Abstract
Methamphetamine (METH) is a strong addictive central nervous system stimulant. METH abuse can alter biological processes and immune functions necessary for host defense. The acquisition and transmission of HIV, hepatitis, and other communicable diseases are possible serious infectious consequences of METH use. METH also accumulates extensively in major organs. Despite METH being a major public health and safety problem globally, there are limited studies addressing the impact of this popular recreational psychostimulant on tissue adaptive immune responses after exposure to T cell dependent [ovalbumin (OVA)] and independent [lipopolysaccharide (LPS)] antigens. We hypothesized that METH administration causes pulmonary and splenic tissue alterations and reduces T cell responses to OVA and LPS in vivo, suggesting the increased susceptibility of users to infection. Using a murine model of METH administration, we showed that METH causes tissue injury, apoptosis, and alters helper and cytotoxic T cell recruitment in antigen challenged mice. METH also reduces the expression and distribution of CD3 and CD28 molecules on the surface of human Jurkat T cells. In addition, METH decreases the production of IL-2 in these T-like cells, suggesting a negative impact on T lymphocyte activation and proliferation. Our findings demonstrate the pleotropic effects of METH on cell-mediated immunity. These alterations have notable implications on tissue homeostasis and the capacity of the host to respond to infection.
Highlights
Methamphetamine (METH) is a strong addictive central nervous system stimulant
METH exposure alters CD4+ helper and CD8+ cytotoxic T lymphocyte populations resulting in increased HIV proliferation in infected individuals16–18. CD4+ T cells recognize peptides presented on MHC class II molecules on antigen (Ag) presenting cells (APCs) and play a central role in modulating adaptive immune responses, whereas, CD8+ T lymphocytes recognize peptides presented by MHC class I molecules, which are found in all nucleated cells
Given that METH users are susceptible to viral infections due to their risky behavior and cytotoxic T lymphocytes are important in the control of these infections, we explored the impact of this psychostimulant on CD8+ T cell recruitment to pulmonary and splenic tissues
Summary
Methamphetamine (METH) is a strong addictive central nervous system stimulant. METH abuse can alter biological processes and immune functions necessary for host defense. We hypothesized that METH administration causes pulmonary and splenic tissue alterations and reduces T cell responses to OVA and LPS in vivo, suggesting the increased susceptibility of users to infection. Given that METH abundantly accumulates in pulmonary and splenic tissues of users and their susceptibility to viral infections, we investigated the impact of this drug on organ architecture and T cell recruitment in the lungs and spleen of C57BL/6 mice after challenge with T-dependent [TD; ovalbumin (OVA)] and T-independent [TI; lipopolysaccharide (LPS)] Ag. we explored the effects of METH on the expression and distribution of T cell surface molecules involved in the activation of cell-mediated immunity. We hypothesized that METH administration may result in tissue injury and reduce T cell responses to OVA and LPS in vivo, suggesting the increased susceptibility of users to infection by commonly transmissible viral pathogens. These alterations may have profound implications on tissue homeostasis and the capacity of METH users to respond to diverse insults, including invading viral pathogens
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