveolar macrophages. Mpn induced AA release 4‐fold from RAW 264.7 cells and 2‐fold from human cells. Bacterial membranes and a derived lipoprotein fraction produced a similar effect. The bacterial lipoprotein mimic and TLR2 ligand, Pam3Cys also produced the same effect in mouse macrophages. Mpn membranes induced phosphorylation of p38 and p42/44 MAP kinases, and cytosolic phospholipase A2 (cPLA2). Inhibition of p42/44 phosphorylation by the MEK1 inhibitor U0126, suppressed AA release. Addition of the cPLA2 inhibitor pyrrolidine also blocked AA release in response to Mpn. Collectively, these data demonstrate Mpn activation of cPLA2 and suggest this eicosanoid production could play a role in asthma exacerbations. NIH PHL 073907.