Sabita Roy

The immunosuppressive effects of chronic morphine treatment are partially dependent on corticosterone and mediated by the mu-opioid receptor.

Mu-opioid receptor mediates chronic restraint stress-induced lymphocyte apoptosis.

Mu and delta receptors mediate morphine effects on phagocytosis by murine peritoneal macrophages.

The role of arginine vasopressin and its receptors in the normal and failing rat heart.

Morphine negatively regulates interferon-gamma promoter activity in activated murine T cells through two distinct cyclic AMP-dependent pathways.

Chronic morphine treatment differentiates T helper cells to Th2 effector cells by modulating transcription factors GATA 3 and T-bet.

Morphine impairs host innate immune response and increases susceptibility to Streptococcus pneumoniae lung infection.

In vivo activation of a mutant mu-opioid receptor by naltrexone produces a potent analgesic effect but no tolerance: role of mu-receptor activation and delta-receptor blockade in morphine tolerance.

Morphine withdrawal contributes to Th cell differentiation by biasing cells toward the Th2 lineage.

Morphine induces CD4+ T cell IL-4 expression through an adenylyl cyclase mechanism independent of the protein kinase A pathway.

Prenatal opiate exposure attenuates LPS-induced fever in adult rats: role of interleukin-1beta.

Transcriptional and epigenetic regulation of interleukin-2 gene in activated T cells by morphine.

Apolipoprotein e deficiency leads to altered brain uptake of alpha tocopherol injected into lateral cerebral ventricles.

Modulation of immune function by morphine: implications for susceptibility to infection.

Morphine induces defects in early response of alveolar macrophages to Streptococcus pneumoniae by modulating TLR9-NF-kappa B signaling.

Morphine withdrawal inhibits IL-12 induction in a macrophage cell line through a mechanism that involves cAMP.

Opioids and infections in the intensive care unit should clinicians and patients be concerned?

Opiate abuse, innate immunity, and bacterial infectious diseases.

SNIP members in a recent international conference: World Summit of Antivirals.

Morphine disrupts interleukin-23 (IL-23)/IL-17-mediated pulmonary mucosal host defense against Streptococcus pneumoniae infection.

Chronic morphine administration delays wound healing by inhibiting immune cell recruitment to the wound site.

PPARgamma gene C161T substitution alters lipid profile in Chinese patients with coronary artery disease and type 2 diabetes mellitus.

In vivo morphine treatment synergistically increases LPS-induced caspase activity in immune organs.

Morphine suppresses tumor angiogenesis through a HIF-1alpha/p38MAPK pathway.

Chronic morphine treatment inhibits LPS-induced angiogenesis: implications in wound healing.

Hypoxia-induced microRNA-424 expression in human endothelial cells regulates HIF-α isoforms and promotes angiogenesis.

Morphine inhibits murine dendritic cell IL-23 production by modulating Toll-like receptor 2 and Nod2 signaling.

Morphine withdrawal stress modulates lipopolysaccharide-induced interleukin 12 p40 (IL-12p40) expression by activating extracellular signal-regulated kinase 1/2, which is further potentiated by glucocorticoids.

Opioid drug abuse and modulation of immune function: consequences in the susceptibility to opportunistic infections.

Morphine induces splenocyte trafficking into the CNS.

Drugs of abuse effects on immunity and microbial pathogenesis.

Hypoxia differentially regulates arterial and venous smooth muscle cell proliferation via PDGFR-β and VEGFR-2 expression.

Role of the mu-opioid receptor in opioid modulation of immune function.

Morphine decreases bacterial phagocytosis by inhibiting actin polymerization through cAMP-, Rac-1-, and p38 MAPK-dependent mechanisms.

Mechanism(s) involved in opioid drug abuse modulation of HAND.

Morphine modulation of toll-like receptors in microglial cells potentiates neuropathogenesis in a HIV-1 model of coinfection with pneumococcal pneumoniae.

Morphine induces bacterial translocation in mice by compromising intestinal barrier function in a TLR-dependent manner.

The role of short-term oxygen administration in the prevention of intimal hyperplasia.

Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a.

Supplemental oxygen reverses hypoxia-induced smooth muscle cell proliferation by modulating HIF-alpha and VEGF levels in a rabbit arteriovenous fistula model.

Morphine inhibits migration of tumor-infiltrating leukocytes and suppresses angiogenesis associated with tumor growth in mice.

Vascular endothelial growth factor signaling in hypoxia and inflammation.

Dynamin 2 along with microRNA-199a reciprocally regulate hypoxia-inducible factors and ovarian cancer metastasis.

Cellular Interactions and Signaling in neuroAIDS: Emerging Issues Colloquium.