Bronchial asthma and Chlamydia pneumoniae antibodies in children aged 4-8 years in Olomouc district.

BACKGROUND: Although several studies have demonstrated an association between infection with Chlamydia pneumoniae and asthma, these were mainly limited to exacerbation of symptoms in adults with known asthma OBJECTIVE: We investigated the role of C. pneumoniae infection in 149 atopic children with chronic cough and asthma, comparing them with 241 control non-atopic subjects presenting at Olomouc hospital between 1999 and 2003 with non-specific symptoms (temperature above normal (subfebrile), abdominal pain, arthralgia, and other symptoms. METHODS: The levels of C. pneumoniae-specific antibodies were measured using Chlamydien-rELISA kits (Medac, Hamburg, Germany). RESULTS: In a group of 83 atopic children with chronic cough, IgM and IgG antibodies to C. pneumoniae were demonstrated in 20 children (24 %). Among children with bronchial asthma, positive antibody was present in 29 children (44 %; /p = 0,052/); of this number, 24 (36 %; /p = 0,06/) had IgM and IgG antibodies while 5 children (8 %) had IgA and IgG antibodies against C. pneumoniae. A group of non-atopic children with non-specific symptoms included 38 children (16 %) with antibody positivity; 27 children (11 %) with IgM and IgG antibodies and 11 children (5 %) with IgA and IgG antibodies against C. pneumoniae. CONCLUSIONS: Asthma in children was associated with elevated levels of IgM and IgG antibodies to C. pneumoniae.

Monocyte chemoattractant protein-1 in patients with peripheral arterial disease.

BACKGROUND: Chemokine-driven migration of inflammatory cells has been implicated in the pathogenesis of atherosclerotic conditions including peripheral arterial disease (PAD). Monocyte chemoattractant protein-1 (MCP-1) is elevated in patients with coronary artery disease and in hypertensive patients. This study therefore investigated MCP-1 in patients with PAD. METHODS: Serum MCP-1 was determined by enzyme-linked immunosorbent assay in 36 healthy, control subjects and in 19 patients with PAD. Statistical analysis utilised the Mann-Whitney test and Spearman correlation (p < 0.05). RESULTS: MCP-1 (pg/ml) was increased in patients compared with in controls (mean+/-standard error of the mean: PAD group, 748+/-60; control group, 459+/-27; p=0.0001). MCP-1 levels tended to decrease with progressing disease. From atherosclerosis risk factors, diabetes inclined to increase MCP-1 levels; hypertension had no effect. Serum MCP-1 correlated with cholesterol, triglycerides, low-density lipoprotein but not high-density lipoprotein. CONCLUSION: Elevation of MCP-1 in the circulation of PAD patients shown in the present pilot study implicates this CC chemokine ligand 2 in inflammatory processes contributing to PAD clinical symptomatology. Further investigations are necessary to evaluate whether MCP-1 can be used as a potential marker of peripheral arterial disease follow-up and/or prognosis.

Expression of macrophage inflammatory protein-3 beta/CCL19 in pulmonary sarcoidosis.

In this study, messenger RNA (mRNA) expression for novel T lymphocyte chemoattractants, leukotactin-1, macrophage inflammatory protein (MIP)-3 alpha and MIP-3 beta was investigated in bronchoalveolar lavage fluid (BALF) cells from patients with sarcoidosis, a T cell-mediated disease with typical CD4+ lymphocyte alveolitis. Of these three chemokines, only MIP-3 beta mRNA was upregulated in sarcoidosis, and therefore, protein levels of this chemokine, its pharmacologic regulation, and association with disease clinical course were explored. MIP-3 beta protein concentrations were elevated in BALF from sarcoid patients compared with control subjects (p = 0.001) and in patients with chest X-ray stage II chemokine protein levels were increased compared with stage I (p = 0.003). MIP-3 beta protein was associated predominantly with alveolar macrophages and correlated with BALF lymphocytes and T cell subsets. mRNA expression for the MIP-3 beta receptor, CC chemokine receptor 7, was increased in sarcoidosis and correlated with MIP-3 beta protein levels. MIP-3 beta mRNA and protein expression in BALF cells was suppressed by dexamethasone and cyclosporine A in vitro. In conclusion, MIP-3 beta is implicated in T lymphocyte recruitment in sarcoidosis, is associated with disease progression, and is downregulated by drugs used for sarcoidosis treatment. This novel chemokine, therefore, represents a candidate for studies of sarcoidosis pathobiologic mechanisms.