PubMed · 2909848
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W Liddle. 1989-01-02. Chronic asthma.. https://pubmed.ncbi.nlm.nih.gov/2909848/
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Gene expression of 5-lipoxygenase (5-LO) and leukotriene A(4) (LTA(4)) hydrolase was analyzed in the peripheral blood of 48 children with active primary nephrotic syndrome (PNS) (group I), 27 children with PNS in remission (group II), and 20 controls. Group I included 34 patients with steroid-sensitive PNS (SSNS) and 14 patients with steroid-resistant PNS (SRNS). Total RNA purified from peripheral blood mononuclear (PBMN) cells was reverse transcribed into cDNA and amplified with specific primers in the polymerase chain reaction. All group I patients and none of the controls expressed 5-LO and LTA(4 )hydrolase. Of group II children, 22.2% expressed 5-LO, while 51.9% expressed LTA(4 )hydrolase. Among group I patients there was a significant positive correlation between the degree of proteinuria and the expression of 5-LO ( r=0.27, P=0.03) and LTA(4 )hydrolase ( r=0.44, P=0.001). There was no difference in the degree of expression of both enzymes between SSNS and SRNS patients. In conclusion, leukotrienes may play a role in the pathogenesis of PNS in children, but they do not participate in the response of these patients to steroids.
The authors report a rare case of a female patient diagnosed with mixed connective tissue disease (MCTD). After a few years in remission, the patient acquired herpes zoster infection followed by a disease flare. Disease activity was accompanied by the development of meningitis. To determine whether the meningitis was caused by the previous herpes virus infection or was aseptic meningitis associated with the activity of MCTD raised important differential diagnostic issues. Repeated laboratory assessments of the patient's sera and cerebrospinal fluid revealed leukocytopenia, high anti-U1 ribonucleoprotein autoantibody level, increased immune complex, and decreased complement concentrations. The administration of corticosteroids resulted in rapid improvements in clinical symptoms and laboratory indicators.
Corticosteroids are routinely administered to women at risk for preterm delivery to induce fetal lung maturation. Antenatal corticosteroids have immunomodulatory effects on fetal immune cells that are poorly understood. We hypothesized that maternal betamethasone would alter in fetal monocytes both the initiation of inflammation in response to pro-inflammatory stimuli and the resolution of inflammation by phagocytosis of apoptotic neutrophils. Preterm lambs at 124 d gestation were delivered 15 h, 1 d, 2 d, or 7 d after 0.5 mg/kg maternal intramuscular betamethasone. Monocytes from cord blood were isolated and cultured and results were compared with monocytes from preterm lambs exposed to maternal saline or monocytes from adult sheep. Phagocytosis of Escherichia coli was not changed, however, phagocytosis of apoptotic neutrophils was low in fetal monocytes but increased after 7 d exposure to maternal betamethasone to the level found in adult monocytes. Hydrogen peroxide production after endotoxin stimulus was significantly reduced to 7.1 +/- 2.2 micromol at 5 h, 8.7 +/- 2.9 micromol at 24 h, and 4.1 +/- 1.9 micromol at 48 h versus 16.4 +/- 3.6 micromol in control animals; at 7 d, the hydrogen peroxide production increased to 74.3 +/- 19.7 micromol (p < 0.05, per 10(6) monocytes). IL-6 production was reduced at 15 h after maternal betamethasone but at no other time point. Maternal betamethasone initially suppressed several fetal monocyte functions, however, at 7 d, measurements of initiation and resolution of inflammation were increased to levels similar to monocytes from adult sheep. The time-dependent changes in maternal betamethasone modulation of the responses of fetal monocytes may influence immune function of the preterm lamb after delivery.