Measurement of interleukin-1 liberation in zymosan air-pouch exudate in mice

1994 ◽  
Vol 41 (1-2) ◽  
pp. 93-95 ◽  
Author(s):  
F. Erdő ◽  
K. Török ◽  
J. I. Székely
Keyword(s):  
Interleukin 1 ◽  
Air Pouch

Interleukin-1-like activity in the exudate of air-pouch inflammation in rats, and its participation in granuloma formation

1989 ◽  
Vol 27 (3-4) ◽  
pp. 359-360 ◽  
Author(s):  
K. Chiba ◽  
H. Shirota ◽  
K. Katayama ◽  
I. Yamatsu
Keyword(s):  
Interleukin 1 ◽  
Granuloma Formation ◽  
Air Pouch

scholarly journals Myeloid Heme Oxygenase-1 Regulates the Acute Inflammatory Response to Zymosan in the Mouse Air Pouch

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Rita Brines ◽  
Laura Catalán ◽  
Maria José Alcaraz ◽  
Maria Luisa Ferrándiz
Keyword(s):  
Inflammatory Response ◽  
Heme Oxygenase ◽  
Interleukin 1 ◽  
Heme Oxygenase 1 ◽  
Prostaglandin E ◽  
Acute Inflammatory Response ◽  
Air Pouch ◽  
Inflammatory Processes ◽  
Anti Inflammatory

Heme oxygenase-1 (HO-1) is induced by many stimuli to modulate the activation and function of different cell types during innate immune responses. Although HO-1 has shown anti-inflammatory effects in different systems, there are few data on the contribution of myeloid HO-1 and its role in inflammatory processes is not well understood. To address this point, we have used HO-1M-KO mice with myeloid-restricted deletion of HO-1 to specifically investigate its influence on the acute inflammatory response to zymosan in vivo. In the mouse air pouch model, we have shown an exacerbated inflammation in HO-1M-KO mice with increased neutrophil infiltration accompanied by high levels of inflammatory mediators such as interleukin-1β, tumor necrosis factor-α, and prostaglandin E2. The expression of the degradative enzyme matrix metalloproteinase-3 (MMP-3) was also enhanced. In addition, we observed higher levels of serum MMP-3 in HO-1M-KO mice compared with control mice, suggesting the presence of systemic inflammation. Altogether, these findings demonstrate that myeloid HO-1 plays an anti-inflammatory role in the acute response to zymosan in vivo and suggest the interest of this target to regulate inflammatory processes.

scholarly journals Carrageenan-induced acute inflammation in the mouse air pouch synovial model. Role of tumour necrosis factor

1997 ◽  
Vol 6 (1) ◽  
pp. 32-38 ◽  
Author(s):  
M. Romano ◽  
R. Faggioni ◽  
M. Sironi ◽  
S. Sacco ◽  
B. Echtenacher ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Prostaglandin E ◽  
Local Inflammation ◽  
Air Pouch ◽  
Necrosis Factor

We used the mouse air pouch model of inflammation to study the interaction between cytokines, prostaglandin E2(PGE2) and cell migration during the various phases of acute local inflammation induced by carrageenan. In serum, the levels of interleukin 1 (IL-1), interleukin 6 (IL-6), tumour necrosis factor (TNF), serum amiloid-A (SAA) and Fe++were never different from controls, indicating that no systemic inflammatory changes were induced. Locally the exudate volume and the number of leukocytes recruited into the pouch increased progressively until 7 days after carrageenan. The same was true for PGE2production. We could not measure IL-1 but the production of IL-6 and TNF reached a maximum after 5-24 h then quickly decreased. Anti-TNF antibodies inhibited cell migration by 50% 24 h after treatment. Pretreatment with interleukin 10 (IL-10) inhibited TNF production almost completely and cell migration by 60%. Carrageenan-induced inflammation was modulated by anti-inflammatory drugs. Pretreatment with dexamethasone (DEX) or indomethacin (INDO) inhibited cell migration and reduced the concentration of TNF in the exudate. Production of PGE2or vascular permeability did not correlate with the number of cells in the pouch. Local TNF seems to play an important role in this model, particularly for leukocyte migration in the first phase of the inflammatory process. In conclusion, the air pouch seems to be a good model for studying the regulation of the early events of local inflammation, particularly the role of cytokines and cell migration.

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