PMID- 16495548
OWN - NLM
STAT- MEDLINE
DCOM- 20060605
LR  - 20181113
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 74
IP  - 3
DP  - 2006 Mar
TI  - Cytosolic phospholipase A2 enzymes are not required by mouse bone marrow-derived 
      macrophages for the control of Mycobacterium tuberculosis in vitro.
PG  - 1751-6
AB  - During the course of infection Mycobacterium tuberculosis predominantly resides 
      within macrophages, where it encounters and is often able to resist the 
      antibacterial mechanisms of the host. In this study, we assessed the role of 
      macrophage phospholipases A2 (PLA2s) in defense against M. tuberculosis. Mouse 
      bone marrow-derived macrophages (BMDMs) expressed cPLA2-IVA, cPLA2-IVB, iPLA2-VI, 
      sPLA2-IIE, and sPLA2-XIIA. The expression of cPLA2-IVA was increased in response 
      to M. tuberculosis, gamma interferon, or their combination, and cPLA2-IVA 
      mediated the release of arachidonic acid, which was stimulated by M. tuberculosis 
      in activated, but not unactivated, macrophages. We confirmed that arachidonic 
      acid is highly mycobactericidal in a concentration- and pH-dependent manner in 
      vitro. However, when M. tuberculosis-infected macrophages were treated with PLA2 
      inhibitors, intracellular survival of M. tuberculosis was not affected, even in 
      inducible nitric oxide synthase-deficient macrophages, in which a major 
      bactericidal mechanism is removed. Moreover, intracellular survival of M. 
      tuberculosis was similar in cPLA2-IVA-deficient and wild-type macrophages. Our 
      results demonstrate that the cytosolic PLA2s are not required by murine BMDMs to 
      kill M. tuberculosis.
FAU - Vandal, Omar H
AU  - Vandal OH
AD  - Department of Microbiology and Immunology, Weill Medical College of Cornell 
      University, 1300 York Avenue, Box 57, New York, NY 10021, USA.
FAU - Gelb, Michael H
AU  - Gelb MH
FAU - Ehrt, Sabine
AU  - Ehrt S
FAU - Nathan, Carl F
AU  - Nathan CF
LA  - eng
GR  - R01 HL072718/HL/NHLBI NIH HHS/United States
GR  - HL72718/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 27YG812J1I (Arachidonic Acid)
RN  - EC 3.1.1.32 (Phospholipases A)
RN  - EC 3.1.1.4 (Phospholipases A2)
SB  - IM
MH  - Animals
MH  - Arachidonic Acid/pharmacology
MH  - Cytosol/*enzymology/immunology/microbiology
MH  - Macrophages/cytology/enzymology/immunology/*microbiology
MH  - Mice
MH  - Mycobacterium tuberculosis/*physiology
MH  - Phospholipases A/antagonists & inhibitors/biosynthesis/*physiology
MH  - Phospholipases A2
PMC - PMC1418652
EDAT- 2006/02/24 09:00
MHDA- 2006/06/06 09:00
PMCR- 2006/07/01
CRDT- 2006/02/24 09:00
PHST- 2006/02/24 09:00 [pubmed]
PHST- 2006/06/06 09:00 [medline]
PHST- 2006/02/24 09:00 [entrez]
PHST- 2006/07/01 00:00 [pmc-release]
AID - 74/3/1751 [pii]
AID - 1467-05 [pii]
AID - 10.1128/IAI.74.3.1751-1756.2006 [doi]
PST - ppublish
SO  - Infect Immun. 2006 Mar;74(3):1751-6. doi: 10.1128/IAI.74.3.1751-1756.2006.