PLoS One. 2014 Jul 11;9(7):e101023. doi: 10.1371/journal.pone.0101023. eCollection 2014.

Helminth induced suppression of macrophage activation is correlated with inhibition of calcium channel activity.External 2231691f894ba696de1310221b0a0dbbb31a7251e75115c265587c3d9d5f507c

Chauhan, A., Sun, Y., Pani, B., Quenumzangbe, F., Sharma, J., Singh, B. B., Mishra, B. B.,
["Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America.", "Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America.", "Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America.", "Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America.", "Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America.", "Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America.", "Department of Basic Sciences, School of Medicine & Health Sciences, The University of North Dakota, Grand Forks, North Dakota, United States of America."]
Helminth parasites cause persistent infections in humans and yet many infected individuals are asymptomatic. Neurocysticercosis (NCC), a disease of the central nervous system (CNS) caused by the cestode Taenia solium, has a long asymptomatic phase correlated with an absence of brain inflammation. However, the mechanisms of immune suppression remain poorly understood. Here we report that murine NCC displays a lack of cell surface maturation markers in infiltrating myeloid cells. Furthermore, soluble parasite ligands (PL) failed to induce maturation of macrophages, and inhibited TLR-induced inflammatory cytokine production. Importantly, PL treatment abolished both LPS and thapsigargin-induced store operated Ca2+ entry (SOCE). Moreover, electrophysiological recordings demonstrated PL-mediated inhibition of LPS or Tg-induced currents that were TRPC1-dependent. Concomitantly STIM1-TRPC1 complex was also impaired that was essential for SOCE and sustained Ca2+ entry. Likewise loss of SOCE due to PL further inhibited NFkB activation. Overall, our results indicate that the negative regulation of agonist induced Ca2+ signaling pathway by parasite ligands may be a novel immune suppressive mechanism to block the initiation of the inflammatory response associated with helminth infections.
PMID: 25013939External 2231691f894ba696de1310221b0a0dbbb31a7251e75115c265587c3d9d5f507c
Validation: In vivo validation Toggle 893349bafcc528f8346c51dc3420151d67b0126b2c122dd1017121c03fa0f69b
  Assay with endogenous proteins Assay with overexpressed proteins Reference
Cell or tissue Cell or tissue TRP channel construct Interactor construct
TRP channel Interactor Method Species Region Species Region
TRPC1 Link 2bd4d11adb659cddf58197a94e201f0a44c55d8d7cb427c624971b42e122c0a4 STIM1 Co-immunoprecipitation Mouse bone marrow derived macrophages 25013939
(Link 2bd4d11adb659cddf58197a94e201f0a44c55d8d7cb427c624971b42e122c0a4: click the arrow icon to show interactions only between the corresponding TRP channel and the interactor)
TRP / Interactor

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