H
Heinz G. Remold
Researcher at Brigham and Women's Hospital
Publications - 141
Citations - 10639
Heinz G. Remold is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Macrophage & Macrophage migration inhibitory factor. The author has an hindex of 51, co-authored 141 publications receiving 10175 citations. Previous affiliations of Heinz G. Remold include University of California, Los Angeles & Beth Israel Deaconess Medical Center.
Papers
More filters
Journal ArticleDOI
Virulent Mycobacterium tuberculosis Strains Evade Apoptosis of Infected Alveolar Macrophages
TL;DR: The existence of mycobacterial virulence determinants that modulate the apoptotic response of AMφ to intracellular infection is suggested and the hypothesis that macrophage apoptosis contributes to innate host defense in tuberculosis is supported.
Journal ArticleDOI
Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis.
Joseph Keane,M K Balcewicz-Sablinska,Heinz G. Remold,Geoffrey L. Chupp,B B Meek,Matthew J. Fenton,Hardy Kornfeld +6 more
TL;DR: The effect of Mycobacterium tuberculosis infection on the viability of healthy (control) human alveolar macrophages was evaluated by staining with ethidium homodimer and calcein to discriminate live from dead cells.
Journal Article
Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha
TL;DR: The effect of TNF-alpha produced by AMphi following infection can be modulated by virulent MTB, using IL-10 as an upstream mediator.
Journal ArticleDOI
Evasion of innate immunity by Mycobacterium tuberculosis : is death an exit strategy?
TL;DR: Virulent Mycobacterium tuberculosis blocks production of the eicosanoid lipid mediator prostaglandin E2 (PGE2) and determines the death modality of the infected macrophage, which has a substantial impact on the outcome of infection.
Journal ArticleDOI
Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis
Samuel M. Behar,Martin Cj,Matthew G. Booty,Tomoyasu Nishimura,Xiaomin Zhao,Huixian Gan,Maziar Divangahi,Maziar Divangahi,Heinz G. Remold +8 more
TL;DR: It is demonstrated that during mycobacterial infection, cell death is regulated by the eicosanoids, prostaglandin E2 (proapoptotic) and lipoxin (LX)A4 (pronecrotic) and, although PGE2 protects against necrosis, virulent Mtb induces LXA4 and inhibits P GE2 production.