Differentiation of monocytes to macrophages induced by influenza virus-infected apoptotic cells

Noboru Uchide1, Kunio Ohyama1, Bo Yuan1

  • 1Department of Biochemistry, School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan1.

Insights

Influenza virus (IV) infection of chorion cells induces apoptosis, releasing factors that differentiate monocytes into macrophages. This process involves soluble factors from apoptotic cells, impacting immune cell function.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Monocytes differentiate into macrophages, crucial immune cells involved in host defense.
  • Apoptosis, or programmed cell death, plays a role in tissue homeostasis and immune regulation.
  • Influenza virus (IV) infection can induce cellular apoptosis.

Purpose of the Study:

  • To investigate the effect of culture supernatant from influenza virus (IV)-infected apoptotic and non-apoptotic cells on monocyte differentiation.
  • To determine if IV-induced apoptosis in specific fetal membrane cells influences monocyte-to-macrophage differentiation.

Main Methods:

  • Human fetal membrane chorion and amnion cells were cultured and infected with IV.
  • Culture supernatants from infected and non-infected cells were collected.
  • The human monocytic leukemia cell line THP-1 was used to assess differentiation via adhesion assays.
  • Morphological analysis and latex particle phagocytosis assays were performed.
  • RT-PCR was used to analyze the expression of scavenger receptor mRNA.

Main Results:

  • IV infection induced apoptotic DNA fragmentation in chorion cells but not amnion cells.
  • Culture supernatant from IV-infected chorion cells induced THP-1 cell adhesion, spreading, and phagocytosis, characteristic of macrophages.
  • Culture supernatant from IV-infected amnion cells did not induce these changes.
  • Incubation with supernatant from IV-infected chorion cells induced class A scavenger receptor mRNA expression in THP-1 cells.

Conclusions:

  • Apoptotic cells resulting from IV infection release soluble factors.
  • These soluble factors promote the morphological and functional differentiation of monocytes (THP-1 cells) into macrophages.
  • This suggests a novel mechanism by which viral infection and apoptosis can modulate immune cell populations.

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