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Disorders of Leukocytes01:27

Disorders of Leukocytes

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Leukocyte disorders can lead to either leukopenia, characterized by an abnormally low leukocyte count, or leukocytosis, marked by a very high leukocyte number.
Leukopenia may result from bone marrow disorders, autoimmune diseases, and infectious diseases. For example, conditions such as multiple myeloma and aplastic anemia can impair the bone marrow's ability to produce adequate leukocytes. Similarly, autoimmune diseases like lupus and viral infections such as HIV can prompt the immune...
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Persistent Cutaneous Leishmania major Infection Promotes Infection-Adapted Myelopoiesis.

Fabio Luiz Bandeira Ferreira1,2, Olivier Séguin1, Albert Descoteaux1

  • 1Centre Armand Frappier Santé Biotechnologie, Institut National de la Recherche Scientifique, Laval, QC H7V 1B7, Canada.

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|March 26, 2022
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Summary

Persistent Leishmania major infection activates hematopoietic stem/progenitor cells (HSPCs) and myeloid precursors, increasing myeloid cell production. This occurs even without direct bone marrow parasite presence, impacting host-pathogen interactions.

Keywords:
Leishmania majorcutaneous leishmaniasishematopoietic stem/progenitor cellinflammationmyelopoiesis

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Area of Science:

  • Immunology
  • Hematopoiesis
  • Parasitology

Background:

  • Hematopoietic stem/progenitor cells (HSPCs) generate immune cells and can be activated by inflammation, enhancing myelopoiesis.
  • Previous work linked HSPC activation to parasite persistence in visceral leishmaniasis via increased monocyte production.
  • The role of bone marrow parasite presence in infection-adapted myelopoiesis remained unclear.

Purpose of the Study:

  • To investigate if persistent Leishmania major strains activate HSPCs and myeloid precursors in a mouse model of cutaneous leishmaniasis.
  • To determine if direct bone marrow infection is necessary for infection-adapted myelopoiesis.

Main Methods:

  • Infection of C57Bl/6 mice with persistent Leishmania major strains.
  • Analysis of myeloid cell populations in bone marrow, spleen, and lesion sites.
  • Quantification of HSPCs and myeloid precursors.
  • Measurement of cytokine and chemokine profiles in the bone marrow.

Main Results:

  • Infection led to increased myeloid cells at the lesion site and a rise in myeloid-biased HSPCs in bone marrow and spleen.
  • Spleens showed increased monocytes and monocyte-derived myeloid cells.
  • Bone marrow revealed attenuated type I/II interferon responses but rapid upregulation of myelopoietic cytokines (IL-1β, GM-CSF) for both strains.

Conclusions:

  • Active bone marrow infection is not required for infection-adapted myelopoiesis.
  • Cutaneous leishmaniasis can induce systemic changes in bone marrow output.
  • Host-pathogen interaction analysis must consider bone marrow alterations.