Septic arthritis caused by Haemophilus influenzae associated with endocarditis.

Septic arthritis with Haemophilus influenzae is infrequent in adults and often associated with an extra-articular septic focus. We report the case of a septic arthritis caused by H. influenzae in an elderly (89-year-old) female patient in whom an transoesophageal echocardiogram showed an aortic valve endocarditis.

Metal fume fever.

Metal fume fever (MFF) is an acute self-limited, flu-like illness resulting from inhalation of metal oxides. Despite the well-documented history of MFF in the medical literature, the illness may remain unrecognized because it may mimic a viral illness. The case of a patient with MFF due to galvanized steel welding presenting to the emergency room is described.

Alveolar macrophage interleukin (IL)-10 and IL-12 production in atopic asthma.

Inflammation in asthma is characterized by a Th2 response. In many experimental systems, this response can be regulated by interleukin (IL)-10 and IL-12. IL-10 deactivates T cells, and IL-12 reorients the response toward a Th1 pattern. Alveolar macrophages (AM) can secrete both of these cytokines, and thus regulate T-cell behavior in asthma. They can enhance the Th2 response by turning off their secretion of IL-10 and IL-12, or tend to downregulate it by producing these cytokines. To elucidate that point, we assayed the AM IL-10 and IL-12 from 11 asthmatic patients and four controls. Six asthmatics were treated by inhaled corticosteroids. AM were recovered by bronchoalveolar lavage (BAL). They were isolated and cultured for 24 h without stimulation or in the presence of lipopolysaccharide (LPS). IL-10 and the p40 subunit of IL-12 were assayed in the BAL fluid and in AM culture supernatants by ELISA. Spontaneous AM IL-10 production was higher in asthmatics, particularly in the treated group. The AM IL-10 production after stimulation by LPS was also elevated in asthmatics, but was mainly so in untreated patients. IL-12 levels were higher in BAL fluids from untreated patients than from controls. The IL-12 production of LPS-stimulated-AM from these patients was increased. These results show that AM are at least primed for the production of IL-10 and IL-12 in asthma, and suggest that these cells could be involved in the resolution of the asthmatic inflammation.

Altered compartmentalization of transforming growth factor-beta in asthmatic airways.

BACKGROUND: Asthma is characterized by alterations of the bronchial epithelium associated with inflammatory cell infiltrates and sub-epithelial fibrosis. Transforming Growth Factor-beta (TGF-beta) is an anti-inflammatory and fibrosing cytokine normally present in bronchial epithelial cells and also potentially produced by inflammatory cells. Thus, TGF-beta could play a role in the asthmatic process, and its expression could be modified in asthmatic airways. OBJECTIVE: To test this latter hypothesis, we studied the bronchial distribution of TGF-beta in asthmatic patients. METHODS: TGF-beta 1, 2, 3 distribution was studied by immunohistochemistry in bronchial biopsies from 12 asthmatic patients and 10 non-asthmatic subjects. RESULTS: Bronchial epithelial cells from asthmatics were negative or faintly positive while a bright staining was detected in these from non-asthmatics (P < 0.01). In both groups, when inflammatory cells were present beneath the basement membrane, they were stained by the anti-TGF-beta antibody. CONCLUSION: This study shows an altered compartimentalization of TGF-beta in asthma. (a) TGF-beta is scarse in asthmatic bronchial epithelial cells, which could favour the perennization of the bronchial inflammation, and (b) TGF-beta is present in inflammatory cells beneath the basement membrane, where it could be involved in the frequent sub-epithelial fibrosis.