Influence on inflammation cytokines in passive immunotherapy for allergic rhinitis guinea pigs / 中国免疫学杂志

Objective:To explore the influence on inflammation cytokines for anti-IL-1βand TNF-αIgY intranasal treatment in guinea pigs with allergic rhinitis.Methods:The allergic rhinitis model in guinea pigs was established using ovalbumin(OVA).Hartley guinea pigs were randomly divided into the control group(group C,n=17),the allergic rhinitis model group(group M,n=27),the 0.1%anti-IL-1βand TNF-αIgY treatment group(group Z1,n=21)and the fluticasone propionate treatment group(group Z2,n=21). At 2 h,4 h and 8 h after the last treatment,blood was got by heart puncture,as well as nose was lavaged using 0.9% saline and the nasal lavage fluid( NLF) was collected.The level of cytokines was examined using ELISA kits.Results: In the peripheral blood, the levels of IL-1β,IL-5,IL-9,IL-13,IL-18,IL-33 and TGF-β1 from 2 h to 8 h;TNF-αand OVA-specific IgE from 2 h to 4 h;and IL-22 from 4 h to 8 h were significantly decreased in the 0.1%anti-IL-1βand TNF-αIgY treatment group compared with the allergic rhinitis model group(P<0.05).In the NLF,the levels of IL-1β,IL-5,IL-9,IL-13,IL-22,IL-33,TNF-α,TGF-β1 and OVA-specific IgE from 2 h to 8 h;and IL-18 at 2 h were significantly decreased in the 0.1% anti-IL-1βand TNF-αIgY treatment group compared with the allergic rhinitis model group ( P<0.05 ) .Conclusion: Anti-IL-1βand TNF-αIgY intranasal treatment can significantly reduce inflammation cytokine levels in allergic rhinitis guinea pigs.

Distribution and expression of visfatin-positive cells in the spleen of lipopolysaccharide-stimulated piglets / Distribución y expresión de células visfatin positivas en el bazo de lechones estimulados con lipopolisacáridos

The histological changes in the spleen and the immunohistochemical expression of visfatin in lipopolysaccharide-stimulated piglets are reported to examine the relation between visfatin and inflammation. The results are as follows: (1) After LPS treated, the spleen displayed thicker capsules and trabecula, the thinner periarterial lymphatic sheath, and the more expandable splenic sinusoid, with an increase in the number of splenic nodules, lymphocytes, ellipsoids of the marginal zone, red blood cells and macrophagocytes. (2) Visfatin-positive cells were mainly distributed in the red pulp of the spleen, with less in splenic nodules and periarterial lymphatic sheath. In the LPS-treated group, the signal intensity and quantity of the visfatin-positive cells were significantly higher in the red pulp and the ellipsoids of the spleen (P<0.01), whereas lower in the periarterial lymphatic sheath. These results indicate that LPS stimulation induces inflammation, causing the histological changes of the piglet spleen and activating humoral immune response. Moreover, variation of visfatin in the spleen suggests that lymphocytes and macrophages are the potent source of visfatin which participates in the humoral immune response in the inflammation.

Se presentan los cambios histológicos en el bazo y la expresión inmunohistoquímica de visfatin en lechones estimulados mediante lipopolisacáridos (LPS) con el objetivo de estudiar la relación entre visfatin e inflamación. Los resultados fueron los siguientes: (1) Después del tratamiento por LPS se observaron en el bazo cápsulas más gruesas y trabéculas, una vaina linfática periarterial más delgada, y más sinusoides esplénicos expandible, con un aumento en el número de nódulos esplénicos, linfocitos, elipsoides de la zona marginal, como también un aumento de las células rojas de la sangre y los macrofagocitos. (2) Las células visfatina-positivas se distribuyeron principalmente en la pulpa roja del bazo, con una cantidad menor en los nódulos esplénicos y la vaina linfática periarterial. En el grupo tratado con LPS, la intensidad de la señal y número de células positivas fueron significativamente mayor en la pulpa roja y los elipsoides del bazo (P<0,01), mientras que estas fueron menores en la vaina linfática periarterial. Estos resultados indican que la estimulación con LPS induce la inflamación provocando cambios histológicos del bazo de los lechones y la activación de la respuesta inmune humoral. Por otra parte, la variación de visfatin en el bazo sugiere que los linfocitos y los macrófagos son una fuente potente de visfatin en la respuesta inmune humoral de la inflamación.

Endothelial nitric oxide synthase gene polymorphisms associated with susceptibility to high altitude pulmonary edema in Chinese railway construction workers at Qinghai-Tibet over 4 500 meters above sea level / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To examine whether the polymorphisms of endothelial nitric oxide synthase (eNOS) gene are associated with the susceptibility to high altitude pulmonary edema (HAPE) in Chinese railway construction workers at Qinghai-Tibet where the altitude is over 4 500 m above sea level.</p><p><b>METHODS</b>A case-control study was conducted including 149 HAPE patients in the construction workers and 160 healthy controls randomly recruited from their co-workers, matching the patients in ethnicity, age, sex, lifestyle, and working conditions. Three polymorphisms of eNOS gene, T-786C in promoter, 894G/T in exon 7, and 27bp variable number tandem repeat (VNTR) in intron 4, were genotyped using polymerase chain reaction (PCR) and confirmed with DNA sequencing.</p><p><b>RESULTS</b>The frequencies of 894T allele and heterozygous G/T of the 894G/T variant were significantly higher in HAPE patients group than in the control group (P=0.0028 and P=0.0047, respectively). However, the frequencies of the T-786C in promoter and the 27bp VNTR in intron 4 were not significantly different between the two groups. Haplotypic analysis revealed that the frequencies of two haplotypes (H3,T-T-b, b indicates 5 repeats of 27 bp VNTR; H6, C-G-a, a indicates 4 repeats of 27 bp VNTR) were significantly higher in HAPE patients (both Pü0.0001). On the contrary, the frequencies of H1 (T-G-b) and H2 (T-G-a) were lower in HAPE patients than in healthy controls (both Pü0.001).</p><p><b>CONCLUSIONS</b>Two haplotypes (T-T-b and C-G-a) may be strongly associated with susceptibility to HAPE. Compared with the individual alleles of eNOS gene, the interaction of multiple genetic markers within a haplotype may be a major determinant for the susceptibility to HAPE.</p>