Apoptosis as the adaptation mechanism in survival of Trichinella spiralis in the host

Parasitol Res. 2011 Oct;109(4):997-1002. doi: 10.1007/s00436-011-2343-2. Epub 2011 Apr 5.

Abstract

The study evaluates the role of apoptosis-inducing factor (AIF) in the process of striated muscle cell transformation after occupation by Trichinella spiralis. Its relationship with other apoptosis-related factors [apoptotic protease-activating factor 1, Bcl-2 associated protein X (BAX), Bcl-2, caspase 3, survivin, poly (ADP-ribose) polymerase-1 (PARP-1), and endothelial and inducible (iNOS) nitric oxide synthase] was evaluated by immunohistochemistry. In the context of low BAX and caspase 3 expression and strong distribution of AIF in the sarcoplasm and nucleus at the very early stage of infection, we suppose that AIF-mediated signaling is involved in the apoptosis activation in the area of Trichinella occupation. In the time course of nurse cell formation, survivin and caspase 3 migrated into the enlarged nuclei with strong PARP-1 expression. In the end of encapsulation of Trichinella, expression of all proapoptotic factors ceased and only survivin in the nuclei and Bcl-2 positivity in the cytoplasm persisted in the formed nurse cell. The expression of sarcoplasmic iNOS was absent during the process of muscle cell de-differentiation and reappeared within the nurse cell. It seems that upregulation and downregulation of factors of apoptosis in the skeletal muscle cell represents an adaptive mechanism providing a comfortable niche for the parasite.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological*
  • Animals
  • Apoptosis / physiology*
  • Apoptosis Inducing Factor / genetics
  • Apoptosis Inducing Factor / metabolism
  • Apoptotic Protease-Activating Factor 1 / genetics
  • Apoptotic Protease-Activating Factor 1 / metabolism
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Cell Nucleus / metabolism
  • Cell Nucleus / parasitology
  • Cell Nucleus / ultrastructure
  • Enzyme Activation
  • Gene Expression Regulation
  • Host-Parasite Interactions*
  • Immunohistochemistry
  • Larva / physiology*
  • Mice
  • Mice, Inbred BALB C
  • Mitochondria / enzymology*
  • Mitochondria / parasitology
  • Mitochondria / ultrastructure
  • Muscle Cells / metabolism*
  • Muscle Cells / parasitology
  • Muscle Cells / ultrastructure
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases / genetics
  • Poly(ADP-ribose) Polymerases / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • Trichinella spiralis / physiology*
  • Trichinellosis* / metabolism
  • Trichinellosis* / parasitology
  • bcl-2-Associated X Protein / genetics
  • bcl-2-Associated X Protein / metabolism

Substances

  • Apoptosis Inducing Factor
  • Apoptotic Protease-Activating Factor 1
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • NOS2 protein, human
  • Nitric Oxide Synthase Type II
  • Parp1 protein, mouse
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases
  • Caspase 3