ABSTRACT
The anaerobic Gram-positive bacterium Propionibacterium avidum is a common inhabitant of the skin with low pathogenicity. We report a case of P. avidum sacroilitis, psoas abscess and osteomyelitis in a 67-year-old male who had recently undergone surgical repair of an inguinal hernia. The organism was recovered from blood cultures, a bone biopsy specimen and specimens from the abscess. The spectrum of bone and joint infections caused by Propionibacterium is discussed. Infection by Propionibacterium spp. should be considered in patients with bone and joint infections.
Subject(s)
Arthritis/microbiology , Gram-Positive Bacterial Infections/microbiology , Osteomyelitis/microbiology , Propionibacterium/isolation & purification , Psoas Abscess/microbiology , Sacroiliac Joint/microbiology , Surgical Wound Infection/microbiology , Aged , Anti-Bacterial Agents/administration & dosage , Anti-Bacterial Agents/therapeutic use , Arthritis/diagnosis , Arthritis/etiology , Biopsy, Needle , Diagnosis, Differential , Gram-Positive Bacterial Infections/diagnosis , Gram-Positive Bacterial Infections/drug therapy , Hernia, Inguinal/surgery , Humans , Male , Osteomyelitis/diagnosis , Psoas Abscess/diagnosis , Psoas Abscess/drug therapy , Radionuclide Imaging , Sacroiliac Joint/diagnostic imaging , Surgical Wound Infection/diagnosis , Surgical Wound Infection/drug therapy , Tomography, X-Ray ComputedABSTRACT
The common leukocyte antigen CD45 plays a central role in T cell activation in coupling the T cell receptor (TCR) to the phosphatidylinositol pathway via interactions with TCR-associated protein tyrosine kinases lck and fyn. We here demonstrate that engagement of CD45 by monoclonal antibodies (mAb) on activated T cells induces tumor necrosis factor (TNF)-alpha as well as TNF-beta, interleukin (IL)-2 and IL-3 gene expression. When human alloreactive T cells are stimulated with mAb 4B2, which recognizes a determinant common to all CD45 isoforms, a vigorous production of TNF-alpha mRNA was detected, which peaked 2 h later. Anti-CD45 mAb cross-linking was required. In contrast, neither mAb 10G10, which recognizes an epitope distinct from the one recognized by mAb 4B2, nor mAb UCHL-1, a CD45RO-specific antibody, induced any significant increase in TNF-alpha transcription. Nuclear run-on transcription assays demonstrated that CD45 cross-linking caused transcriptional activation of the TNF-alpha gene. De novo protein synthesis was not required, since incubation with cycloheximide (CHX) did not block transcriptional activation. CHX in contrast up-regulated TNF-alpha gene expression and increased transcript half-life, an effect that was under control of post-transcriptional mechanisms. Engagement of CD45 by itself did not affect transcript stability. CD45 ligation resulted in TNF-alpha secretion. These results indicate that in addition to its role in TCR/CD3-mediated T cell activation, CD45, in an epitope-specific manner, may act as a primary signaling molecule, leading to the transcriptional regulation and secretion of a major pro-inflammatory cytokine.
