Right Pleural Effusion in Fitz-Hugh-Curtis Syndrome

Right pleural effusion was diagnosed in a 36-year-old woman with right upper quadrant pain and fever. Enhanced pelvic computed tomography performed because of irregular genital bleeding revealed the pelvic inflammatory disease. Upon further questioning, the patient confirmed that she had recently undergone therapy for Chlamydia trachomatis infection. Therefore she was given an injection of tetracycline because we suspected Fitz-Hugh-Curtis syndrome (FHCS), a pelvic inflammatory disease characterized by perihepatitis associated with chlamydial infection. A remarkable clinical response to antibiotics was noted. The right upper quadrant pain was due to perihepatitis, and the final diagnosis was FHCS. Right pleural effusion may be caused by inflammation of the diaphragm associated with perihepatitis. Once chlamydial infection reaches the subphrenic liver, conditions in the closed space between the liver and diaphragm due to inflammatory adhesion may be conductive to chlamydial proliferation. The possibility of FHCS should be considered in patients and carefully distinguished from other abdominal diseases

Selective modulation of Wnt ligands and their receptors in adipose tissue by chronic hyperadiponectinemia.

BACKGROUND: Adiponectin-transgenic mice had many small adipocytes in both subcutaneous and visceral adipose tissues, and showed higher sensitivity to insulin, longer life span, and reduced chronic inflammation. We hypothesized that adiponectin regulates Wnt signaling in adipocytes and thereby modulates adipocyte proliferation and chronic inflammation in adipose tissue. MATERIALS AND METHODS: We examined the expression of all Wnt ligands and their receptors and the activity of Wnt signaling pathways in visceral adipose tissue from wild-type mice and two lines of adiponectin-transgenic mice. The effects of adiponectin were also investigated in cultured 3T3-L1 cells. RESULTS: The Wnt5b, Wnt6, Frizzled 6 (Fzd6), and Fzd9 genes were up-regulated in both lines of transgenic mice, whereas Wnt1, Wnt2, Wnt5a, Wnt9b, Wnt10b, Wnt11, Fzd1, Fzd2, Fzd4, Fzd7, and the Fzd coreceptor low-density-lipoprotein receptor-related protein 6 (Lrp6) were reduced. There was no difference in total β-catenin levels in whole-cell extracts, non-phospho-β-catenin levels in nuclear extracts, or mRNA levels of β-catenin target genes, indicating that hyperadiponectinemia did not affect canonical Wnt signaling. In contrast, phosphorylated calcium/calmodulin-dependent kinase II (p-CaMKII) and phosphorylated Jun N-terminal kinase (p-JNK) were markedly reduced in adipose tissue from the transgenic mice. The adipose tissue of the transgenic mice consisted of many small cells and had increased expression of adiponectin, whereas cyclooxygenase-2 expression was reduced. Wnt5b expression was elevated in preadipocytes of the transgenic mice and decreased in diet-induced obese mice, suggesting a role in adipocyte differentiation. Some Wnt genes, Fzd genes, and p-CaMKII protein were down-regulated in 3T3-L1 cells cultured with a high concentration of adiponectin. CONCLUSION: Chronic hyperadiponectinemia selectively modulated the expression of Wnt ligands, Fzd receptors and LRP coreceptors accompanied by the inhibition of the Wnt/Ca(2+) and JNK signaling pathways, which may be involved in the altered adipocyte cellularity, endogenous adiponectin production, and anti-inflammatory action induced by hyperadiponectinemia

Analysis of the Wnt ligand family, their receptors and cyclooxygenase-2 in skeletal muscle from wild-type mice and adiponectin-transgenic mice.

<p>mRNA levels of the Wnt ligand family (A), Frizzled receptors (B), and the cyclooxygenase-2 gene (C) in skeletal muscle from adiponectin-transgenic mice shown as ratios to those of wild-type C57BL/6 mice at the age of 20 weeks (n = 4, each). Means and SD. *p<0.05, **p<0.01 vs. wild-type mice.</p

Analysis of the Wnt ligand family and their receptors in adipose tissue from wild-type mice and adiponectin-transgenic mice.

<p>mRNA levels of the Wnt ligand family (A), Frizzled receptors (B), non-Fzd Wnt receptors (C) and coreceptors (D) in adipose tissue from line 11 (closed bars) and line 13 (open bars) of male adiponectin-transgenic mice. Data are shown as ratios to wild-type C57BL/6 mice at the age of 20 weeks (n = 6–10, for each group). mRNA levels were determined by quantitative real-time RT-PCR and normalized to <i>Gapdh</i> mRNA. Means and SD, *p<0.05, **p<0.01 vs. wild-type mice.</p

Analysis of the non-canonical Wnt signaling pathway in adipose tissue from wild-type mice and line 11 (closed bars) and line 13 (open bars) of transgenic mice at the age of 20 weeks.

<p>(A) Expression of <i>RhoA</i> in adiponectin-transgenic mice shown as a ratio to that in wild-type mice (n = 6–10, for each group). Western blot analysis of total and phosphorylated CaMKII (B) and the relative protein levels of p-CaMKII (C) in transgenic mice compared with wild-type mice (n = 5, each). Western blot analysis of total and phosphorylated JNK (D) and the relative protein levels of p-JNK (E) in transgenic mice compared with wild-type mice (n = 4, each). Means and SD, *p<0.01 vs. wild-type mice.</p

Effects of adiponectin on Wnt signaling components of 3T3-L1 cells.

<p>mRNA levels of the Wnt ligand family (A), Wnt receptors (B), and Fabp4 (C) in 3T3-L1 cells cultured with 50 (open bars), 150 (dotted bars), and 300 µg/ml (closed bars) of adiponectin shown as ratios to those of 3T3-L1 cells without adiponectin supplementation (n = 3, each). Means and SD. *p<0.05, **p<0.01. Protein levels of total and phosphorylated forms of CaMKII (D) and JNK (H) and relative protein levels of p-CaMKII (E, F, G) and p-JNK (I, J, K) in 3T3-L1 cells incubated with Wnt5a (open bars), Wnt5a and 50 (E, I), 150 (F, J), or 300 µg/ml (G, K) of adiponectin (dotted bars), or 50 (E, I), 150 (F, J), or 300 µg/ml (G, K) of adiponectin alone (hatched bars) compared with non-treated 3T3-L1 cells. The dose-response experiments were carried out independently at each concentration. Western blot analyses were performed twice with essentially the same results. Dots indicate individual data points (E, F, G, I, J, K). Ad, adiponectin.</p