scholarly journals Sequential release of TNFα and phospholipase A2in a rat model of LPS-induced pleurisy

1997 ◽  
Vol 6 (3) ◽  
pp. 211-215
Author(s):  
C. Cicala ◽  
M. Bucci ◽  
F. D′Acquisto ◽  
L. Parente ◽  
G. Cirino

The levels of extracellular phospholipase A2(sPLA2) and TNFα, and cell accumulation were measured in the pleural washings obtained at different times following the induction ofEscherichia colilipopolysaccharide (LPS, 100 μg/cavity) pleurisy in rats. TNFα peaked at 2 hours (3036 ± 160.3 units/ml) and decreased thereafter. Conversely, levels of sPLA2peaked at 48 hours (1.97 ± 0.64 ng/ml) and were increased further (14.02 ± 4.16 ng/ml) by pretreatment with anti-TNFα antibody. Cell accumulation was not affected by antibody pretreatment. These data indicate that the sPLA2enzyme is involved in LPS-induced pleurisy. The enzyme seems not to be stimulated by TNFα which may be involved in the downregulation of sPLA2in this model of inflammation.

2001 ◽  
Vol 183 (18) ◽  
pp. 5230-5238 ◽  
Author(s):  
Geoffrey R. Langen ◽  
Jill R. Harper ◽  
Thomas J. Silhavy ◽  
S. Peter Howard

ABSTRACT DegP is a periplasmic protease that is a member of both the ςE and Cpx extracytoplasmic stress regulons ofEscherichia coli and is essential for viability at temperatures above 42°C. [U-14C]acetate labeling experiments demonstrated that phospholipids were degraded indegP mutants at elevated temperatures. In addition, chloramphenicol acetyltransferase, β-lactamase, and β-galactosidase assays as well as sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis indicated that large amounts of cellular proteins are released from degP cells at the nonpermissive temperature. A mutation in pldA, which encodes outer membrane phospholipase A (OMPLA), was found to rescue degPcells from the temperature-sensitive phenotype. pldA degP mutants had a normal plating efficiency at 42°C, displayed increased viability at 44°C, showed no degradation of phospholipids, and released far lower amounts of cellular protein to culture supernatants. degP and pldA degP mutants containing chromosomal lacZ fusions to Cpx and ςE regulon promoters indicated that both regulons were activated in the pldA mutants. The overexpression of the envelope lipoprotein, NlpE, which induces the Cpx regulon, was also found to suppress the temperature-sensitive phenotype ofdegP mutants but did not prevent the degradation of phospholipids. These results suggest that the absence of OMPLA corrects the degP temperature-sensitive phenotype by inducing the Cpx and ςE regulons rather than by inactivating the phospholipase per se.


2021 ◽  
Vol 45 (1) ◽  
pp. 49-52
Author(s):  
Doni Keyang ◽  
Syama N Prabhu ◽  
Ajay Pratap Singh ◽  
Neeraj Gangwar ◽  
Ambika Arun ◽  
...  

2009 ◽  
Vol 77 (11) ◽  
pp. 5163-5169 ◽  
Author(s):  
Samira Khaldi ◽  
Gilles Gargala ◽  
Laetitia Le Goff ◽  
Simon Parey ◽  
Arnaud Francois ◽  
...  

ABSTRACT Cryptosporidium spp. are a cause of self-limited diarrhea in immunocompetent hosts. In immunocompetent rats, Cryptosporidium parvum infection induced digestive hypersensitivity, a key pathophysiological factor in functional digestive disorders such as irritable bowel syndrome (IBS). In such a rat model, we sought to document whether jejunal hypersensitivity depends on C. parvum isolate and is associated with a mast cell accumulation. Five-day-old rats were orally administered 105 oocysts of either Nouzilly (NoI) or Iowa (IoI) C. parvum isolate. NoI-infected rats exhibited the lowest food intake on days 7 and 14 postinfection (p.i.). On day 7 p.i., small intestine villus atrophy, crypt hyperplasia, and inflammatory cell infiltration were prominent in NoI-infected rats, with higher numbers of Cryptosporidium forms than in IoI-infected rats. Compared to uninfected control rats, jejunal intraepithelial lymphocytes (IELs) were increased only in NoI-infected rats on day 14 p.i. On day 50 p.i., jejunal hypersensitivity to distension was found only in NoI-infected rats; this hypersensitivity is associated with activated mast cell accumulation. The number of mast cells in the jejunal lamina propria was increased from day 36 p.i. in NoI-infected rats and only at day 120 p.i. in IoI-infected rats. Our data suggest that both the severity of infection (weight loss, reduced food intake, villus atrophy, and IEL accumulation) and the onset of a jejunal hypersensitivity after infection in association with an activated mast cell accumulation are isolate dependent and related to NoI infection. This cryptosporidiosis rat model is a relevant model for the study of underlying mechanisms of postinfectious IBS-like symptoms.


Nephron ◽  
1995 ◽  
Vol 69 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Tetsuro Matsumoto ◽  
Masashi Haraoka ◽  
Yoshimitsu Mizunoe ◽  
Koichi Takahashi ◽  
Shuta Kubo ◽  
...  

1979 ◽  
Vol 86 (4) ◽  
pp. 1129-1138 ◽  
Author(s):  
Yumiko TAMORI ◽  
Masahiro NISHIJIMA ◽  
Shoshichi NOJIMA

Biochemistry ◽  
1989 ◽  
Vol 28 (3) ◽  
pp. 1139-1147 ◽  
Author(s):  
Anton J. G. Horrevoets ◽  
Tilman M. Hackeng ◽  
Hubertus M. Verheij ◽  
Ruud Dijkman ◽  
Gerard H. De Haas

1999 ◽  
Vol 181 (10) ◽  
pp. 3281-3283 ◽  
Author(s):  
Niek Dekker ◽  
Jan Tommassen ◽  
Hubertus M. Verheij

ABSTRACT Bacteriocin release protein is known to activate outer membrane phospholipase A (OMPLA), which results in the release of colicin fromEscherichia coli. In vivo chemical cross-linking experiments revealed that the activation coincides with dimerization of OMPLA. Permeabilization of the cell envelope and dimerization were characterized by a lag time of 2 h.


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