Evidence For Reciprocal Interaction Research Articles

Current status and prospects of intestinal microbiome studies.

The incidence and prevalence of inflammatory bowel disease (IBD) in Asia has witnessed a rapid increase within a few decades. The genetic susceptibility and epidemiologic backgrounds in the Asian population have been found to be different from that of Western populations. There is an extensive crosstalk between gut microbiota and human hosts, with evidence of reciprocal interactions. It is well known that gut microbiota can affect the host immune system and in turn, host genetic backgrounds can affect gut microbiota reciprocally. Evidences have implicated gut microbes in the development of IBD, but no causative microorganisms have been identified. Recent advances in sequencing technology and computational analysis have now made identification of complex gut microbiomes accessible. Further research targeting gut microbiota could help in identifying biomarkers to predict clinical response, and therapeutic modalities that might affect their resilience.

Induction of oligodendrocyte differentiation by Olig2 and Sox10: Evidence for reciprocal interactions and dosage-dependent mechanisms

Recent studies have suggested that oligodendrocyte development is likely to be under the control of a hierarchy of lineage-specific transcription factors. In the developing mouse spinal cord, expression of Olig2, Sox10 and Nkx2.2 is sequentially up-regulated in cells of oligodendrocyte lineage. These transcription factors play essential roles in oligodendrocyte specification and differentiation. However, the regulatory relationship and functional interactions among these transcription factors have not been determined. In this study, we systematically investigated the function and hierarchical relationship of Olig2, Sox10 and Nkx2.2 transcription factors in the control of oligodendrocyte differentiation. It was found that over-expression of Olig2 is sufficient to induce Sox10, Nkx2.2 and precocious oligodendrocyte differentiation in embryonic chicken spinal cord. Sox10 expression alone is also sufficient to stimulate ectopic oligodendrocyte differentiation and weakly induce Nkx2.2 expression. Although genetic evidence indicated that Sox10 functions downstream of Olig2, Sox10 activity can modulate Olig2 expression. In addition, we presented evidence that the control of oligodendrocyte differentiation by Olig2, Sox10 and Nkx2.2 is a dosage-dependent developmental process and can be affected by both haploinsufficiency and over-dosage.

Medial basal hypothalamic monoamine activity associated with intracerebroventricular p-chlorophenylalanine-induced hyperphagia

There is evidence for reciprocal interactions between the brain monoamine neurotransmitters serotonin and noradrenaline which may play a critical role in homeostasis. The aim of the present study was to establish the effect of drug-induced damage to the serotoninergic system on noradrenergic activity in the hypothalamus. Bilateral intracerebroventricular injections of p-chlorophenylalanine (PCPA; 3 mg/kg in 2 × 6 μl) were made to induce destruction in the serotoninergic system. Relative to saline-injected controls, PCPA-injected rats began overeating by 3 days postinjection. On day 10, when the experimental rats were consuming approximately 120% that of controls, animals were 4-h food deprived, sacrificed and the medial basal hypothalamus was removed for later analysis (by gas chromatography/mass spectrometry) of noradrenaline (NA), serotonin (5-HT) and dopamine (DA) and their principal metabolites dihydroxyphenylethyleneglycol (DHPG), 5-hydroxyindoleacetic acid (5-IAAA) and 3,4-dihydroxyphenylacetic acid (DOPAC), respectively. The ratio of metabolite to monoamine provided an index of functional activity. Trunk blood was collected for analysis of serum insulin and glucose. PCPA-injected animals had higher levels of DHPG ( P < 0.05), an increase in the DHPG/NA ratio ( P <0.02), lower serum insulin ( P < 0.05) and increased serum glucose ( P < 0.05). There were significant correlations between noradrenergic activity (DHPG/NA ratio) and: (1) food intake (day 9 and 10 average; r = 0.62, P < 0.05); and (2) serum glucose ( r = 0.59, P < 0.05). In contrast, PCPA treatment only marginally lowered levels of 5-HT and 5-HIAA with no change in the 5-HIAA/5-HT ratio and no changes in DA or DOPAC or the DOPAC/DA ratio. Neither serotoninergic nor dopaminergic activity was related to any of the intake, body weight, insulin or glucose measures. We conclude that intracerebroventricular PCPA chronically elevates hypothalamic noradrenergic activity and this, rather than decreased serotoninergic activity, may lead to the observed hyperphagia, hyperglycemia and hypoinsulinemia.

Further evidence for reciprocal interactions between the annual sexual and thyroid cycles in male Peking ducks

The possible relationships between the annual reproductive and thyroid cycles were explored in two groups of either orchidectomized (six), or thyroidectomized (six) Peking ducks, which were compared with a large group of intact controls. LH, testosterone, and thyroxine were measured on blood samples collected monthly. Castrates exhibited an annual cycle in LH, which at its highest point was five times above the peak levels found in intact birds and culminated in August–September when the thyroxine cycle in the birds started to decrease. From January through July the thyroxine concentrations in the castrates were at maximal levels, similar to those that were attained in intact birds only in June. Thyroidectomy if performed during the reproductive season in April suppressed the biphasic pattern of the reproductive hormone cycle during the postnuptial phase and delayed from June to October the postnuptial decrease in the hormones. During this phase LH levels were twice as high and testosterone titers were equal to those in sexually active drakes. In intact ducks the increasing testosterone levels in winter and spring appear, therefore, to depress the thyroid while the annual peak in thyroxine secretion in June may act as an essential (primary?) factor in causing the cessation of the reproductive season. The autumnal decrease in LH testosterone, and thyroxine appears to be unrelated to any testis-thyroid interactions or to the negative feedback of testosterone on LH.