Acute Hepatic Necrosis Induced by Brucella Infection in Hyperthyroid Mice

نویسندگان

  • G. Mary Bradley
  • Wesley W. Spink
چکیده

When small numbers of Brucella melitensis were inoculated into ABC mice, occasional hepatic granulomas without necrosis were demonstrated. The greatest multiplication of brucellae was detected in the spleens. Because it had been previously observed that ACTH or cortisone markedly accelerated the multiplication of brucellae in the livers of infected mice with destruction of liver cells, it was considered that triiodothyronine might likewise exaggerate a brucella infection by stimulating endogenous adrenal secretion. Although adrenal hypertrophy was produced, infection of mice treated with triiodothyronine resulted in severe hepatic necrosis or infarcts without the multiplication of brucellae in either the livers or spleens. The lesions were not encountered in untreated infected mice or in control mice treated with triiodothyronine. The necrosis was associated with minimal inflammatory reaction. The necrosis was not induced in mice treated with triiodothyronine and given brucella endotoxin. The precise genesis of the acute hepatic necrosis cited in these experiments remains undefined. Triiodothyronine did not cause deaths in mice infected with Br. melitensis. The infection was neither enhanced nor suppressed.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Acute Brucella melitensis M16 infection model in mice treated with tumor necrosis factor-alpha inhibitors.

INTRODUCTION There is limited data in the literature about brucellosis related to an intracellular pathogen and anti-tumor necrosis factor alpha (anti-TNFα) medication. The aim of this study was to evaluate acute Brucella infections in mice receiving anti-TNFα drug treatment. METHODOLOGY Anti-TNFα drugs were injected in mice on the first and fifth days of the study, after which the mice were ...

متن کامل

Orthotopic Liver Transplantation for Etanercept-Induced Acute Hepatic Failure; a case report

The occurrence of hepatotoxicity following etanercept (tumor necrosis factor-alpha antagonist) prescription, has been studied well. However, an acute hepatic failure leading to liver transplant as an adverse effect of this drug has not been reported in the literature. In this article, we are going to present a case of acute liver failure followed by liver transplantation, in a 32 years old man ...

متن کامل

Nramp1 is not a major determinant in the control of Brucella melitensis infection in mice.

Brucella, the causative agent of brucellosis in animals and humans, can survive and proliferate within macrophages. Macrophages mediate mouse resistance to various pathogens through the expression of the Nramp1 gene. The role of this gene in the control of Brucella infection was investigated. When BALB/c mice (Nramp1(s)) and C.CB congenic mice (Nramp1(r)) were infected with Brucella melitensis,...

متن کامل

اثر محافظتی عصاره زردچوبه (Curcuma longa) در مسمومیت کبدی حاد ناشی از استامینوفن در موش آزمایشگاهی

Background and Objective: Acetaminophen is widely used as an analgesic and antipyretic drug, and when given in high doses can causes hepatic and renal injury in both human and animal. The liver damage in form of centrilobular necrosis is induced by using acetaminophen, depends on the cytochrome P-450 activities. In the present study hepatoprotective effects of Curcuma longa extract on hepatic i...

متن کامل

Susceptibility of IFN regulatory factor-1 and IFN consensus sequence binding protein-deficient mice to brucellosis.

IFN-gamma is a key cytokine controlling Brucella infection, and the diverse functions of this cytokine are mediated by IFN regulatory factors (IRFs) such as IRF-1, IRF-2, and IFN consensus sequence binding protein (ICSBP). However, the roles of these three IRFs in Brucella infection have not been investigated. The infection of each IRF-deficient mouse strain provides an opportunity to determine...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • The Journal of Experimental Medicine

دوره 110  شماره 

صفحات  -

تاریخ انتشار 1959