Enterobacter cloacae infection of the shoulder in a 52-year-old woman without apparent predisposing risk factor: a case report and literature review.

BACKGROUND: Enterobacter cloacae (E. cloacae) is one of the commensal flora in the human intestinal tract and a prevalent nosocomial pathogen, which rarely causes infectious osteoarthritis in immunocompetent patients without recent trauma or surgery. Here, we report the first case of septic monoarthritis of the shoulder caused by E. cloacae in an immunocompetent patient. CASE PRESENTATION: A 52-year-old female with a 6-year history of right shoulder pain was referred to our emergency department due to fever, acute severe shoulder pain, and swelling. Blood test showed elevated inflammatory markers. The patient denied any recent invasive surgical procedure and trauma. She was misdiagnosed with a frozen shoulder, and the anti-inflammatory painkiller celecoxib for symptomatic treatment was ineffective. Magnetic resonance imaging (MRI) showed a shoulder joint abscess and supraspinatus tendon tear. The joint aspirate culture showed E. cloacae. After late diagnosis, she was treated with levofloxacin and underwent surgical debridement and irrigation. Her follow-up data revealed that she did not suffer from shoulder swelling and severe pain. CONCLUSION: This is a rare case of E. cloacae infected arthritis of the shoulder in an immunocompetent patient with a rotator cuff tear, indicating that even if the symptoms and age of the patients match the characteristics of frozen shoulder, the possibility of septic arthritis should be considered in the presence of fever and increasing inflammatory markers. The cases of our literature review suggest that the patients subjected to invasive procedure may develop a subsequent E. cloacae osteoarticular infection, regardless of being asymptomatic after the procedure.

Semaphorin 4A acts in a feed-forward loop with NF-κB pathway to exacerbate catabolic effect of IL-1ß on chondrocytes.

Inflammation is fundamental in osteoarthritis (OA) pathogenesis. Semaphorin 4A (Sema4A) has been implicated in immune-associated diseases, however, its role in OA remains unclear. In this study, we show that Sema4A is upregulated in knee OA articular cartilage as well as in chondrocytes exposed to IL-1ß treatment in vitro. Moreover, IL-1ß-induced Sema4A upregulation is abrogated in the presence of BAY 11-7082, a specific inhibitor of NF-κB pathway, suggesting that the activation of NF-κB is required for Sema4A upregulation under this pathological condition. Intriguingly, Sema4A in turn activates NF-κB through facilitating Rac1/AKT-dependent IκBα phosphorylation and subsequent degradation. Functionally, Sema4A aggravates the catabolic effect of IL-1ß on chondrocytes, which can be largely attributed to exacerbated NF-κB activation, since NF-κB inhibition remarkably abolishes this effect. In conclusion, our study suggests that Sema4A is a novel regulator of NF-κB-dependent catabolic events in chondrocytes, which may underlie OA pathogenesis.