author={Ursula Wiedermann and X.‐J. Chen and Lennart Enerb{\"a}ck and Lars {\AA}ke Hanson and Helena Kahu and Ulf I Dahlgren},
  journal={Scandinavian Journal of Immunology},
The authors studied the influence of vitamin A deficiency on immediate and delayed type hypersensitivity as well as granulocyte‐mediated inflammatory reactions in vitamin A depleted and control rats. The number of circulating leucocytes was 43% higher in the vitamin A deficient than in the control animals. The leucocytosis was a result of a general increase of white blood cells and was not due to an increase in one particular type. The ratio between CD4+ and CD8+ T cells was unchanged. The… 

Vitamin A as an anti-inflammatory agent

  • R. Reifen
  • Medicine, Biology
    Proceedings of the Nutrition Society
  • 2002
The present review suggests that vitamin A deficiency induces inflammation and aggravates existing inflammatory states, and Supplementation with vitamin A in selected cases could ameliorate inflammation.

Vitamin A Deficiency in Mice Enhances the Colonic Level of Purine Enzyme Activity

VAD causes upregulation of purine enzyme, which together with an increased number of inflammatory cells might exacerbate colonic injuries in VAD condition, and increased expression of adenosine deaminase in Vad mice colon is shown.

Vitamin A, infection, and immune function.

Vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished, presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.

Vitamin A deficiency exacerbates inflammation in a rat model of colitis through activation of nuclear factor-kappaB and collagen formation.

The data suggest that vitamin A deficiency induces colonic inflammation, which is amplified by deficiency and ameliorated by supplementation of the vitamin.

PNS1200007 290..297

Vitamin A deficiency increases a Th1 response in the presence of obesity and thus, increases the inflammatory process involved in chronic inflammation and fat deposition.

Repeated allergen challenge in rats increases vitamin A consumption.

It is concluded that vitamin A utilization is increased during repeated allergen challenge and allergic bronchitis, most probably due to increased demand for epithelial repair.

Vitamin A status does not influence neopterin production during illness or health in South African children

The results indicate that, contrary to what is observed in rodents under experimental conditions, poor vitamin A status is not associated with altered regulation of IFN-γ production in children.

Vitamin A deficiency injures lung and liver parenchyma and impairs function of rat type II pneumocytes.

Evidence is provided that vitamin A deficiency produces profound morphologic alterations in liver and lung parenchyma and impairs pneumocyte function, as well as in the small arteries and arterioles, but not in the larger ones.

Decreased vitamin A levels in common variable immunodeficiency: vitamin A supplementation in vivo enhances immunoglobulin production and downregulates inflammatory responses

The possible role of vitamin A deficiency in Common variable immunodeficiency is examined, which is a group of B‐cell deficiency syndromes with impaired antibody production and recurrent bacterial infections as the major manifestations.



Vitamin A deficiency predisposes to Staphylococcus aureus infection

The results suggest that the increased susceptibility to S. aureus infection observed in the vitamin-A-deficient rats is due to a concerted action of antigen-specific T-cell hyperactivity, impaired function of the phagocytes, and decreased complement activity.

The effect of vitamin A deficiency on the in vitro cellular immune response of rats.

The effect of vitamin A deficiency on the response of splenic lymphocytes to mitogenic stimulation was determined in an experimental rat model and showed a marked leukopenia, a decrease in the number of circulating lymphocytes and an increase in thenumber of circulating neutrophils.

Vitamin A deficiency decreases natural killer cell activity and interferon production in rats.

The data suggest that vitamin A deficiency affect the nonspecific arm of the immune system, possibly by altering the functional capacity of cells to produce lymphokines needed for the generation of an appropriate cytolytic response.

Increased Interleukin-1 Activity in the Injured Vitamin A-Deficient Cornea

The results demonstrate a correlation between IL-1 levels and severity of inflammation in the injured vitamin A-deficient rat cornea, and is the first report describing the induction ofIL-1 in the vitamin A -deficient cornea by thermal and mechanical injuries.

Vitamin A deficiency results in a priming environment conducive for Th1 cell development

The results show that during vitamin A deficiency, the priming environment included constitutive interleukin (IL)‐12 and IFN‐γ transcripts, but it was devoid of constitutive IL‐4 and IL‐10 transcripts, and the distorted constitutive and inducible cytokine gene expression patterns that occurred when vitamin A levels were low would be expected strongly to favor T helper type‐1 development and limit T helpers type‐2 cell growth and differentiation.

Increased translocation of Escherichia coli and development of arthritis in vitamin A-deficient rats

Vitamin A deficiency led to a decrease in the ability to control the localization of intestinal bacteria and an increase in translocation, which was followed by development of arthritis regardless of substantial levels of antibacterial antibodies.

Aberrant T-cell function in vitro and impaired T-cell dependent antibody response in vivo in vitamin A-deficient rats.

The increased IL-2 and IFN-gamma levels may reflect an up-regulation of Th1 cell function, while the decreased IgA, IgE and IL-6 levels indicate a suppression of Th2 cells.

Antigen-specific immune response impairment in the chick as influenced by dietary vitamin A.

A large vitamin A bolus did not cause immune response impairment and, on the contrary, restored normal immune functions in previously vitamin A-depleted chicks, implying a regulatory role for vitamin A in the immune system rather than a constitutive one.

Antibody production in vitamin A‐depleted rats is impaired after immunization with bacterial polysaccharide or protein antigens

The studies indicate that retinol status is an important determinant of the humoral immune response to certain types of antigen and suggest that antibody production to capsular polysaccharides and T cell‐dependent antigens is particularly dependent on adequate retinols status.

Neutrophil mediated inflammatory response in murine lupus.

It is concluded that the PMNC mediated inflammatory potential is not affected in severely diseased lupus mice, and the increased numbers of circulating PMNC together with intact PMNC function may explain why severely immune deficient l upus mice seldom show clinical signs of bacterial infection.