Prolonged “Slight” Fever in Rats Induced by Administration of Freund’s Complete Adjuvant: Effects of Indomethacin and NO-Related Drugs

1994 ◽  
pp. 385-389
Author(s):  
I. N. Semenenya ◽  
A. V. Gourine ◽  
V. N. Gourine
Keyword(s):  
Freund’S Complete Adjuvant ◽  
Freund's Complete Adjuvant ◽  
Slight Fever ◽  
Adjuvant Effects

Experimental Amyloidosis Induced by Immune Complex

1971 ◽  
Vol 29 ◽  
pp. 582-583
Author(s):  
A. Kawaoi
Keyword(s):  
Immune Complex ◽  
Systemic Amyloidosis ◽  
Human Diseases ◽  
Experimental Amyloidosis ◽  
Freund’S Complete Adjuvant ◽  
Freund's Complete Adjuvant ◽  
Immunological Approach ◽  
Experimentally Induced

Numbers of immunological approach have been made to the amyloidosis through the variety of predisposing human diseases and the experimentally induced animals by the greater number of agents. The results suggest an important role of impaired immunity involving both humoral and cell-mediated aspects.Recently the author has succeeded in producing amyloidosis in the rabbits and mice by the injections of immune complex of heat denatured DNA.The aim of this report is to demonstrate the details of the ultrastructure of the amyloidosis induced by heterologous insoluble immune complex. Eleven of twelve mice, dd strain, subcutaneously injected twice a week with Freund's complete adjuvant and four of seven animals intraperitonially injected developed systemic amyloidosis two months later from the initial injections. The spleens were electron microscopically observed.

Opioid Peptide–expressing Leukocytes

2001 ◽  
Vol 95 (2) ◽  
pp. 500-508 ◽  
Author(s):  
Heike L. Rittner ◽  
Alexander Brack ◽  
Halina Machelska ◽  
Shaaban A. Mousa ◽  
Monika Bauer ◽  
...  
Keyword(s):  
Immune Cells ◽  
Cold Water ◽  
Inflammatory Diseases ◽  
Sensory Nerve ◽  
Opioid Peptide ◽  
Cell Surface Antigens ◽  
Swim Stress ◽  
Freund’S Complete Adjuvant ◽  
Beta Endorphin ◽  
Freund's Complete Adjuvant

Background Inflammatory pain can be effectively controlled by an interaction of opioid receptors on peripheral sensory nerve terminals with opioid peptides released from immune cells upon stressful stimulation. To define the source of opioid peptide production, we sought to identify and quantify populations of opioid-containing cells during the course of Freund's complete adjuvant-induced hind paw inflammation in the rat. In parallel, we examined the development of stress-induced local analgesia in the paw. Methods At 2, 6, and 96 h after Freund's complete adjuvant inoculation, cells were characterized by flow cytometry using a monoclonal pan-opioid antibody (3E7) and antibodies against cell surface antigens and by immunohistochemistry using a polyclonal antibody to beta-endorphin. After magnetic cell sorting, the beta-endorphin content was quantified by radioimmunoassay. Pain responses before and after cold water swim stress were evaluated by paw pressure thresholds. Results In early inflammation, 66% of opioid peptide-producing (3E7+) leukocytes were HIS48+ granulocytes. In contrast, at later stages (96 h), the majority of 3E7+ immune cells were ED1+ monocytes or macrophages (73%). During the 4 days after Freund's complete adjuvant inoculation, the number of 3E7+ cells increased 5.6-fold (P < 0.001, Kruskal-Wallis test) and the beta-endorphin content in the paw multiplied 3.9-fold (P < 0.05, Kruskal-Wallis test). In parallel, cold water swim stress-induced analgesia increased by 160% (P < 0.01, analysis of variance). Conclusions The degree of endogenous pain inhibition is proportional to the number of opioid peptide-producing cells, and distinct leukocyte lineages contribute to this function at different stages of inflammation. These mechanisms may be important for understanding pain in immunosuppressed states such as cancer, diabetes, or AIDS and for the design of novel therapeutic strategies in inflammatory diseases.

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