Pinocytic rates of macrophages from mice immunized against Toxoplasma gondii and macrophages stimulated to inhibit toxoplasma in vitro

Jones, Thomas C.; Len, L

doi:10.1128/iai.14.4.1011-1013.1976

Cited by 6 publications

(2 citation statements)

References 4 publications

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“…This could occur for example when exposed to a nonspecific inflammatory environment. In this regard, it is of interest that in every instance in which an in vitro microbistatic or microbicidal activity has been generated against protozoa, macrophages were obtained from peritoneal exudates, sensitized animals, or had been manipulated in vitro by exposure to heart-infusion broth, thioglycollate medium, or Ficoll-Hypaque (4,(6)(7)(8)31). Efforts are in progress to define the conditions under which a trypanocidal activity can be evoked under in vitro conditions.…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma cruzi: the immunological induction of macrophage plasminogen activator requires thymus-derived lymphocytes.

Nogueira¹,

Gordon²,

Cohn³

1977

The Journal of Experimental Medicine

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In this article we describe methods in which unstimulated mouse peritoneal macrophages were induced to secrete high livels of plasminogen activator under in vitro conditions. The exposure of sensitized peritoneal or spleen cell populations from Trypanosoma cruzi-infected animals to either viable or heat-killed trypanosomes lead to the release of an inducing factor(s). Maximal levels of plasminogen activator secretion are achieved by the incubation of such factors (s) with unstimulated macrophages for 48 h. A significant increase in enzyme secretion was already observed after a 24 h incubation. The production of the inducing factor(s) by sensitized cells was immunologically specific and unrelated antigens did not stimulate the production of the factor(s) by sensitized peritoneal or spleen cell populations. The inducing factor(s) was produced by nylon-wool-fractionated spleen and peritoneal cells which had been depleted of marcrophages. Pretreatment of sensitized spleen cells with anti-theta serum and C abolished the production of the activating factor(s). The active supernatant fluids were able to induce secretion of macrophage plasminogen activator across H-2 barriers. Attempts to induce trypanocidal activity in unstimulated macrophages have not been successful.

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Section: Discussionmentioning

confidence: 99%

Trypanosoma cruzi: the immunological induction of macrophage plasminogen activator requires thymus-derived lymphocytes.

Nogueira¹,

Gordon²,

Cohn³

1977

The Journal of Experimental Medicine

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“…This may occur by virtue of Rho regulating actin stress fiber formation, which is necessary to coordinate caveolin-associated membrane domains (Stahlhut and van Deurs, 2000; Prieto-Sánchez et al, 2006). However, Toxoplasma does not appear to induce host cell stress fiber assembly (Morisaki et al, 1995; Coppens et al, 2006), and the rates of endocytosis/pinocytosis are not increased by infection (Jones and Len, 1976; Sweeney et al, 2010). Thus, we hypothesize that Toxoplasma utilizes Rho signaling to activate JNK through a more direct approach.…”

Section: Discussionmentioning

confidence: 99%

The Activin Receptor, Activin-Like Kinase 4, Mediates Toxoplasma Gondii Activation of Hypoxia Inducible Factor-1

Lis

Wiley

Vaughan

et al. 2019

Front. Cell. Infect. Microbiol.

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To grow and cause disease, intracellular pathogens modulate host cell processes. Identifying these processes as well as the mechanisms used by the pathogens to manipulate them is important for the development of more effective therapeutics. As an example, the intracellular parasite Toxoplasma gondii induces a wide variety of changes to its host cell, including altered membrane trafficking, cytoskeletal reorganization, and differential gene expression. Although several parasite molecules and their host targets have been identified that mediate- these changes, few are known to be required for parasite replication. One exception is the host cell transcription factor, hypoxia-inducible factor-1 (HIF-1), which is required for parasite replication in an oxygen-dependent manner. Toxoplasma activates HIF-1 by stabilizing the HIF-1α subunit, and this is dependent on the signaling from the Activin-Like Kinase (ALK) receptor superfamily. Here, we demonstrate that specific overexpression of the ALK family member, ALK4, increased HIF-1 activity in Toxoplasma-infected cells, and this increase required ALK4 kinase activity. Moreover, Toxoplasma stimulated ALK4 to dimerize with its co-receptor, ActRII, and also increased ALK4 kinase activity, thereby demonstrating that Toxoplasma activates the ALK4 receptor. ALK4 activation of HIF-1 was independent of canonical SMAD signaling but rather was dependent on the non-canonical Rho GTPase and JNK MAP kinase signaling pathways. Finally, Toxoplasma increased rates of ALK4 ubiquitination and turnover. These data provide the first evidence indicating that ALK4 signaling is a target for a microbial pathogen to manipulate its host cell.

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Immunity to Malaria and Related Intracellular Protozoa

Trager

1986

Living Together

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Pinocytic rates of macrophages from mice immunized against Toxoplasma gondii and macrophages stimulated to inhibit toxoplasma in vitro

Cited by 6 publications

References 4 publications

Trypanosoma cruzi: the immunological induction of macrophage plasminogen activator requires thymus-derived lymphocytes.

Trypanosoma cruzi: the immunological induction of macrophage plasminogen activator requires thymus-derived lymphocytes.

The Activin Receptor, Activin-Like Kinase 4, Mediates Toxoplasma Gondii Activation of Hypoxia Inducible Factor-1

Immunity to Malaria and Related Intracellular Protozoa

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