Anesthesiologists at work: an increase in pro-inflammatory and Th2 cytokine production, and alterations in proliferative immune responses

The skin is constantly exposed to various types of chemical stresses that challenge the immune cells, leading to the activation of T cell-mediated hypersensitivity reactions including atopic dermatitis. Previous studies have demonstrated that a variety of natural compounds are effective against development of atopic dermatitis by modulating immune responses. Cardamonin is a natural compound abundantly found in cardamom spices and many other medicinal plant species. In the present study, we attempted to examine whether cardamonin could inhibit oxazolone-induced atopic dermatitis in vivo. Our results show that topical application of cardamonin onto the ear of mice suppressed oxazolone-induced inflammation in the ear and hyperplasia in the spleen. Cardamonin also inhibited oxazolone-induced destruction of connective tissues and subsequent infiltration of mast cells into the skin. In addition, we found that the production of Th2 cytokines is negatively regulated by NRF2, and the induction of NRF2 by cardamonin contributed to suppressing oxazolone-induced Th2 cytokine production and oxidative damages in vivo. Together, our results demonstrate that cardamonin is a promising natural compound, which might be effective for treatment of atopic dermatitis.

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Immune responses during the acute stages of infection with the intestinal trematode Echinostoma caproni

Parasitology ◽

10.1017/s0031182099006009 ◽

2000 ◽

Vol 120 (6) ◽

pp. 565-571 ◽

Cited By ~ 34

Author(s):

L. R. BRUNET ◽

S. JOSEPH ◽

D. W. DUNNE ◽

B. FRIED

Keyword(s):

Immune Responses ◽

Cytokine Production ◽

Humoral Response ◽

Spleen Cells ◽

Echinostoma Caproni ◽

Th2 Cytokine ◽

Mesenteric Lymph ◽

Cytokine Pattern ◽

Th1 Cytokine ◽

Ifn Γ

This study investigated the nature of the immune response of C57BL/6 mice infected with the trematode Echinostoma caproni. To determine the preferential development of either a Th1 or Th2 cytokine pattern during early stages of infection, cytokine production by spleen and mesenteric lymph node (MLN) cells during the first 3 weeks of infection was followed. Whereas spleen cells failed to respond to antigen stimulation, MLN cells produced IFN-γ and to a lesser extent IL-4. IL-5 levels were elevated throughout the period studied. The humoral response was consistent with a Th1 cytokine pattern as antigen-specific IgG2a antibodies were preferentially developed. We investigated whether IFN-γ is critical for establishment of E. caproni infection. Worm burden in infected mice treated with a single injection of anti-IFN-γ mAb was significantly reduced compared to that of animals treated with a control antibody.

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TIM-1 and TIM-3 enhancement of Th2 cytokine production by mast cells

Blood ◽

10.1182/blood-2006-11-058800 ◽

2007 ◽

Vol 110 (7) ◽

pp. 2565-2568 ◽

Cited By ~ 106

Author(s):

Susumu Nakae ◽

Motoyasu Iikura ◽

Hajime Suto ◽

Hisaya Akiba ◽

Dale T. Umetsu ◽

...

Keyword(s):

T Cell ◽

Mast Cells ◽

Immune Responses ◽

Cytokine Production ◽

Interleukin 4 ◽

Th2 Cells ◽

T Helper ◽

Th2 Cytokine ◽

Peritoneal Mast Cells

Members of the T-cell immunoglobulin– and mucin-domain–containing molecule (TIM) family have roles in T-cell–mediated immune responses. TIM-1 and TIM-2 are predominantly expressed on T helper type 2 (Th2) cells, whereas TIM-3 is preferentially expressed on Th1 and Th17 cells. We found that TIM-1 and TIM-3, but neither TIM-2 nor TIM-4, were constitutively expressed on mouse peritoneal mast cells and bone marrow–derived cultured mast cells (BMCMCs). After IgE + Ag stimulation, TIM-1 expression was down-regulated on BMCMCs, whereas TIM-3 expression was up-regulated. We also found that recombinant mouse TIM-4 (rmTIM-4), which is a ligand for TIM-1, as well as an anti–TIM-3 polyclonal Ab, can promote interleukin-4 (IL-4), IL-6, and IL-13 production without enhancing degranulation in BMCMCs stimulated with IgE + Ag. Moreover, the anti–TIM-3 Ab, but neither anti–TIM-1 Ab nor rmTIM-4, suppressed mast-cell apoptosis. These observations suggest that TIM-1 and TIM-3 may be able to influence T-cell–mediated immune responses in part through effects on mast cells.

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