Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.22.36 (caspase-1)
 6,285 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Escherichia coli (E. coli) infections in mouse mammary glands are rarely described and poorly characterized. In order to investigate the host immune response during coliform mastitis, several inflammatory parameters were evaluated at 24 and 48h following inoculation of mouse mammary glands with E. coli. Successfully challenged mice showed high values of the acute phase protein serum amyloid A (SAA) in blood. Systemic concentrations of the major inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were also increased as compared to control mice, while interleukin-1 (IL-1) levels remained negligible. Infected mammary glands showed a significant increase of all cytokine levels as compared to control glands. In accordance, mammary expression of the biologically inactive proform of IL-1beta was strongly up-regulated. Remarkably, data obtained in wild type as well as caspase-1 knockout mice showed that IL-1beta maturation seemed to occur independently from caspase-1. Finally, E. coli infection also triggered activation of the nuclear transcription factor-kappaB (NF-kappaB) in the mammary gland. In conclusion, the current study provides novel insights on the contribution of major regulatory proteins to the acute inflammatory host response at the local and systemic level during E. coli mastitis in mice.
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PMID:Inflammatory mediators in Escherichia coli-induced mastitis in mice. 1824 14

In this study we identified a potential pro-apoptotic caspase gene, Bombyx mori(B. mori)ICE-2 (BmICE-2) which encoded a polypeptide of 284 amino acid residues, including a (169)QACRG(173) sequence which surrounded the catalytic site and contained a p20 and a p10 domain. BmICE-2 expressed in Escherichia coli (E. coli) exhibited high proteolytic activity for the synthetic human initiator caspase-9 substrates Ac-LEHD-pNA, but little activity towards the effector caspase-3 substrates Ac-DEVD-pNA. When BmICE-2 was transiently expressed in BmN-SWU1 silkworm B. mori cells, we found that the high proteolytic activity for Ac-LEHD-pNA triggered caspase-3-like protease activity resulting in spontaneous cleavage and apoptosis in these cells. This effect was not replicated in Spodoptera frugiperda 9 cells. In addition, spontaneous cleavage of endogenous BmICE-2 in BmN-SWU1 cells could be induced by actinomycin D. These results suggest that BmICE-2 may be a novel pro-apoptotic gene with caspase-9 activity which is involved apoptotic processes in BmN-SWU1 silkworm B. mori cells.
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PMID:BmICE-2 is a novel pro-apoptotic caspase involved in apoptosis in the silkworm, Bombyx mori. 2449 40

Infection of the mammary gland with live bacteria elicits a pathogen-specific host inflammatory response. To study these host-pathogen interactions wild type mice, NF-kappaB reporter mice as well as caspase-1 and IL-1beta knockout mice were intramammarily challenged with Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). The murine mastitis model allowed to compare the kinetics of the induced cytokine protein profiles and their underlying pathways. In vivo and ex vivo imaging showed that E. coli rapidly induced NF-kappaB inflammatory signaling concomitant with high mammary levels of TNF-alpha, IL-1 alpha and MCP-1 as determined by multiplex analysis. In contrast, an equal number of S. aureus bacteria induced a low NF-kappaB activity concomitant with high mammary levels of the classical IL-1beta fragment. These quantitative and qualitative differences in local inflammatory mediators resulted in an earlier neutrophil influx and in a more extensive alveolar damage post-infection with E. coli compared to S. aureus. Western blot analysis revealed that the inactive proIL-1beta precursor was processed into pathogen-specific IL-1beta fragmentation patterns as confirmed with IL-1beta knockout animals. Additionally, caspase-1 knockout animals allowed to investigate whether IL-1beta maturation depended on the conventional inflammasome pathway. The lack of caspase-1 did not prevent extensive proIL-1beta fragmentation by either of S. aureus or E. coli. These non-classical IL-1beta patterns were likely caused by different proteases and suggest a sentinel function of IL-1beta during mammary gland infection. Thus, a key signaling nodule can be defined in the differential host innate immune defense upon E. coli versus S. aureus mammary gland infection, which is independent of caspase-1.
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PMID:Non-classical proIL-1beta activation during mammary gland infection is pathogen-dependent but caspase-1 independent. 2516 21