Immunomodulation of caprine lentiviral infection by interleukin-16

R Nimmanapalli1, C Sharmila, P G Reddy

  • 1Department of Pathobiology, College of Veterinary Medicine, Nursing & Allied Health, Tuskegee University, Tuskegee, AL 36088, United States. ramadevi.nimmanapalli@gmail.com

Insights

Interleukin-16 (IL-16) boosts immune cell movement and may inhibit viral integration in goats. This proinflammatory cytokine, IL-16, shows potential in managing caprine arthritis-encephalitis virus (CAEV) infection.

Area of Science:

  • Immunology
  • Virology
  • Cytokine Biology

Background:

  • Interleukin-16 (IL-16) is a proinflammatory cytokine implicated in various immune responses.
  • Previous studies demonstrated elevated IL-16 mRNA and protein in caprine arthritis-encephalitis virus (CAEV)-infected goats.

Purpose of the Study:

  • To investigate the immunomodulatory effects of IL-16 in vitro.
  • To determine the mechanism of IL-16 action in goats, specifically its interaction with CD4.
  • To assess the impact of IL-16 on CAEV proviral DNA integration.

Main Methods:

  • Utilized peripheral blood mononuclear cells (PBMCs) from CAEV-infected and uninfected goats.
  • Administered human recombinant IL-16 (rhIL-16) and assessed its effects on PBMC chemotaxis.
  • Investigated IL-16's mechanism of action using anti-goat CD4 monoclonal antibody.
  • Quantified CAEV proviral DNA in monocytes treated with rhIL-16.
  • Analyzed lymphocyte activation markers via flow cytometry.

Main Results:

  • rhIL-16 significantly enhanced PBMC chemotaxis in both control and CAEV-infected goats.
  • IL-16-induced chemotaxis was inhibited by anti-goat CD4 antibody, indicating CD4 as the primary receptor.
  • Treatment with rhIL-16 led to a reduction in CAEV proviral DNA in caprine monocytes.
  • Flow cytometry revealed a trend towards increased lymphocyte activation markers following IL-16 treatment.

Conclusions:

  • IL-16 modulates immune cell function in goats, primarily through CD4 interaction.
  • IL-16 exhibits an inhibitory effect on CAEV viral integration.
  • Elevated IL-16 during CAEV infection may play a role in controlling viral replication.

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