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Yu Wu, Tingting Wu, Jun Wu, Lei Zhao, Qing Li, Zac Varghese, John F Moorhead, Stephen H Powis, Yaxi Chen and Xiong Z Ruan

impaired glucose tolerance and diabetes ( Xiang et al . 2010 a ). Obesity, insulin resistance, and T2DM are closely associated with chronic inflammation characterized by abnormal cytokine production, increased acute-phase reactants and other mediators, and

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J. A. P. Da Silva, S. H. Peers, M. Perretti and D. A. Willoughby


The influence of gender and sex hormones upon both the hypothalamic-pituitary-adrenal (HPA) axis and the immune and inflammatory responses is well recognized, but it is not clear to what extent the two effects are interdependent. We have investigated this interaction using a chronic inflammation model. Corticosterone levels were measured in mature BALB/c male and female mice, which were intact, sham-operated or gonadectomized. No significant differences were found between groups in baseline corticosterone, but systemic inflammation (cotton-induced granulomas) resulted in stimulation of the HPA axis in a reproducible pattern. Corticosterone levels were higher in sham-operated females than in males, but gonadectomy had opposing effects in the two genders, resulting in reduced levels in females but significantly increased levels in males. A similar pattern emerged after stimulation by ether exposure or injection of interleukin-1β. In the chronic inflammatory model, replacement of ovariectomized females with physiological levels of progesterone restored a response similar to that of intact females. Physiological levels of 5α-dihydrotestosterone prevented the increase in corticosterone levels caused by castration in males and also resulted in reduced corticosterone levels in sham-operated females. Oestradiol treatment did not affect corticosterone levels. Release of interleukin-1 by peritoneal macrophages from intact and gonadectomized mice with chronic inflammation followed a similar pattern, females releasing more than males. These data suggest a complex inter-relationship between sex steroids, inflammatory stimuli and the HPA axis, such that females have a greater tendency than males to generate activating signals and in addition have a greater sensitivity to such factors.

Journal of Endocrinology (1993) 136, 389–397

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S Otabe, N Wada, T Hashinaga, X Yuan, I Shimokawa, T Fukutani, K Tanaka, T Ohki, S Kakino, Y Kurita, H Nakayama, Y Tajiri and K Yamada

chronic inflammation, and the possible effects of adiponectin on sirtuin levels. To answer these questions, we established KK/Ta mice expressing human adiponectin in the liver. The KK/Ta mouse is an animal model of metabolic syndrome exhibiting moderate

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Kanta Kon, Hiroshi Tsuneki, Hisakatsu Ito, Yoshinori Takemura, Kiyofumi Sato, Mitsuaki Yamazaki, Yoko Ishii, Masakiyo Sasahara, Assaf Rudich, Takahiro Maeda, Tsutomu Wada and Toshiyasu Sasaoka

( Mcp1 ) mRNA levels by 2-SORA-MK1064 and DORA-12. These results indicate that daily resting-phase administration of 2-SORA-MK1064 and DORA-12, but not 1-SORA-1, attenuated chronic inflammation in the liver of db/db mice. The levels of

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JA Baugh and SC Donnelly

The diverse actions of macrophage migration inhibitory factor (MIF) within the immuno-neuroendocrine system are yet to be fully understood, but it is clear that MIF plays a pivotal role in the regulation of both the innate and adaptive immune response. An emerging body of data presently indicates that MIF's position within the cytokine cascade is to act in concert with glucocorticoids to control the 'set point' and magnitude of the immune and inflammatory response. In this article we will review the actions of MIF within the immune system and discuss the overlapping and contrasting aspects of MIF and glucocorticoid biology. In particular we will focus on the role of MIF within the immuno-neuroendocrine interface and suggest molecular mechanisms by which MIF may counter-regulate glucocorticoid function. Finally we will discuss emerging evidence that functional MIF gene-promoter polymorphisms render one susceptible to elevated MIF expression, and the development of an exaggerated immune/inflammatory response that potentiates the progression to chronic inflammatory disease.

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A Boelen, J Kwakkel, W M Wiersinga and E Fliers

increased hypothalamic interleukin (IL)-1β mRNA expression ( Boelen et al. 2004 ). It is known that chronic inflammation in mice, induced by an s.c. injection of turpentine in each hind limb also results in altered peripheral thyroid hormone metabolism

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J Kwakkel, H C van Beeren, M T Ackermans, M C Platvoet-ter Schiphorst, E Fliers, W M Wiersinga and A Boelen

, timing, and severity of illness. 1) Turpentine-induced abscess in the hindlimb, a model of local chronic inflammation. 2) Streptococcus pneumoniae infection, a lethal model that results in severe pneumonia and sepsis. Muscle D2 expression and D2

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S F Ahmed and C Farquharson

chronic inflammation which is often associated with altered systemic and local cytokine milieu. The mechanisms by which these inflammatory cytokines modulate linear growth and skeletal development are poorly understood, but an involvement of members of the

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Richard R Almon, Debra C DuBois, William Lai, Bai Xue, Jing Nie and William J Jusko

examined. Adding to the picture of chronic inflammation in the GK rats are the expression patterns of two interferon-induced genes: Fig. 6 B, interferon-induced protein with tetratricopeptide repeats 1 ( Ifit1 ) and Fig. 6 C, interferon-inducible GTPase

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Yingxin Xian, Zonglan Chen, Hongrong Deng, Mengyin Cai, Hua Liang, Wen Xu, Jianping Weng and Fen Xu

Introduction Obesity is widely considered as a state with low-grade chronic inflammation ( de Heredia et al. 2012 ). Elevated circulating levels of inflammatory cytokines, such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-6