Inducing maternal inflammation promotes leptin production in offspring but does not improve allergic symptoms in a mouse model of allergic rhinitis.

AIMS: The intrauterine environment is considered to affect immunological development in fetus, leading to an increased risk of developing allergy. In particular, maternal lipopolysaccharides (LPS) administration might regulate the development of allergic disease in offspring. Several studies have shown that being obese relates to a higher prevalence of allergic diseases compared to normal weight. The present study explored the effects of inducing maternal inflammation with LPS before pregnancy on body weight, physical composition including body fat, adipokine production, and pathology of allergic rhinitis in offspring. MAIN METHODS: Female mice received a single intraperitoneal injection of LPS (2 µg/g BW). After 5 days of LPS administration, female mice were mated with males, and experimental allergic rhinitis was induced in female offspring. Immunization and nasal challenge with ovalbumin (OVA) were performed at 7 and 8 weeks of age. Allergic rhinitis-like symptoms, OVA-specific IgE and adipokines in sera, body weight, fat pad weight, and cytokine production by splenocytes in these 9-week-old offspring. KEY FINDINGS: Maternal LPS administration results in a significant increase in body weight, visceral fat accumulation, and serum leptin concentration, and the dominance of Th1 in Th balance. Nevertheless, there was no statistical difference in OVA-specific IgE titer and allergic-like symptoms between the groups. SIGNIFICANCE: In conclusion, maternal LPS promoted leptin production and altered Th balance in mice offspring, but not improved allergic symptoms in a mouse model of allergic rhinitis. It might suggest that inflammation during pregnancy plays a role in the adipose tissue function which could diversely influence allergic inflammation in offspring.

Nutritional status in relation to adipokines and oxidative stress is associated with disease activity in patients with rheumatoid arthritis.

OBJECTIVE: We assessed whether disease activity was associated with dietary habits, nutritional status, adipokines, and oxidative stress in patients with rheumatoid arthritis. METHODS: The subjects were 37 patients with RA. The assessment of the nutritional status included anthropometric and biochemical parameters. A food-frequency questionnaire and a 3-d diet record to assess dietary intake were used. The serum levels of adipokines and oxidative stress markers in sera and saliva were measured. The disease activity was determined using the 28 Disease Activity Score (DAS28). We divided the subjects into high (DAS28 ≥3.2) and low (DAS28 <3.2) disease activity groups. RESULTS: The serum leptin and albumin levels were significantly lower, whereas the inflammatory markers were increased, in the high disease activity group. The dietary intake assessment showed a lower intake of fish oil and a lower ratio of monounsaturated fatty acid intake in the high disease activity group. There was a negative correlation between the DAS28 and the dietary intake of the ratio of monounsaturated fatty acid to total fatty acid intake. The serum oxidative stress marker (reactive oxygen metabolites) showed a positive correlation to the DAS28. The salivary reactive oxygen metabolites also correlated with C-reactive protein and serum reactive oxygen metabolites. CONCLUSION: Altered serum adipokine levels with decreased albumin may reflect the deterioration that is associated with rheumatoid arthritis. An increased oxidative stress was observed in sera and saliva. Intakes of ω-3 polyunsaturated fatty acids, fish oil, and monounsaturated fatty acid seem to affect disease activity and may have beneficial effects by decreasing inflammation.

Analysis of adipose tissues and stromal vascular cells in a murine arthritis model.

PURPOSE: Changes in body composition in rheumatoid arthritis (RA), including a reduction in skeletal muscle mass and the accumulation of visceral fat, have been identified, and the interaction between immune abnormality and metabolic disorders has received much attention. The effect of a high-fat (HF) diet and the role of adipose tissue in an arthritis model were investigated. METHODS: The effect of an HF diet on the histopathology of joints in murine type II collagen-induced arthritis (CIA) was evaluated. The morphology and adipokine production of adipose tissues were analyzed, and macrophages in the stromal vascular fraction (SVF) were counted by flow cytometry. Serum adipokine levels were measured by ELISA. RESULTS: Significant exacerbation of joint destruction and aggravated pathological conditions were observed in CIA mice that were fed an HF diet. However, the boundary length of adipose tissue tended to decrease and the levels of adipokines (leptin and adiponectin) were lowered by the induction of arthritis. In HF/CIA mice, nevertheless, the production of MCP-1 in adipose tissues and the accumulation of macrophages in the SVF were significantly higher than CON/CIA group. The serum leptin/adiponectin (L/A) ratio was positively correlated with the number of macrophages in the SVF and MCP-1 production by adipose tissue, particularly in the CIA group. CONCLUSION: Functional alterations of adipose tissues could be originated from HF diet during developing arthritis. An abnormal activation of macrophages and an increased production of MCP-1 in adipose tissues might be both involved in joint destruction and inflammation.